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Chi Zhou

  • Assistant Professor, Animal and Comparative Biomedical Sciences
Contact
  • (520) 621-2457
  • William J. Parker Agricultural, Rm. N109
  • Tucson, AZ 85721
  • chizhou@email.arizona.edu
  • Bio
  • Interests
  • Courses
  • Scholarly Contributions

Biography

Chi Zhou, Ph.D.

Lab website: https://chizhou.lab.arizona.edu/

Positions:

2020 - current   Assistant Professor of Physiology
, School of Animal and Comparative Biomedical Sciences, the University of Arizona, Tucson, AZ, USA.

2019 - 2020       Assistant Scientist (Research Assistant Professor), Perinatal Research Lab, Department of Ob/Gyn, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.

2014 - 2019       Postdoctoral Fellow (Reproductive Physiology),  Perinatal Research Lab, Department of Ob/Gyn, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.

Teaching experiences:

2019 -2020        Co-Lecturer in a graduate-level course Obstetrics/Gynecology 710 “Reproductive Endocrine Physiology”, University of Wisconsin-Madison, Madison, WI, USA.

2016 - 2018       Co-Lecturer in a graduate-level course ERP875 “Endocrine Physiology”, University of Wisconsin-Madison, Madison, WI, USA.

Honors:

2019-2022        American Heart Association (AHA), Career Development Award, USA.

2019                  Outstanding Paper by an Associate Member Award, Perinatal Research Society (PRS), Brooklyn Park, MN, USA.

2019                  SRI NIH Travel Grant Award, Society for Reproductive Investigation (SRI), Paris, France.

2017-2018         American Heart Association (AHA), Postdoctoral Fellowship, USA.

2016                  Young Investigator Award, Perinatal Research Society (PRS), Itasca, IL, USA.

Invited Lectures/Seminars:

2020 Mar.          Vascular Biology Research Colloquium, Cardiovascular Research Center, UW-Madison, WI.

2020 Jan.           Department of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD.

2019 Nov.          Animal and Avian Sciences Department, University of Maryland, College Park, MD.

2019 Nov.          Department of Physiology, College of Medicine, University of Florida, FL.

2019 Sept.         Basic biomedical Science, Sanford School of Medicine, University of South Dakota, SD.

2019 Sept.         School of Animal and Comparative Biomedical Sciences, University of Arizona, AZ.

2019 Aug.          Institute for Genomic Medicine, Nationwide Children’s Hospital, OH.

2019 Aug.          Department of Obstetrics and Gynecology, NorthShore University Health System, University of Chicago Pritzker School of Medicine, IL.

2019 April.        Animal Reproduction & Biotechnology Laboratory, Department of Biomedical Science, Colorado State University, CO.

2019 Jan.           Vascular Biology Research Colloquium, Cardiovascular Research Center, UW-Madison, WI.

2017 Nov.          Vascular Biology Research Colloquium, Cardiovascular Research Center, UW-Madison, WI.

Scientific membership:

2016-current:   Perinatal Research Society.

2015-current:   Society for Reproductive Investigation.

2015-current:   American Heart Association.

2013-current:   Society for the Study of Reproduction.

Professional service:

2019 Nov.          Abstracts Reviewer for the 67th annual scientific meeting of the Society for Reproductive Investigation (SRI), Vancouver, Canada.

2019 Mar.          Poster Judge for the 66th annual scientific meeting of the Society for Reproductive Investigation (SRI), Paris, France.

2018 Nov.          Abstracts Reviewer for the 66th annual scientific meeting of the Society for Reproductive Investigation (SRI), Paris, France.

2018 Mar.          Modulator of the “Preeclampsia II” scientific session at the 65th annual Scientific meeting of the Society for Reproductive Investigation (SRI), San Diego, CA, USA.

2016 Nov.          Abstracts Reviewer for the 64th annual Scientific meeting of the Society for Reproductive Investigation (SRI), Orlando, FL, USA.

