Zheng Research Team




The main focus of Dr. Zheng's laboratory is to determine how fetal and placental endothelial function is regulated, particularly during pregnancy complications with ultimate goals to control blood flow to the fetus. This is important as changes in fetal and fetoplacental blood flows are directly correlated with fetal growth and survival as well as neonatal birth weights and survivability. Specifically, the Zheng laboratory is to investigate 1) how pregnancy complications (e.g., preeclampisa) affect gene expression and function of fetoplacental endothelial cells, 2) if these genes and function are associated with risk of adult-onset cardiovascualr diseases, and 3) how locally produced factors (e.g., growth factors) and environmental factors (e.g., dioxin and oxygen) can affect fetal and placental vascular endothelial function as well as what are signaling molecules inside cells involved in. The Zheng laboratory is also interested in investigating mechanisms controlling ovarian cancer growth as well as therapeutic intervention for ovarian cancer and other gynecologic pathologies. Zheng laboratory has/will use state of the art technology to identify genes which are potenetially used as biomarkers/therapeutic tragets for preventing and treating  pregnancy complications-related cardiovascular diseases.  His laboratory has/will aim to  dissect cellular and molecular mechanisms controlling fetal endothelial function, which are poorly understood so far.  


Current Members:

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Jing Zheng

Principal Investigator 

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Past Members:


Role of Endogenous AhR Ligand in Pregnancy

Start Date: 9/1/2019 --- End Date: 8/31/2020

Sponsor: UL1TR002373 (NCATS/NIH)

The goal of this project is to determine the role of AhR ligands in vascular development and function during pregnancy.


Publications:

Li Y, Wang K, Zou QY, Zhou C, Magness RR, Zheng J. A possible role of aryl hydrocarbon receptor in preterm birth. Med Hypotheses. 2015; 84:494-497. PMC4380652.


Li Y, Wang K, Zou QY, Magness RR, Zheng J. 2,3,7,8-Tetrachlorodibenzo-p-dioxin differentially suppresses angiogenic responses in human placental vein and artery endothelial cells. Toxicology 2015; 336:70-78.  PMC4593512.


Wu YM, Chen X, Liu CH, Bao S, He QZ, Zhou Q, Li Y, Zheng J, Duan T, Wang K. Potential involvement of placental AhR in unexplained recurrent spontaneous abortion.  Reprod Toxicol 2016; 59: 45-52.


Li Y, Wang K, Zou QY, Jiang YZ, Zhou C, Zheng J. An endogenous aryl hydrocarbon receptor ligand suppresses angiogenic responses of human artery and vein endothelial cells: differential roles of AhR.  Reprod Toxicol 2017; 74:181-188.  PMC5718942.


Pang LP, Li Y, Zou QY, Zhou C, Lei W, Zheng J*, Huang SA*. ITE inhibits proliferation of pulmonary artery endothelial cells independent of AhR. Exp Lung Res 2017; 43:283-292.*Co-correspondence. PMC5909382


Zhu KX, Meng Q, Zhang Z, He Y, Zheng J, Lei W. Aryl hydrocarbon receptor pathway: role, regulation, and intervention in atherosclerosis therapy. Mol Med Rep. 2019; 20(6):4763-4773. 



The role of miRNAs in placental vascular function

Sponsor:

The goal of this project is to determine the role of miRNAs in controlling fetoplacental vascular function.


Publications:

Zhou C, Zou QY, Li H, Liu AX, Wang RF, Magness RR, Zheng J.  Preeclampsia down-regulates microRNAs in fetal endothelial cells: Roles of miR-29a/c-3p in endothelial function.  J Clin Endocrinol Metab 2017; 102: 3470-3479. PMC5587062.


Zhou C, Yan Q, Zou QY, Zhong XQ, Tyler CT, Magness RR, Bird IM, Zheng J. Sexual dimorphism of preeclampsia-dysregulated transcriptomic profiles and cellular function in fetal endothelial cells. Hypertension 2019;74(1):154-163. [An invited editorial commentary by Reckelhoff JF et al appeared in Hypertension DOI:10.1161/HYPERTENSIONAHA.119.12652), stating that this study “determine whether fetal sex alters HUVEC function and to provide insight into potential mechanism responsible for sex differences in increased cardiovascular risk in offspring of pregnancies complicated by preeclampsia”. They also emphasized the need for further investigation of this important work.). PMC6561818.



Vascular function in pregnancy

Sponsor:


Publications:

Li Y, Zhao YJ, Zou QY, Zheng K, WU YM, Zhou C, Wang K, Zheng J. Preeclampsia does not alter vascular growth and expression of CD31 and vascular endothelial-cadherin in human placentas. J Histochem Cytochem. 2015; 63:22-31. PMC4395995.


