Adipose-derived mesenchymal stem cell transplantation promotes adult neurogenesis in the brains of Alzheimer's disease mice

In the present study, we transplanted adipose-derived mesenchymal stem cells into the hippo-campi of APP/PS1 transgenic Alzheimer＇s disease model mice. Immunofluorescence staining revealed that the number of newly generated （BrdU＋） cells in the subgranular zone of the dentate gyrus in the hippocampus was signiifcantly higher in Alzheimer＇s disease mice after adipose-de-rived mesenchymal stem cell transplantation, and there was also a significant increase in the number of BrdU＋/DCX＋neuroblasts in these animals. Adipose-derived mesenchymal stem cell transplantation enhanced neurogenic activity in the subventricular zone as well. Furthermore, adipose-derived mesenchymal stem cell transplantation reduced oxidative stress and alleviated cognitive impairment in the mice. Based on these ifndings, we propose that adipose-derived mes-enchymal stem cell transplantation enhances endogenous neurogenesis in both the subgranular and subventricular zones in APP/PS1 transgenic Alzheimer＇s disease mice, thereby facilitating functional recovery.

Smurf participates in Helicoverpa armigera diapause by regulating the transforming growth factor-βsignaling pathway

Diapause,an important strategy used by insects to avoid adverse environments,is regulated by various cell signaling pathways.The results of our previous studies demonstrated that the transforming growth factor-β(TGF-β)signaling pathway regulated pupal diapause in Helicoverpa armigera,which was accompanied by downregulation of proteins in TGF-βsignaling.However,to date the mechanism underlying this phenomenon remains unknown.Here,we cloned the E3 ubiquitin ligases gene Smurf.In vitro experiments showed that Smurf directly bound to TGF-βreceptor type I(TGFβRI)and Smad2.Overexpressing Smurf promoted ubiquitination of TGFβRI and Smad2,thereby downregulating their protein levels.Conversely,silencing of the Smurf gene suppressed ubiquitination of TGFβRI and Smad2 thereby increasing their protein levels.Results from in vivo co-immunoprecipitation assays revealed that the binding of Smurf to TGFβRI or Smad2 was stronger in diapause pupae than in nondiapause pupae.Injection of Smurf inhibitor A01 into diapause pupae markedly upregulated expression of TGFβRI and Smad2 proteins,leading to resumption of development in diapause pupae.Taken together,these findings suggested that ubiquitin ligase E3 Smurf participated in H.armigera diapause by regulating TGF-βsignaling,and thus could be playing a crucial role in insect diapause.