Sirtinol Treatment Reduces Inflammation in Human Dermal Microvascular Endothelial Cells 英文参考文献.docVIP

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Sirtinol Treatment Reduces Inflammation in Human Dermal Microvascular Endothelial Cells 英文参考文献.doc

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Sirtinol Treatment Reduces Inflammation in Human Dermal Microvascular Endothelial Cells 英文参考文献

SirtinolTreatmentReducesInflammationinHuman DermalMicrovascularEndothelialCells AngelaOrecchia1,ClaudiaScarponi2,FrancescaDiFelice1,ElisaCesarini3,SimonaAvitabile1 ,Antonello Mai4,MariaLuisaMauro3,ValentinaSirri5,GiovannaZambruno1,CristinaAlbanesi2 ,Giorgio Camilloni3,6,CristinaM.Failla1* 1Molecular and Cell Biology Laboratory, IDI-IRCCS, Rome, Italy, 2Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy, 3Department of Biology and Biotechnology‘C.Darwin’,UniversitydiRomaLaSapienza,Rome,Italy,4DepartmentofDrugChemistryandTechnologies,PasteurInstitute,CenciBolognettiFoundation, UniversitydiRomaLaSapienza,Rome,Italy,5RNABiology,FRE3402CNRS,Universite′PierreetMarieCurie,Paris,France,6IstitutodiBiologiaePatologiaMolecolari,CNR, Rome,Italy Abstract Histonedeacetylases(HDAC)arekeyenzymesintheepigeneticcontrolofgeneexpression.Recently,inhibitorsofclassIand classIIHDAChavebeensuccessfullyemployedforthetreatmentofdifferentinflammatorydiseasessuchasrheumatoid arthritis,colitis,airwayinflammationandasthma.Sofar,littleisknownsofaraboutasimilartherapeuticeffectofinhibitors specifically directed against sirtuins, the class III HDAC. In this study, we investigated the expression and localization of endogenoussirtuinsinprimaryhumandermalmicrovascularendothelialcells(HDMEC),acelltypeplayingakeyroleinthe developmentandmaintenanceofskininflammation.Wethenexaminedthebiologicalactivityofsirtinol,aspecificsirtuin inhibitor,inHDMECresponsetopro-inflammatorycytokines.Wefoundthat,eventhoughsirtinoltreatmentaloneaffected only long-term cell proliferation, it diminishes HDMEC inflammatory responses to tumor necrosis factor (TNF)a and interleukin (IL)-1b. In fact, sirtinol significantly reduced membrane expression of adhesion molecules in TNFa?- or IL-1b- stimulatedcells,aswellastheamountofCXCL10andCCL2releasedbyHDMECfollowingTNFatreatment.Notably,sirtinol drasticallydecreasedmonocyteadhesiononactivatedHDMEC.UsingselectiveinhibitorsforSirt1andSirt2,weshoweda predominantinvolvementofSi