Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.

Prostaglandin E2 (PGE2), 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 PGE2-induced human brain endothelial cells (HBECs) migration, and works in a...

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Main Authors: Gausal Azam Khan, Arjun Ghosh
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2025-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0326312
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author Gausal Azam Khan
Arjun Ghosh
author_facet Gausal Azam Khan
Arjun Ghosh
author_sort Gausal Azam Khan
collection DOAJ
description Prostaglandin E2 (PGE2), 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 PGE2-induced human brain endothelial cells (HBECs) migration, and works in a cooperative manner through its three receptors (EP2, EP3 & EP4). However, the detailed signaling mechanism of PGE2-induced HBECs migration remains obscure. In this present study, we investigated the signaling pathway of actin dynamics/polymerization and migration of HBECs by PGE2 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. PGE2 (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 PGE2-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 PGE2-induced ROCK II activity. Furthermore, PGE2-induced MLC phosphorylation also occurs in a time-dependent manner. However, pretreatment of ROCK II inhibitor or silencing of ROCK II significantly abrogated PGE2-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 PGE2-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.
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spelling doaj-art-3ca0df689bce4aa2bc48991aeaaa34322025-08-20T03:58:41ZengPublic Library of Science (PLoS)PLoS ONE1932-62032025-01-01206e032631210.1371/journal.pone.0326312Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.Gausal Azam KhanArjun GhoshProstaglandin E2 (PGE2), 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 PGE2-induced human brain endothelial cells (HBECs) migration, and works in a cooperative manner through its three receptors (EP2, EP3 & EP4). However, the detailed signaling mechanism of PGE2-induced HBECs migration remains obscure. In this present study, we investigated the signaling pathway of actin dynamics/polymerization and migration of HBECs by PGE2 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. PGE2 (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 PGE2-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 PGE2-induced ROCK II activity. Furthermore, PGE2-induced MLC phosphorylation also occurs in a time-dependent manner. However, pretreatment of ROCK II inhibitor or silencing of ROCK II significantly abrogated PGE2-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 PGE2-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.https://doi.org/10.1371/journal.pone.0326312
spellingShingle Gausal Azam Khan
Arjun Ghosh
Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.
PLoS ONE
title Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.
title_full Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.
title_fullStr Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.
title_full_unstemmed Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.
title_short Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.
title_sort prostaglandin e2 dependent migration of human brain endothelial cells is mediated through rho kinase ii
url https://doi.org/10.1371/journal.pone.0326312
work_keys_str_mv AT gausalazamkhan prostaglandine2dependentmigrationofhumanbrainendothelialcellsismediatedthroughrhokinaseii
AT arjunghosh prostaglandine2dependentmigrationofhumanbrainendothelialcellsismediatedthroughrhokinaseii