Journal reviewer:

Biology of Reproduction; Journal of Cellular Physiology, Journal of Clinical Medicine; Nutrients; Medicina; International Immunopharmacology; International Journal of Molecular Sciences; International Journal of Environmental Research and Public Health; Experimental and Molecular Pathology; Cells; Biomolecules; Reproductive Sciences; Scientific Reports

Full list of Peer-Reviewed Publications (https://www.ncbi.nlm.nih.gov/myncbi/1TmkW4baZzbkC/bibliography/public):

Book Edited:

  1. Jing Zheng, PhD., and Chi Zhou, Ph.D. (Editors). Hypoxia and Human Diseases. Intech - Open Access Publisher, 2017. DOI: 10.5772/62960 (https://www.intechopen.com/books/hypoxia-and-human-diseases).

Electronic Publications:

  1. Zhou C, Zheng J. 2018. Sexual dimorphisms of preeclampsia-dysregulated transcriptomic profiles and endothelial function in fetal endothelial cells. NCBI Gene Expression Omnibus (GEO) Data Series # GSE116428 (contain 27 datasets). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116428
  2. Tsoi S, Zhou C. Agilent-031068 EmbryoGene Porcine Array V.1 (EMPV1; Probe Name version). NCBI Gene Expression Omnibus (GEO) Platform # GPL18148.
  3. Zhou C. Gene expression profile changes during blastocysts hatching of embryos produced from parthenogenesis and in vivo. NCBI Gene Expression Omnibus (GEO) Data Series # GSE48290 (contain 12 datasets).
  4. Zhou C. Comparison of hatched blastocyst derived from in vivo (IVV), parthenogenetic activation (PA), and chromatin transfer (CT). NCBI Gene Expression Omnibus (GEO) Data Series # GSE48291 (contain 9 datasets).
  5. Zhou C. Gene expression profile changes during blastocysts hatching of embryos. NCBI Gene Expression Omnibus (GEO) Data Series # GSE48292 (contain 21 datasets).
  6. Tsoi S, Zhou C. Agilent-031068 EmbryoGene Porcine Array Version 1 (EMPV1) [Probe version]. NCBI Gene Expression Omnibus (GEO) Platform # GPL17779.
  7. Tsoi S, Zhou C. Agilent-031068 EmbryoGene Porcine Array Version 1 (EMPV1). NCBI Gene Expression Omnibus (GEO) Platform # GPL14925.
  8. Zhou C. EMPV1 technical repeat. NCBI Gene Expression Omnibus (GEO) Data Series # GSE34157 (contain 1 dataset).

Abstracts, Posters, and Presentations in Conferences:

