FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2890163138> ?p ?o ?g. }

• W2890163138 endingPage "53" @default.
• W2890163138 startingPage "39" @default.
• W2890163138 abstract "BackgroundTransplant arteriosclerosis (TA) remains the major cause of chronic graft failure in solid organ transplantation. The phenotypic modulation of vascular smooth muscle cells (VSMCs) is a key event for the initiation and progression of neointimal formation and TA. This study aims to explore the role and underlying mechanism of phosphoinositide 3-kinases γ (PI3Kγ) in VSMC phenotypic modulation and TA.MethodsThe rat model of aortic transplantation was established to detect PI3Kγ expression and its role in neointimal formation and vascular remodeling in vivo. PI3Kγ shRNA transfection was employed to knockdown PI3Kγ gene. Aortic VSMCs was cultured and treated with TNF-α to explore the role and molecular mechanism of PI3Kγ in VSMC phenotypic modulation.FindingsActivated PI3Kγ/p-Akt signaling was observed in aortic allografts and in TNF-α-treated VSMCs. Lentivirus-mediated shRNA transfection effectively inhibited PI3Kγ expression in medial VSMCs while restoring the expression of VSMC contractile genes, associated with impaired neointimal formation in aortic allografts. In cultured VSMCs, PI3Kγ blockade with pharmacological inhibitor or genetic knockdown markedly abrogated TNF-α-induced downregulation of VSMC contractile genes and increase in cellular proliferation and migration. Moreover, SOX9 located in nucleus competitively inhibited the interaction of Myocardin and SRF, while PI3Kγ inhibition robustly reduced SOX9 expression and its nuclear translocation and repaired the Myocardin/SRF association.InterpretationThese results suggest that PI3Kγ plays a critical role in VSMC phenotypic modulation via a SOX9-dependent mechanism. Therefore, PI3Kγ in VSMCs may represent a promising therapeutic target for the treatment of TA.FundNational Natural Science Foundation of China." @default.
• W2890163138 created "2018-09-27" @default.
• W2890163138 creator A5002846208 @default.
• W2890163138 creator A5003733739 @default.
• W2890163138 creator A5009280516 @default.
• W2890163138 creator A5010806417 @default.
• W2890163138 creator A5018135780 @default.
• W2890163138 creator A5022841543 @default.
• W2890163138 creator A5034855502 @default.
• W2890163138 creator A5043764764 @default.
• W2890163138 creator A5043962446 @default.
• W2890163138 creator A5052024256 @default.
• W2890163138 creator A5064845987 @default.
• W2890163138 creator A5065420469 @default.
• W2890163138 creator A5065451120 @default.
• W2890163138 creator A5079472260 @default.
• W2890163138 creator A5081755685 @default.
• W2890163138 date "2018-10-01" @default.
• W2890163138 modified "2023-10-14" @default.
• W2890163138 title "PI3Kγ promotes vascular smooth muscle cell phenotypic modulation and transplant arteriosclerosis via a SOX9-dependent mechanism" @default.
• W2890163138 cites W1484142455 @default.
• W2890163138 cites W1510552367 @default.
• W2890163138 cites W1524999411 @default.
• W2890163138 cites W1578086713 @default.
• W2890163138 cites W1581446430 @default.
• W2890163138 cites W1945199177 @default.
• W2890163138 cites W1963782714 @default.
• W2890163138 cites W1972664321 @default.
• W2890163138 cites W1977427723 @default.
• W2890163138 cites W1984453879 @default.
• W2890163138 cites W1988224683 @default.
• W2890163138 cites W1992477322 @default.
• W2890163138 cites W1992718251 @default.
• W2890163138 cites W2005760229 @default.
• W2890163138 cites W2012182256 @default.
• W2890163138 cites W2015690952 @default.
• W2890163138 cites W2019222060 @default.
• W2890163138 cites W2028116439 @default.
• W2890163138 cites W2035402287 @default.
• W2890163138 cites W2038169545 @default.
• W2890163138 cites W2039241091 @default.
• W2890163138 cites W2041977741 @default.
• W2890163138 cites W2046564695 @default.
• W2890163138 cites W2047647015 @default.
• W2890163138 cites W2051872988 @default.
• W2890163138 cites W2053587992 @default.
• W2890163138 cites W2057370954 @default.
• W2890163138 cites W2059839442 @default.
• W2890163138 cites W2061440101 @default.
• W2890163138 cites W2072091375 @default.
• W2890163138 cites W2094451792 @default.
• W2890163138 cites W2103802459 @default.
• W2890163138 cites W2106294342 @default.
• W2890163138 cites W2110360170 @default.
• W2890163138 cites W2111695359 @default.
• W2890163138 cites W2113414181 @default.
• W2890163138 cites W2121331806 @default.
• W2890163138 cites W2121860616 @default.
• W2890163138 cites W2122740586 @default.
• W2890163138 cites W2126705092 @default.
• W2890163138 cites W2128455103 @default.
• W2890163138 cites W2129070301 @default.
• W2890163138 cites W2130020347 @default.
• W2890163138 cites W2130251290 @default.
• W2890163138 cites W2130995100 @default.
• W2890163138 cites W2136081121 @default.
• W2890163138 cites W2139418412 @default.
• W2890163138 cites W2155846133 @default.
• W2890163138 cites W2160773533 @default.
• W2890163138 cites W2168438265 @default.
• W2890163138 cites W2168662912 @default.
• W2890163138 cites W2168946030 @default.
• W2890163138 cites W2168983272 @default.
• W2890163138 cites W2189029396 @default.
• W2890163138 cites W2287481555 @default.
• W2890163138 cites W2322586828 @default.
• W2890163138 cites W2471777514 @default.
• W2890163138 cites W2507636691 @default.
• W2890163138 cites W268674102 @default.
• W2890163138 cites W2753350383 @default.
• W2890163138 cites W2800521804 @default.
• W2890163138 cites W2801683398 @default.
• W2890163138 cites W4213297656 @default.
• W2890163138 cites W635062304 @default.
• W2890163138 doi "https://doi.org/10.1016/j.ebiom.2018.09.013" @default.
• W2890163138 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6197754" @default.
• W2890163138 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30241919" @default.
• W2890163138 hasPublicationYear "2018" @default.
• W2890163138 type Work @default.
• W2890163138 sameAs 2890163138 @default.
• W2890163138 citedByCount "11" @default.
• W2890163138 countsByYear W28901631382020 @default.
• W2890163138 countsByYear W28901631382022 @default.
• W2890163138 countsByYear W28901631382023 @default.
• W2890163138 crossrefType "journal-article" @default.
• W2890163138 hasAuthorship W2890163138A5002846208 @default.
• W2890163138 hasAuthorship W2890163138A5003733739 @default.
• W2890163138 hasAuthorship W2890163138A5009280516 @default.

• next