JournalofCellularBiochemistryVolume120,Issue9
RESEARCHARTICLEHumanumbilicalcordmesenchymalstemcellsderivedexosomesexertantiapoptosiseffectviaactivatingPI3K/Akt/mTORpathwayonH9C2cellsHuiLiuDepartmentofCardiology,StateKeyLaboratoryofCardiovascularDiseases,FuwaiHospital,NationalCenterforCardiovascularDiseases,ChineseAcademyofMedicalSciencesandPekingUnionMedicalCollege,Beijing,People"sRepublicofChina
SearchformorepapersbythisauthorXiaoluSunCorrespondingAuthor
E-mailaddress:fwxiaolusun@yahoo.com
DepartmentofCardiology,StateKeyLaboratoryofCardiovascularDiseases,FuwaiHospital,NationalCenterforCardiovascularDiseases,ChineseAcademyofMedicalSciencesandPekingUnionMedicalCollege,Beijing,People"sRepublicofChina
CorrespondenceXiaoluSunandGuoganWang,No.167,NorthLishiRoad,XichengDistrict,100037Beijing,People"sRepublicofChina.Email:fwxiaolusun@yahoo.com(XS);wangguog@hotmail.com(GW)
SearchformorepapersbythisauthorXuheGongDepartmentofCardiology,BeijingFriendshipHospital,CapitalMedicalUniversity,Beijing,People"sRepublicofChina
SearchformorepapersbythisauthorGuoganWangCorrespondingAuthor
E-mailaddress:wangguog@hotmail.com
http://orcid.org/0000-0001-9451-3007
DepartmentofCardiology,StateKeyLaboratoryofCardiovascularDiseases,FuwaiHospital,NationalCenterforCardiovascularDiseases,ChineseAcademyofMedicalSciencesandPekingUnionMedicalCollege,Beijing,People"sRepublicofChina
CorrespondenceXiaoluSunandGuoganWang,No.167,NorthLishiRoad,XichengDistrict,100037Beijing,People"sRepublicofChina.Email:fwxiaolusun@yahoo.com(XS);wangguog@hotmail.com(GW)
SearchformorepapersbythisauthorHuiLiu
DepartmentofCardiology,StateKeyLaboratoryofCardiovascularDiseases,FuwaiHospital,NationalCenterforCardiovascularDiseases,ChineseAcademyofMedicalSciencesandPekingUnionMedicalCollege,Beijing,People"sRepublicofChina
SearchformorepapersbythisauthorXiaoluSunCorrespondingAuthor
E-mailaddress:fwxiaolusun@yahoo.com
DepartmentofCardiology,StateKeyLaboratoryofCardiovascularDiseases,FuwaiHospital,NationalCenterforCardiovascularDiseases,ChineseAcademyofMedicalSciencesandPekingUnionMedicalCollege,Beijing,People"sRepublicofChina
CorrespondenceXiaoluSunandGuoganWang,No.167,NorthLishiRoad,XichengDistrict,100037Beijing,People"sRepublicofChina.Email:fwxiaolusun@yahoo.com(XS);wangguog@hotmail.com(GW)
SearchformorepapersbythisauthorXuheGongDepartmentofCardiology,BeijingFriendshipHospital,CapitalMedicalUniversity,Beijing,People"sRepublicofChina
SearchformorepapersbythisauthorGuoganWangCorrespondingAuthor
E-mailaddress:wangguog@hotmail.com
http://orcid.org/0000-0001-9451-3007
DepartmentofCardiology,StateKeyLaboratoryofCardiovascularDiseases,FuwaiHospital,NationalCenterforCardiovascularDiseases,ChineseAcademyofMedicalSciencesandPekingUnionMedicalCollege,Beijing,People"sRepublicofChina
CorrespondenceXiaoluSunandGuoganWang,No.167,NorthLishiRoad,XichengDistrict,100037Beijing,People"sRepublicofChina.Email:fwxiaolusun@yahoo.com(XS);wangguog@hotmail.com(GW)
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ShareonEmailFacebookTwitterLinkedInRedditWechatInrecentyears,asanalternativetostemcelltherapyforcardiovasculardiseases(CVD),exsomeshaveattractedwideattentionamongresearchers.Thepresentstudyaimedtoinvestigatetheroleofhumanumbilicalcordmesenchymalstemcells(UC‐MSCs)derivedexosomesplayonH9C2cellsapoptosisandpossIBLemechanisms.
ExosomeswereisolatedfromnormalUC‐MSCsculturemediaandhypoxicpreconditioningculturemedia.Transmissionelectronmicroscopywasusedtoobservethemorphologyofexosomes.Nanoparticletrackinganalysiswasusedtodetectthesizedistributionandconcentrationofexosomes.WesternblotanalysiswasusedtoanalyzedthesurfaceMarkerCD63ofexosomes.H9C2cellswereinducedapoptosisbyhypoxiaandserumdeprivation(H/SD)andthenweretreatedrespectivelybygroup.CellCountingKit‐8assaywasusedtodetectviABIlityofH9C2cells.ApoptosiswasdetectedbyHocheststainingandannexinV‐FITC/PI.Theexpressionlevelsofrelatedproteinsofapoptosis,autophagy,andPI3K/Akt/mTORpathwaywereanalyzedbyWesternblotanalysis.ImmunofluorescencewasusedtoanalyzeLC3Bexpression.
HypoxicpreconditioningincreasedtheexosomessecretionofUC‐MSCs.UC‐MSCsderivedexosomescouldinhibitH/SD‐inducedH9C2cellsapoptosis.HypoxicpreconditioningstrengthenedthisantiapoptosiseffectofUC‐MSCs.HypoxicpreconditioningUC‐MSCsderivedexosomes(H‐Exo)downregulatedLC3B‐II/Iandbeclin‐1andupregulatedP62,p‐Akt/Aktandp‐mTOR/mTOR.TheantiapoptoticeffectofH‐ExocouldbeattenuatedbytreatmentwithLY294002andrapamycin.
UC‐MSCsderivedexosomescouldinhibitH9C2cellsapoptosisinducedbyH/SDthroughregulatingautophagyviaPI3K/Akt/mTORpathway.HypoxiapreconditioningcouldenhanceaboveeffectsthroughincreasingexosomessecretionofUC‐MSCs.
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