  1. Chi Zhou, Qin Yan, Xin-wen Chang, Ronald R. Magness, Ian M. Bir1, and Jing Zheng. Preeclampsia differentially dysregulates female and male fetal endothelial function: roles of miR29a/c. Abstract and Poster in “52nd annual scientific meeting of the Society of the Study of Reproduction (SSR)”, San Jose, CA, USA July. 18-21, 2019.
  2. Chi Zhou, Qin Yan, Xin-Wen Chang, Ronald R. Magness, Ian M. Bird, and Jing Zheng. Preeclampsia differentially dysregulates transcriptomic profiles and function in female and male fetal endothelial cells. Abstract and Poster in the “66th annual scientific meeting of the Society for Reproductive Investigation (SRI)”, Paris, France, Mar. 12-16, 2019.
  3. Chi Zhou, Yan Qin, Qing-Yun Zou, Chanel Tyler, Xin-Qi Zhong, Ronald R. Magness, Ian M. Bird, and Jing Zheng. Sexual dimorphism of preeclampsia-dysregulated transcriptomic profiles and endothelial function in fetal endothelial cells. Abstract and Oral presentation in “51st Annual Scientific Meeting of the Society for the Study of Reproduction” New Orleans, Louisiana, July 10-13, 2018.
  4. Chi Zhou, Yan Qin, Qing-Yun Zou, Chanel T. Tyler, Xing-qi Zhong, Ronald R. Magness, and Jing Zheng. Preeclampsia dysregulates endothelial function-associated genes/pathways in fetal endothelial cells. Abstract and Poster in “Society for Reproductive Investigation 65th Annual Scientific Meeting” San Diego, CA, Mar. 6-10, 2018.
  5. Chi Zhou, Qing-Yun, Ronald R. Magness, and Jing Zheng. Preeclampsia dysregulates genes associated with cellular responses to cytokine/chemokine stimulus in male fetal endothelial cells. Abstract and Poster in “50th Annual Scientific Meeting of the Society for the Study of Reproduction” Washington D.C., July 13-16, 2017.
  6. Chi Zhou, Qing-Yun Zou, Ai-Xia Liu, Rui-Fang Wang, Ronald R. Magness, and Jing Zheng. Preeclampsia downregulates microRNAs in fetal endothelial cells: Roles of miR-29a/c-3p in endothelial function. Abstract and Poster in “Society for Reproductive Investigation 64th Annual Scientific Meeting” Orlando, USA, March 15-18, 2017.
  7. Chi Zhou, Rui-fang Wang, Qing-Yun Zou, Ronald R. Magness, and Jing Zheng. Identification of a novel association between mir-29a/c and preeclampsia in human fetal endothelial cells. Abstract and Poster in “Society for Reproductive Investigation 63rd Annual Scientific Meeting” Montreal, Canada, March16-19, 2016.
  8. Chi Zhou, Yan Li, Ronald R. Magness, Jing Zheng. Altered transcriptional regulation of CYP1A1 and AhR in human placentas from preterm birth. Abstract and Poster in “Society for Reproductive Investigation 62nd Annual Scientific Meeting” San Francisco, USA, March 25-28, 2015.
  9. Chi Zhou, Stephen Tsoi, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. Gene expression profiling of in vivo-derived female and male day 11 embryos. Poster in the “4th Embryo Genomics Meeting” Quebec City, Canada, October 9-11, 2013.
  10. Chi Zhou, Stephen Tsoi, Walter Dixon, George Foxcroft, Michael Dyck. Stage-specific gene expression profile differences during early porcine embryonic development, Abstract, and Poster in “Reproductive Health: Nano to Global” SSR's 46th Annual Meeting, Montreal, Quebec, Canada, July 21-26, 2013.
  11. Chi Zhou, Stephen Tsoi, Walter Dixon, George Foxcroft, Michael Dyck. Comparative transcriptomic analyses between in vivo derived porcine 4-cell and morula embryos. Oral presentation in the “9th International Conference on Pig Reproduction (ICPR)”, Olsztyn, Poland, June 9 - 12, 2013.
  12. Chi Zhou, Stephen Tsoi, Walter Dixon, George Foxcroft, Michael Dyck. Stage-specific gene expression profile differences during early porcine embryonic development, Abstract, and Poster in “Applied Reproductive Biology: Making It Relevant” SSR's 45th Annual Meeting, The Pennsylvania State University State College, Pennsylvania, August 12-15, 2012.
  13. Chi Zhou, Stephen Tsoi, Walter Dixon, George Foxcroft, Michael Dyck. Comparative gene expression profiling of in vivo derived early porcine embryos from different stages, Abstract, Poster and Oral presentation in “Symposium on Functional Genomics of Early Livestock Development” Banff, Canada, July 24 -26, 2012.
  14. Chi Zhou, Stephen Tsoi, Walter Dixon, George Foxcroft, Michael Dyck. Gene expression profile analysis of early porcine embryos, Oral presentation in “EmbryoGENE Annual General Meeting” Banff, Canada, July 23-24, 2012.
