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Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II
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Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II
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Journal Article
Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II
2025
Overview
Prostaglandin E 2 (PGE 2 ), that plays a crucial role in angiogenesis as well as in ischemic and inflammatory disorders of the brain, is associated with breakdown of the blood-brain barrier (BBB). Previously, we had shown that PGE 2 -induced human brain endothelial cells (HBECs) migration, and works in a cooperative manner through its three receptors (EP 2 , EP 3 & EP 4 ). However, the detailed signaling mechanism of PGE 2 -induced HBECs migration remains obscure. In this present study, we investigated the signaling pathway of actin dynamics/polymerization and migration of HBECs by PGE 2 in vitro. Expression of ROCK was analyzed by ELISA and RT-PCR. Actin polymerization was evaluated by NBD-phallacidin immunofluorescence staining. HBECs expressed only ROCK II. PGE 2 (100 pM) induced ROCK II expression occurs in dose-and-time-dependent manner. ROCK II inhibition by Y27632 (150nM), as well as ROCK II silencing significantly attenuated PGE 2 -induced migration of HBECs. We further showed that pretreatment of PKA inhibitor (H-89; 0.5 μM) or adenylate cyclase inhibitor (ddA; 1μM) completely inhibited PGE 2 -induced ROCK II activity. Furthermore, PGE 2 -induced MLC phosphorylation also occurs in a time-dependent manner. However, pretreatment of ROCK II inhibitor or silencing of ROCK II significantly abrogated PGE 2 -induced MLC phosphorylation as well as F-actin polymerization. Our ex-vivo aortic ring angiogenesis study also showed that pretreatment of ROCK II inhibitor significantly inhibited ECs sprouting. These results suggest that PGE 2 -induced HBECs migration is mediated through PKA, ROCK II and MLC phosphorylation as well as F-actin polymerization, indicating that modulation of these pathways may aid in the future treatment of dysregulated angiogenesis in cerebrovascular diseases.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Animals
/ Aorta
/ Blood-Brain Barrier - cytology
/ Blood-Brain Barrier - pathology
/ Blood-Brain Barrier - physiology
/ Brain
/ Cells
/ Cerebrovascular Disorders - pathology
/ Cerebrovascular Disorders - physiopathology
/ Endothelial Cells - pathology
/ Endothelial Cells - physiology
/ Enzyme-linked immunosorbent assay
/ Humans
/ Ischemia
/ Kinases
/ Mice
/ Proteins
/ Research and Analysis Methods
/ rho-Associated Kinases - metabolism
/ Rocks
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