Adipose-derived mesenchymal stem cells (ADMSCs)-based therapy is a promising modality for the treatment of @entity583 in the future. However, the majority of transplanted cells are readily lost after transplantation because of @entity519 and oxidative stress. An efficient means to enhance the ability of ADMSCs to survive under pathologic conditions is required. In our study, we explored the effects of exendin-4 (Ex-4) on ADMSCs apoptosis in vitro induced by @entity273 , focusing in particular on mitochondrial apoptotic pathways and @entity68417 ( @entity12317 ) survival signaling. We demonstrated that ADMSCs subjected to @entity274 for 12h exhibited impaired mitochondrial function and higher apoptotic rate. However, Ex-4 (1-20nM) preconditioning for 12h could protect ADMSCs against @entity274 -mediated apoptosis in a dose-dependent manner. Furthermore, Ex-4 pretreatment upregulated the levels of @entity224 dismutase and @entity2041 as well as downregulating the production of reactive @entity26 species and @entity1234 . Western blots revealed that increased antiapoptotic proteins @entity588 and @entity22557 as well as decreased proapoptotic proteins @entity589 and @entity4674 appeared in ADMSCs with Ex-4 incubation, which inhibited the @entity8187 -involved mitochondrial apoptosis pathways with evidence showing inactivation of @entity8187 /3 and preservation of mitochondrial membrane potential. Furthermore, we illustrated that Ex-4 enhanced @entity584 phosphorylation, which increased the expression of @entity12317 . Notably, blockade of the @entity10412 / @entity584 pathway or knockdown of @entity12317 with siRNA obviously abolished the protective effects of Ex-4 on mitochondrial function and ADMSCs apoptosis under @entity274 . In summary, this study confirmed that @entity274 induced ADMSCs apoptosis through mitochondria-dependent cell death pathways, and Ex-4 preconditioning may reduce such apoptosis of ADMSCs through the @entity10412 / @entity584 - @entity12317 pathways.

Exendin-4 protects adipose-derived mesenchymal stem cells from apoptosis induced by @entity273 through the XXXX / @entity584 - @entity12317 pathways.

@entity68417 :: ('6423;5293', 'Gene') :: ['PI3K/Akt-secreted frizzled-related protein 2'] @entity274 :: ('CHEBI:16240', 'Chemical') :: ['H2O2'] @entity588 :: ('596', 'Gene') :: ['Bcl-2'] @entity12317 :: ('6423', 'Gene') :: ['Sfrp2'] @entity22557 :: ('329;330', 'Gene') :: ['c-IAP1/2'] @entity589 :: ('581', 'Gene') :: ['Bax'] @entity4674 :: ('54205', 'Gene') :: ['cytochrome c'] @entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen'] @entity2041 :: ('MESH:D005978', 'Chemical') :: ['glutathione'] @entity584 :: ('207', 'Gene') :: ['Akt'] @entity8187 :: ('842', 'Gene') :: ['caspase-9'] @entity273 :: ('MESH:D006861', 'Chemical') :: ['hydrogen peroxide'] @entity519 :: ('MESH:D000860', 'Disease') :: ['hypoxia'] @entity1234 :: ('MESH:D008315', 'Chemical') :: ['malondialdehyde'] @entity10412 :: ('5293', 'Gene') :: ['PI3K'] @entity583 :: ('MESH:D009203', 'Disease') :: ['myocardial infarction'] @entity224 :: ('MESH:D013481', 'Chemical') :: ['superoxide']
@entity10412 :: (5293,Gene) :: ['PI3K']