  15. Chi Zhou, Stephen Tsoi, Walter Dixon, George Foxcroft, Michael Dyck. Verification of a porcine embryo-specific microarray platform. Abstract, Poster and Oral presentation “Banff Pork Seminar”, Banff, AB, Canada, January 17 -20, 2012.
  16. Chi Zhou, Stephen Tsoi, Walter Dixon, George Foxcroft, Michael Dyck. Comparative transcriptomic analysis of in vivo-derived early porcine embryos from 4 different developmental stages. Abstract and Poster in “International Plant and Animal Genome XX Conference”, San Diego, California, United States, January 14-18, 2012.
  17. Chi Zhou, Stephen Tsoi, Audrey Cameron, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. Transcriptomic effect of porcine luteinizing hormone (pLH) Induced ovulation on blastocyst stage porcine embryos. Poster in 3rd Embryo Genomics Meeting, Bonn, Germany, September 20-22, 2011.
  18. Chi Zhou, Stephen Tsoi, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. Identification and Characterization of Novel Genes from Blastocyst-Stage Porcine Embryos Using 454 Sequencing. Abstract and Poster in “Reproduction and the World’s Future” 44th Annual Meeting of the Society for the Study of Reproduction, Portland, Oregon, United States, July 31-August 4, 2011.
  19. Chi Zhou, Stephen Tsoi, Audrey Cameron, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. Gene expression profiling of blastocyst stage embryos from porcine luteinizing hormone (pLH) treated gilts. Abstract, Poster and Oral presentation in “EmbryoGENE Annual General Meeting” Quebec City, Quebec, Canada, June 7-9, 2011.
  20. Chi Zhou, Stephen Tsoi, Jason Grant, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. Characterization of unknown expression sequence tags (ESTs) from porcine blastocyst stage embryos using 454 sequencing. Abstract, Poster and Oral presentation in “Banff Pork Seminar”, Banff, AB, Canada, January 18 -21, 2011.
  21. Chi Zhou, Stephen Tsoi, Susan Novak, Jason Grant, Walter Dixon, George Foxcroft, Michael Dyck. Comparative gene expression profiling of in vivo-derived expanded and hatched porcine blastocyst-stage embryos. Abstract and Poster “The Intersection Between Genetics, Genomics, and Reproductive Biology”43rd Annual Meeting of the Society for the Study of Reproduction, Milwaukee, Wisconsin, United States, July 30-August 3, 2010.
  22. Chi Zhou, John Dobrinsky, Stephen Tsoi, Walter Dixon, George Foxcroft, M.K. Dyck. Gene expression profiling of ART derived pre-implantation porcine embryos. Poster and Oral presentation “EmbryoGENE Annual General Meeting”, Edmonton, Canada, June 14 - 17, 2010.
  23. Chi Zhou, Stephen Tsoi, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. Validation of reference genes for relative real-time quantitative PCR analysis with porcine embryos. Abstract and Poster “AICLGT AGM 2010: Genomics and Livestock Quality Improvement: Bringing It All Together"- Calgary, AB, Canada, May 11 -13, 2010.
  24. Chi Zhou, Susan Novak, Stephen Tsoi, Jason Grant, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. Gene expression profiling of the porcine blastocyst stage embryo. Abstract, Poster and Oral presentation in the “Banff Pork Seminar”, Banff, AB, Canada, January 19 -22, 2010.
  25. Stephen Tsoi, Chi Zhou, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. The porcine blastocyst transcriptome generated from 454-sequencing platform. Abstract and Poster in “International Plant and Animal Genome XVIII Conference”, San Diego, California, United States, January 9-13, 2010.
  26. Chi Zhou, Stephen Tsoi, Walter T. Dixon, George R. Foxcroft, Michael K. Dyck. Real-time quantitative PCR analysis of gene expression in a single pre-implantation porcine embryo. Abstract and Poster in “Alberta Bovine Genomics AGM 2009: Enabling Protein Value Chains"- Edmonton, AB, Canada, April 29 -30, 2009.
  27. Chi Zhou, Chun-hou Li, Wei-min Zhang, Xiao-ping Jia. Quantitative PCR analysis of CYP4 gene expression in PCB1254 treated green mussel (Perna viridis Linnaeus). Abstract and Oral presentation in 2007 Forum on Fishery Science and Technology, Qingdao, China, October 22-25, 2007(Collection of Abstracts of Forum on Fishery Science and Technology·2007:112).