Zhang HH, Wang W, Feng L, Yang YY, Zheng J, Magness RR, Huang L, Dong-bao Chen. S-nitrosylation of cofilin-1 serves as a novel pathway for VEGF2-stimulated endothelial cell migration. J Cell Physiol. 2015; 230: 406-417.


Zheng J and Zhou C. 2017. Hypoxia and Human Diseases. Zheng J, PhD and Zhou C, PhD. (ed). InTech-Open Access Publisher.


Vargas VE, Landeros RV, Lopez GE, Zheng J, Magness RR. Uterine artery leptin receptors during the ovarian cycle and pregnancy regulate angiogenesis in ovine uterine artery endothelial cells. Biol Reprod 2017; 96: 866-876.  PMC5819836.


Landeros RV, Jobe SO, Aranda-Pino G, Lopez GE, Zheng J, Magness RR. Activation of mitogen-activated protein kinases facilitates catecholestrogen-induced uterine artery endothelial cell proliferation. J Physiol. (London) 2017; 15;595:4663-4676. PMC5509880.


Zou QY, Zhao YZ, Li H, Wang XZ, Liu AX, Zhong XQ, Yan Q, Li Y, Zhou C, Zheng J.  GNA11 differentially mediates fibroblast growth factor 2- and vascular endothelial growth factor A-induced cellular responses in human fetoplacental endothelial cells. J Physiol (London). 2018: 596: 2333-2344. PMC6002203.


Zou QY, Zhao YJ, Liu AX, Zhong XQ, Yan Q, Li Y, Zhou C, Yi FX, Bird IM, and Zheng J. G protein α subunit 14 mediates fibroblast growth factor 2-induced cellular responses in human endothelial cells.  J Cell Physiol. 2019;234:10184-10195. PMC6426666.


Zhou C, Zou QY, Jiang YZ, and Zheng J. Role of oxygen in fetoplacental endothelial responses: hypoxia, physiological normoxia, or hyperoxia? Am J Physiol-Cell Physiol (Invited Review). 2020;318(5):C943‐C953.



Past Projects

Sponsor:


Publications:

Distinct roles of HIF1A in endothelial adaptations to physiological and ambient oxygen.

Jiang YZ, Li Y, Wang K, Dai CF, Huang SA, Chen DB, Zheng J. Mol Cell Endocrinol. 2014; 391: 60-7. PMC4079002.


Expression of G-protein subunit α-14 is increased in human placentas from preeclamptic pregnancies.

Zhao YJ, Zou QY, Li Y, Li HH, Li XF, Wang K, Zheng J. J Histochem Cytochem 2014; 62: 347-54. PMC4005364.


ITE and TCDD differentially regulate the vascular remodeling of rat placenta via the activation of AhR.

Wu YM, Chen X, Zhou Q, He QZ, Kang JH, Zheng J, Wang K, Duan T. PLoS One 2014; 9: e86549. PMC3901702.


Regulation of placental angiogenesis.

Chen DB, Zheng J. Microcirculation (Invited Review) 2014; 21: 15-25. PMC5589442


Estradiol-17β and its metabolites attenuate vitamin c-suppressed human ovarian cancer cell proliferation.

Li HH, Zhao YJ, Li Y, Dai DF, Jobe SO, Li XF, Yang XS, Patankar MS, Magness RR, Zheng J. Reprod Sci. 2014; 21:102-11. PMC3857769.


Enhanced cellular responses and distinct gene profiles in human fetoplacental artery endothelial cells under chronic low oxygen.

Jiang YZ, Wang K, Li Y, Dai CF, Wang P, Kendziorski C, Chen DB, Zheng J. Biol Reprod. 2013; 89:133. PMC4076354.


An endogenous aryl hydrocarbon receptor ligand inhibits proliferation and migration of human ovarian cancer cells.

Wang K, Li Y, Jiang YZ, Dai CF, Patankar MS, Song JS, Zheng J. Cancer Lett 2013; 340:63-71. PMC3781955.


Transcriptional and functional adaptations of endothelial cells to physiological chronic low oxygen.

Jiang YZ, Wang K, Li Y, Dai CF, Wang P, Kendziorski C, Chen DB, Zheng J. Biol Reprod 2013; 88:114. PMC4013893.


Transcriptional and functional adaptations of endothelial cells to physiological chronic low oxygen.

Jiang YZ, Wang K, Li Y, Dai CF, Wang P, Kendziorski C, Chen DB, Zheng J. Biol Reprod 2013; 88:114. PMC4013893.