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This study investigated the effects of HSPA<\/jats:styled-content>12B on lipopolysaccharide (LPS<\/jats:styled-content>)\u2010induced inflammatory responses in human umbilical vein endothelial cells (HUVEC<\/jats:styled-content>s) and the possible mechanisms involved. A HUVEC<\/jats:styled-content>s inflammatory model was induced by LPS<\/jats:styled-content>. Overexpression of HSPA<\/jats:styled-content>12B in HUVEC<\/jats:styled-content>s was achieved by infection with recombinant adenoviruses encoding green fluorescence protein\u2010HSPA<\/jats:styled-content>12B. Knockdown of HSPA<\/jats:styled-content>12B was achieved by siRNA<\/jats:styled-content> technique. Twenty four hours after virus infection or siRNA<\/jats:styled-content> transfection, HUVEC<\/jats:styled-content>s were stimulated with 1\u00a0\u03bcg\/ml LPS<\/jats:styled-content> for 4\u00a0hrs. Endothelial cell permeability ability was determined by transwell permeability assay. The binding rate of human neutrophilic polymorphonuclear leucocytes (PMN<\/jats:styled-content>) with HUVEC<\/jats:styled-content>s was examined using myeloperoxidase assay. Cell migrating ability was determined by the wound\u2010healing assay. The mRNA<\/jats:styled-content> and protein expression levels of interested genes were analyzed by RT<\/jats:styled-content>\u2010qPCR<\/jats:styled-content> and Western blot, respectively. The release of cytokines interleukin\u20106 and tumour necrosis factor\u2010\u03b1 was measured by ELISA<\/jats:styled-content>. HSPA<\/jats:styled-content>12B suppressed LPS<\/jats:styled-content>\u2010induced HUVEC<\/jats:styled-content> permeability and reduced PMN<\/jats:styled-content> adhesion to HUVEC<\/jats:styled-content>s. HSPA<\/jats:styled-content>12B also inhibited LPS<\/jats:styled-content>\u2010induced up\u2010regulation of adhesion molecules and inflammatory cytokine expression. By contrast, knockdown of HSPA<\/jats:styled-content>12B enhanced LPS<\/jats:styled-content>\u2010induced increases in the expression of adhesion molecules and inflammatory cytokines. Moreover, HSPA<\/jats:styled-content>12B activated PI<\/jats:styled-content>3K\/Akt signalling pathway and pharmacological inhibition of this pathway by Wortmannin completely abrogated the protection of HSPA<\/jats:styled-content>12B against inflammatory response in HUVEC<\/jats:styled-content>s. Our results suggest that HSPA<\/jats:styled-content>12B attenuates LPS<\/jats:styled-content>\u2010induced inflammatory responses in HUVEC<\/jats:styled-content>s via<\/jats:italic> activation of PI<\/jats:styled-content>3K\/Akt signalling pathway.<\/jats:p>","DOI":"10.1111\/jcmm.12464","type":"journal-article","created":{"date-parts":[[2014,12,24]],"date-time":"2014-12-24T13:50:25Z","timestamp":1419429025000},"page":"544-554","source":"Crossref","is-referenced-by-count":29,"title":["HSPA<\/scp>12B inhibits lipopolysaccharide\u2010induced inflammatory response in human umbilical vein endothelial cells"],"prefix":"10.1111","volume":"19","author":[{"given":"Jun","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Geriatrics The First Affiliated Hospital of Nanjing Medical University Nanjing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xuehan","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Geriatrics The First 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