Degrees

  • Ph.D. Animal Science/Reproductive Physiology
    • University of Alberta, Edmonton, Canada
    • Comparative gene expression profiling of early porcine embryos generated from different assisted reproductive technology systems

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Interests

Teaching

Reproductive Physiology

Research

Pregnancy Complications, Placental Biology, Fetal Endothelial Function, Sexual Dimorphisms of Fetal Endothelial/Vascular Programming, Preeclampsia, Obesity

Courses

2020-21 Courses

  • Directed Research
    ACBS 492 (Spring 2021)
  • Independent Study
    ACBS 399 (Winter 2020)
  • Honors Independent Study
    PSIO 399H (Fall 2020)

Related Links

UA Course Catalog

Scholarly Contributions

Journals/Publications

  • Li, Y., Zhou, C., Lei, W., Wang, K., & Zheng, J. (2020). Roles of Aryl Hydrocarbon Receptor in Endothelial Angiogenic Responses†. Biology of reproduction.
    More info
    Aryl hydrocarbon receptor (AhR) is a transcription factor, which can be activated by a plethora of structure-diverse ligands. Historically, AhR is known for its involvements in regulation of metabolism of xenobiotics. However, normal physiological roles of AhR have been defined in other essential biological processes, including vascular growth and function, reproduction, and immunoresponses. In contrast, aberrant expression and activation of the AhR signaling pathway occur in a variety of human diseases, many of which (e.g., preeclampsia, atherosclerosis, and hypertension) could be associated with endothelial dysfunction. Indeed, emerging evidence has shown that either exogenous or endogenous AhR ligands can induce endothelial dysfunction in either an AhR dependent or independent manner, possibly reliant on the blood vessel origin (artery and vein) of endothelial cells. Given that the AhR signaling pathway has the broader impacts on endothelial and cardiovascular function, AhR ligands, AhR, and their downstream genes could be considered novel therapeutic targets for those endothelial related-diseases. This review will discuss the current knowledge of AhR's mediation on endothelial function and potential mechanisms underlying these actions with a focus on placental endothelial cells.
  • Zhou, C., Zou, Q. Y., Jiang, Y. Z., & Zheng, J. (2020). Role of oxygen in fetoplacental endothelial responses: hypoxia, physiological normoxia, or hyperoxia?. American journal of physiology. Cell physiology, 318(5), C943-C953.
    More info
    During pregnancy, placental vascular growth, which is essential for supporting the rapidly growing fetus, is associated with marked elevations in blood flow. These vascular changes take place under chronic physiological low O (less than 2-8% O in human; chronic physiological normoxia, CPN) throughout pregnancy. O level below CPN pertinent to the placenta results in placental hypoxia. Such hypoxia can cause severe endothelial dysfunction, which is associated with adverse pregnancy outcomes (e.g., preeclampsia) and high risk of adult-onset cardiovascular diseases in children born to these pregnancy complications. However, our current knowledge about the mechanisms underlying fetoplacental endothelial function is derived primarily from cell models established under atmospheric O (~21% O at sea level, hyperoxia). Recent evidence has shown that fetoplacental endothelial cells cultured under CPN have distinct gene expression profiles and cellular responses compared with cells cultured under chronic hyperoxia. These data indicate the critical roles of CPN in programming fetal endothelial function and prompt us to re-examine the mechanisms governing fetoplacental endothelial function under CPN. Better understanding these mechanisms will facilitate us to develop preventive and therapeutic strategies for endothelial dysfunction-associated diseases (e.g., preeclampsia). This review will provide a brief summary on the impacts of CPN on endothelial function and its underlying mechanisms with a focus on fetoplacental endothelial cells.
  • Zhou, C., Yan, Q., Zou, Q. Y., Zhong, X. Q., Tyler, C. T., Magness, R. R., Bird, I. M., & Zheng, J. (2019). Sexual Dimorphisms of Preeclampsia-Dysregulated Transcriptomic Profiles and Cell Function in Fetal Endothelial Cells. Hypertension, 74(1), 154-163.
    More info
