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Jing Zheng

Researcher at University of Wisconsin-Madison

Publications -  85
Citations -  2912

Jing Zheng is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Angiogenesis & Vascular endothelial growth factor A. The author has an hindex of 29, co-authored 77 publications receiving 2631 citations. Previous affiliations of Jing Zheng include Guangdong Medical College.

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Endothelial vasodilator production by uterine and systemic arteries. II. Pregnancy effects on NO synthase expression

TL;DR: During pregnancy, expression of uterine artery endothelium-derived (not VSM) ecNOS constitutive isoform is increased, whereas expression in systemic vessels shows little or no change.
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Preeclampsia Up-Regulates Angiogenesis-Associated MicroRNA (i.e., miR-17, -20a, and -20b) That Target Ephrin-B2 and EPHB4 in Human Placenta

TL;DR: Three highly expressed miRNA (miR-17, -20a, and -20b) were found significantly increased in PE compared with healthy term placentas and regulate EPHB4 and ephrin-B2 expression in trophoblast and endothelial cells via the same "seed" sequence, suggesting their roles in early placental development.
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Membrane Estrogen Receptor-Dependent Extracellular Signal-Regulated Kinase Pathway Mediates Acute Activation of Endothelial Nitric Oxide Synthase by Estrogen in Uterine Artery Endothelial Cells

TL;DR: Acute activation of eNOS to produce NO in UAEC by estrogen is at least partially through an ERK pathway, possibly via estrogen receptor localized on the plasma membrane, and may provide a novel mechanism for NO-mediated rapid uterine vasodilatation by estrogen.
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Regulation of Placental Angiogenesis

TL;DR: The genetic and molecular aspects of normal placental angiogenesis as well as the signaling mechanisms by which the dominant angiogenic factor vascular endothelial growth factor regulates placentalAngiogenesis are summarized with a focus on placental endothelial cells.
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Differential Expression of Vascular Endothelial Growth Factor (VEGF), Endocrine Gland Derived-VEGF, and VEGF Receptors in Human Placentas from Normal and Preeclamptic Pregnancies

TL;DR: Combined with previous reports that VEGFR-1 mediates trophoblast function and inhibits VEGF-induced angiogenesis and endothelium-dependent vasodilation, these data suggest that the increased VEG FR-1 expression may alter V EGF- mediated function on troPHoblast and endothelial cells in PE placentas.