Sandy S. Jun
University of Texas Southwestern Medical Center
5 Papers
61 Citations
Sandy S. Jun is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Fetus & Endothelium. The author has an hindex of 3, co-authored 5 publications.
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Papers
Estrogen Upregulates Endothelial Nitric Oxide Synthase Gene Expression in Fetal Pulmonary Artery Endothelium
Amy N. MacRitchie,Sandy S. Jun,Zhong Chen,Zohre German,Ivan S. Yuhanna,Todd S. Sherman,Philip W. Shaul +6 more
TL;DR: Estrogen upregulates eNOS gene expression in fetal PAECs through the activation of PAEC estrogen receptors, thereby optimizing the capacity for NO-mediated pulmonary vasodilation at birth.
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Glucocorticoids Downregulate Cyclooxygenase-1 Gene Expression and Prostacyclin Synthesis in Fetal Pulmonary Artery Endothelium
TL;DR: Prostacyclin (prostaglandin I2 [PGI2] is a key mediator of pulmonary vascular function during early postnatal life, and its production in the pulmonary vasculature rises markedly during that period because of increasing expression of cyclooxygenase type 1 (COX-1).
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Estrogen upregulates cyclooxygenase gene expression in fetal pulmonary artery endothelial cells. • 164
TL;DR: The total number of cells needed for cell reprograming, including mitochondria, has not yet been determined, but initial results suggest that the number ofocytes needed for reprogramming is low.
Glucocorticoids Downregulate Cyclooxygenase-1 Gene Expression and Prostacyclin Synthesis in Fetal Pulmonary Artery Endothelium via Activation of Endothelial Glucocorticoid Receptors ♦ 116
TL;DR: The findings indicate that glucocorticoids downregulate COX-1 expression and PGI2 synthesis in fetal PAECs through the activation of PAEC GR and effects on COx-1 gene transcription, which may modulate pulmonary P GI2 production in the perinatal period, and it may also play a role in the effects of glucoc Corticoids on the systemic circulation at a variety of ages.
Estrogen upregulates cyclooxygenase-1 gene expression in ovine fetal pulmonary artery endothelium.
TL;DR: Findings indicate that physiologic levels of estrogen cause upregulation of COX-1 expression and PGI2 synthesis in fetal PAEC via activation of PAEC ER, and this process may play a critical role in optimizing the capacity for P GI2-mediated pulmonary vasodilation at birth.