Kao Y.-CChen Z.-HWang W.-YLee C.-HPO-LING KUO2022-04-252022-04-2520210006291Xhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85108441826&doi=10.1016%2fj.bbrc.2021.06.055&partnerID=40&md5=1fedc877a47e42317d37338cd6838596https://scholars.lib.ntu.edu.tw/handle/123456789/607265Fibroblast migration is closely regulated by the mechanical characteristics in surrounding microenvironment. While increased interstitial hydrostatic pressure (HP) is a hallmark in many pathological and physiological conditions, little is known about how the HP affects fibroblast motility. Using cell-culture chips with elevated HP conditions, we showed that 20 cmH2O HP significantly accelerated fibroblast migration. The HP-induced migration acceleration was dependent on the augmentation of transforming growth factor-β1, and correlated with the activation of filamin A via the phosphorylation of p38 mitogen-activated protein kinase. Our results suggest that interstitial HP elevation associated with various pathological states could significantly regulate fibroblast migration. ? 2021 The AuthorsCell motilityFibroblastFilaminInterstitial hydrostatic pressurep38TGF-βfilamin Amitogen activated protein kinase p38transforming growth factor betafilaminFlnA protein, mouseArticlecell culturecell migrationcell motilitycontrolled studyfibroblasthydrostatic pressureMAPK signalingNIH 3T3 cell lineprotein expressionprotein functionprotein phosphorylationprotein secretionupregulationanimalcell motioncytologymetabolismmousephosphorylationAnimalsCell MovementFibroblastsFilaminsHydrostatic PressureMiceNIH 3T3 Cellsp38 Mitogen-Activated Protein KinasesPhosphorylationTransforming Growth Factor beta[SDGs]SDG3journal article10.1016/j.bbrc.2021.06.055341745372-s2.0-85108441826