    Preeclampsia impairs fetoplacental vascular function and increases risks of adult-onset cardiovascular disorders in children born to preeclamptic mothers, implicating that preeclampsia programs fetal vasculature in utero. However, the underlying mechanisms remain elusive. We hypothesize that preeclampsia alters fetal endothelial gene expression and disturbs cytokines- and growth factors-induced endothelial responses. RNA sequencing analysis was performed on unpassaged human umbilical vein endothelial cells (HUVECs) from normotensive and preeclamptic pregnancies. Functional assays for endothelial monolayer integrity, proliferation, and migration were conducted on passage 1 HUVECs from normotensive and preeclamptic pregnancies. Compared with normotensive cells, 926 and 172 genes were dysregulated in unpassaged female and male HUVECs from preeclamptic pregnancies, respectively. Many of these preeclampsia-dysregulated genes are associated with cardiovascular diseases (eg, heart failure) and endothelial function (eg, cell migration, calcium signaling, and endothelial nitric oxide synthase signaling). TNF (tumor necrosis factor)-α-, TGF (transforming growth factor)-β1-, FGF (fibroblast growth factor)-2-, and VEGFA (vascular endothelial growth factor A)-regulated gene networks were differentially disrupted in unpassaged female and male HUVECs from preeclamptic pregnancies. Moreover, preeclampsia decreased endothelial monolayer integrity in responses to TNF-α in both female and male HUVECs. Preeclampsia decreased TGF-β1-strengthened monolayer integrity in female HUVECs, whereas it enhanced FGF-2-strengthened monolayer integrity in male HUVECs. Preeclampsia promoted TNF-α-, TGF-β1-, and VEGFA-induced cell proliferation in female, but not in male HUVECs. Preeclampsia inhibited TNF-α-induced cell migration in female HUVECs, but had an opposite effect on male HUVECs. In conclusion, preeclampsia differentially dysregulates cardiovascular diseases- and endothelial function-associated genes/pathways in female and male fetal endothelial cells in association with the sexual dimorphisms of preeclampsia-dysregulated fetal endothelial function.
  • Zou, Q. Y., Zhao, Y. J., Zhou, C., Liu, A. X., Zhong, X. Q., Yan, Q., Li, Y., Yi, F. X., Bird, I. M., & Zheng, J. (2019). G Protein α Subunit 14 Mediates Fibroblast Growth Factor 2-Induced Cellular Responses in Human Endothelial Cells. Journal of cellular physiology, 234(7), 10184-10195.
    More info
    During pregnancy, a tremendous increase in fetoplacental angiogenesis is associated with elevated blood flow. Aberrant fetoplacental vascular function may lead to pregnancy complications including pre-eclampsia. Fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor A (VEGFA) are crucial regulators of fetoplacental endothelial function. G protein α subunit 14 (GNA14), a member of Gαq/11 subfamily is involved in mediating hypertensive diseases and tumor vascularization. However, little is known about roles of GNA14 in mediating the FGF2- and VEGFA-induced fetoplacental endothelial function. Using human umbilical vein endothelial cells (HUVECs) cultured under physiological chronic low oxygen (3% O ) as a cell model, we show that transfecting cells with adenovirus carrying GNA14 complementary DNA (cDNA; Ad-GNA14) increases (p 
  • Zou, Q. Y., Zhao, Y. J., Li, H., Wang, X. Z., Liu, A. X., Zhong, X. Q., Yan, Q., Li, Y., Zhou, C., & Zheng, J. (2018). GNA11 differentially mediates fibroblast growth factor 2- and vascular endothelial growth factor A-induced cellular responses in human fetoplacental endothelial cells. The Journal of physiology, 596(12), 2333-2344.
    More info
    Fetoplacental vascular growth is critical to fetal growth. Fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor A (VEGFA) are two major regulators of fetoplacental vascular growth. G protein α subunit 11 (GNA11) transmits signals from many external stimuli to the cellular interior and may mediate endothelial function. It is not known whether GNA11 mediates FGF2- and VEGFA-induced endothelial cell responses under physiological chronic low O . In the present study, we show that knockdown of GNA11 significantly decreases FGF2- and VEGFA-induced fetoplacental endothelial cell migration but not proliferation and permeability. Such decreases in endothelial migration are associated with increased phosphorylation of phospholipase C-β3. The results of the present study suggest differential roles of GNA11 with respect to mediating FGF2- and VEGFA-induced fetoplacental endothelial function.
  • Li, Y., Wang, K., Zou, Q. Y., Jiang, Y. Z., Zhou, C., & Zheng, J. (2017). ITE Suppresses Angiogenic Responses in Human Artery and Vein Endothelial Cells: Differential Roles of AhR. Reproductive toxicology, 74, 181-188.
    More info
    Aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor is involved in regulation of many essential biological processes including vascular development and angiogenesis. 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) is an AhR ligand, which regulates immune responses and cancer cell growth. However, the roles of the ITE/AhR pathway in mediating placental angiogenesis remains elusive. Here, we determined if ITE affected placental angiogenic responses via AhR in human umbilical vein (HUVECs) and artery endothelial (HUAECs) cells in vitro. We observed that ITE dose- and time-dependently inhibited proliferation and viability of HUAECs and HUVECs, whereas it inhibited migration of HUAECs, but not HUVECs. While AhR siRNA significantly suppressed AhR protein expression in HUVECs and HUAECs, it attenuated the ITE-inhibited angiogenic responses of HUAECs, but not HUVECs. Collectively, ITE suppressed angiogenic responses of HUAECs and HUVECs, dependent and independent of AhR, respectively. These data suggest that ITE may regulate placental angiogenesis.
