<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Khan GA</submitter><funding>Deanship of Scientific Research, King Faisal University</funding><pagination>e0326312</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12185010</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(6)</volume><pubmed_abstract>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 &amp; 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 o</pubmed_abstract><journal>PloS one</journal><pubmed_title>Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.</pubmed_title><pmcid>PMC12185010</pmcid><funding_grant_id>KFU 252130 to GAK</funding_grant_id><pubmed_authors>Ghosh A</pubmed_authors><pubmed_authors>Khan GA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Prostaglandin E2 dependent migration of human brain endothelial cells is mediated through Rho-Kinase-II.</name><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 &amp; 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 o</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-06-03T07:03:37.029Z</modification><creation>2026-04-25T03:21:58.034Z</creation></dates><accession>S-EPMC12185010</accession><cross_references><pubmed>40549735</pubmed><doi>10.1371/journal.pone.0326312</doi></cross_references></HashMap>