JAK/STAT3SignalingPathwayIsInvolvedinPromotingtheProliferationand MigrationofBronchialSmoothMuscleCellsInducedbyInterleukin-17 / 中山大学学报(医学科学版)

ABSTRACT

@#：【Objective】Toinvestigatetheeffectsofinterleukin-17（IL-17）ontheproliferationandmigrationof bronchialsmoothmusclecells（BSMC）andtheroleofJAK/STAT3signalingpathwayinthisprocess.【Methods】BSMC weretreatedwithdifferentconcentrationsofIL-17fordifferenttimestodeterminethebestoftheexperimentalcondition. ThenMTTassaywasusedtodetectcellviability.CellproliferationstatesweredetectedbyBrdUstaining，andthecell cyclewasassessedbyPIstainingusingaflowcytometer.Transwellcellmigrationassaywasfurtherusedtodetectcell migrationability.TheexpressionofJAK，p-JAK，STAT3andp-STAT3inBSMCafterbeingtreatedwithIL-17was detectedbyWesternblotting.JAK/STAT3signalingpathwayspecificblockerAG490wasusedtoinvestigatetheroleof JAK/STAT3signalingpathwayinIL-17-inducedBSMCproliferationandmigration.TheeffectsofIL-17oncellproliferation， migration and JAK/STAT3 signaling pathway related protein expression were evaluated after blocking the JAK/STAT3 signaling.【Results】IL-17enhancedtheproliferation（P<0.05），promotedthecellcycletransitions（P<0.05）andsig⁃nificantlyincreasesthemigrationability（P<0.05）inBSMC.ThisprocesswasaccompaniedbytheenhancementofJAK/ STAT3signalingpathwayinBSMC（P<0.05）.InhibitionofJAK/STAT3signalingpathwayalleviatedBSMCproliferation andmigrationinducedbyIL-17（P<0.05） .【Conclusions】JAK/STAT3signalingpathwayparticipatesinthestimulation processofIL-17ontheproliferationandmigrationofBSMC.AG490inhibitstheenhancementofJAK/STAT3signaling pathwayinBSMCinducedbyinterleukin-17.