  • Pang, L. P., Li, Y., Zou, Q. Y., Zhou, C., Lei, W., Zheng, J., & Huang, S. A. (2017). ITE inhibits growth of human pulmonary artery endothelial cells. Experimental lung research, 43(8), 283-292.
    More info
    Pulmonary arterial hypertension (PAH), a deadly disorder is associated with excessive growth of human pulmonary artery endothelial (HPAECs) and smooth muscle (HPASMCs) cells. Current therapies primarily aim at promoting vasodilation, which only ameliorates clinical symptoms without a cure. 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) is an endogenous aryl hydrocarbon receptor (AhR) ligand, and mediates many cellular function including cell growth. However, the roles of ITE in human lung endothelial cells remain elusive. Herein, we tested a hypothesis that ITE inhibits growth of human pulmonary artery endothelial cells via AhR.
  • Zhou, C., Zou, Q. Y., Li, H., Wang, R. F., Liu, A. X., Magness, R. R., & Zheng, J. (2017). Preeclampsia Downregulates MicroRNAs in Fetal Endothelial Cells: Roles of miR-29a/c-3p in Endothelial Function. The Journal of clinical endocrinology and metabolism, 102(9), 3470-3479.
    More info
    Preeclampsia is a leading cause of fetal and maternal morbidity and mortality during pregnancy. Although the etiology of preeclampsia is unknown, preeclampsia offspring have increased risks of developing cardiovascular disorders in adulthood, implicating that preeclampsia programs fetal vasculature in utero.
  • Li, Y., Wang, K., Zou, Q. Y., Zhou, C., Magness, R. R., & Zheng, J. (2015). A possible role of aryl hydrocarbon receptor in spontaneous preterm birth. Medical hypotheses, 84(5), 494-7.
    More info
    Preterm birth (PTB) is defined as birth before 37 weeks of gestation and is a leading cause of neonatal mortality and morbidity. To date, the etiology of spontaneous PTB (sPTB) remains unclear; however, intrauterine bacterial infection-induced inflammation is considered to be one of the major triggers. Aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor. Upon activation, AhR signaling mediates many biological processes. AhR is abundantly expressed in human placentas, primarily in trophoblasts, and several fetal organs and tissues. The activation of AhR signaling can modulate inflammatory responses via promoting production of pro-inflammatory cytokines by the placenta and fetal membranes. These cytokines could enhance expression and/or activity of cyclooxygenase-2 (COX2) in human trophoblasts and amniotic epithelia, which in turn stimulate synthesis and release of prostaglandins (PGs; e.g., PGE2 and PGF2α). Given the discovery of a number of natural and endogenous AhR ligands in human, we hypothesize that in a subset of patients with high AhR expression in placentas and fetal membranes, repeated exposure to these AhR ligands hyperactivates AhR, inducing hyperactivation of the cytokines/COX2/PGs pathway, resulting in myometrial contractions, ultimately leading to sPTB. We further hypothesize that hyperactivation of this AhR pathway can induce sPTB either directly or in synergy with the bacterial infection. Proof of this hypothesis may provide a novel mechanism underlying sPTB.
  • Li, Y., Zhao, Y. J., Zou, Q. Y., Zhang, K., Wu, Y. M., Zhou, C., Wang, K., & Zheng, J. (2015). Preeclampsia does not alter vascular growth and expression of CD31 and vascular endothelial cadherin in human placentas. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 63(1), 22-31.
    More info
    Preeclampsia is characterized by maternal endothelial dysfunction (e.g., increased maternal vascular permeability caused by the disassembly of endothelial junction proteins). However, it is unclear if preeclampsia is associated with impaired vascular growth and expression of endothelial junction proteins in human placentas. Herein, we examined vascular growth in placentas from women with normal term (NT) and preeclamptic (PE) pregnancies using two endothelial junction proteins as endothelial markers: CD31 and vascular endothelial-cadherin (VE-Cad). We also compared protein and mRNA expression of CD31 and VE-Cad between NT and PE placentas, and determined the alternatively spliced expression of CD31 using PCR. We found that CD31 and VE-Cad were immunolocalized predominantly in villous endothelial cells. However, capillary number density (total capillary number per unit villous area) and capillary area density (total capillary lumen area per unit villous area) as well as CD31 and VE-Cad protein and mRNA levels were similar between NT and PE placentas. PCR in combination with sequence analysis revealed a single, full-length CD31, suggesting that there are no alternatively spliced isoform of CD31 expressed in placentas. These data indicate that preeclampsia does not significantly affect vascular growth or the expression of endothelial junction proteins in human placentas.
  • Dyck, M. K., Zhou, C., Tsoi, S., Grant, J., Dixon, W. T., & Foxcroft, G. R. (2014). Reproductive technologies and the porcine embryonic transcriptome. Animal reproduction science, 149(1-2), 11-8.
    More info
    The domestic pig is not only an economically-important livestock species, but also an increasingly recognized biomedical animal model due to its physiological similarities with humans. As a result, there is a strong interest in the factors that affect the efficient production of viable embryos and offspring in the pig using either in vivo or in vitro production methods. The application of assisted reproductive technologies (ART) has the potential to increase reproductive efficiency in livestock. These technologies include, but are not limited to: artificial insemination (AI), fixed-time AI, embryo transfer, cryopreservation of sperm/oocytes/embryos, in vitro fertilization and somatic cell nuclear transfer (cloning). However, the application of ART is much less efficient in the pig than in many other mammalian species such as cattle. Until recently, the underlying causes of these inefficiencies have been difficult to study, but advances in molecular biology techniques for studying gene expression have resulted in the availability of a variety of options for gene expression profiling such as microarrays, and next generation sequencing technologies. Capitalizing on these technologies the effects of various ARTs on the porcine embryonic transcriptome has been determined and the impact on the related biological pathways and functions been evaluated. The implications of these results on the efficiency of ARTs in swine, as well potential consequences for the developing embryo and resulting offspring, are reviewed.
  • Zhou, C., Dobrinsky, J., Tsoi, S., Foxcroft, G. R., Dixon, W. T., Stothard, P., Verstegen, J., & Dyck, M. K. (2014). Characterization of the altered gene expression profile in early porcine embryos generated from parthenogenesis and somatic cell chromatin transfer. PloS one, 9(3), e91728.
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    The in vitro production of early porcine embryos is of particular scientific and economic interest. In general, embryos produced from in vitro Assisted Reproductive Technologies (ART) manipulations, such as somatic cell chromatin transfer (CT) and parthenogenetic activation (PA), are less developmentally competent than in vivo-derived embryos. The mechanisms underlying the deficiencies of embryos generated from PA and CT have not been completely understood. To characterize the altered genes and gene networks in embryos generated from CT and PA, comparative transcriptomic analyses of in vivo (IVV) expanded blastocysts (XB), IVV hatched blastocyst (HB), PA XB, PA HB, and CT HB were performed using a custom microarray platform enriched for genes expressed during early embryonic development. Differential expressions of 1492 and 103 genes were identified in PA and CT HB, respectively, in comparison with IVV HB. The "eIF2 signalling", "mitochondrial dysfunction", "regulation of eIF4 and p70S6K signalling", "protein ubiquitination", and "mTOR signalling" pathways were down-regulated in PA HB. Dysregulation of notch signalling-associated genes were observed in both PA and CT HB. TP53 was predicted to be activated in both PA and CT HB, as 136 and 23 regulation targets of TP53 showed significant differential expression in PA and CT HB, respectively, in comparison with IVV HB. In addition, dysregulations of several critical pluripotency, trophoblast development, and implantation-associated genes (NANOG, GATA2, KRT8, LGMN, and DPP4) were observed in PA HB during the blastocyst hatching process. The critical genes that were observed to be dysregulated in CT and PA embryos could be indicative of underlying developmental deficiencies of embryos produced from these technologies.
  • Tsoi, S., Zhou, C., Grant, J. R., Pasternak, J. A., Dobrinsky, J., Rigault, P., Nieminen, J., Sirard, M. A., Robert, C., Foxcroft, G. R., & Dyck, M. K. (2012). Development of a porcine (Sus scofa) embryo-specific microarray: array annotation and validation. BMC genomics, 13, 370.
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    The domestic pig is an important livestock species and there is strong interest in the factors that affect the development of viable embryos and offspring in this species. A limited understanding of the molecular mechanisms involved in early embryonic development has inhibited our ability to fully elucidate these factors. Next generation deep sequencing and microarray technologies are powerful tools for delineation of molecular pathways involved in the developing embryo.

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