HSPB8 Promotes the Fusion of Autophagosome and Lysosome during Autophagy in Diabetic Neurons.

HSPB8 Promotes the Fusion of Autophagosome and Lysosome during Autophagy in Diabetic Neurons. Int J Med Sci. 2017;14(13):1335-1341 Authors: Li XC, Hu QK, Chen L, Liu SY, Su S, Tao H, Zhang LN, Sun T, He LJ Abstract Although autophagy has been proposed to play an emerging role in diabetic neuropathy, autophagy and its possible role remains unclear. Moreover, only few studies about diabetes have explored the autophagy mediated by heat shock protein beta-8 (HSPB8) and Bcl-2 associated athanogene 3 (BAG3). In the present study, we examined the autophagy induced by high glucose levels in an in vivo rat model of diabetes induced by streptozotocin (STZ) and an in vitro model of retinal ganglion cell-5 (RGC5) cells under high glucose conditions. In the spinal cord tissues of the STZ-induced diabetic rats, the levels of light chain 3 (LC3) and Beclin-1-marked autophagy rose with increasing HSPB8 and BAG3 levels. By confocal immunofluorescence, HSPB8 and LC3 were observed to be co-localized in the spinal cord tissues. In the RGC5 cells, high-glucose stimulation upregulated the expression of LC3-Ⅱ, Beclin-1, and HSPB8 in a dose-dependent manner. When the RGC5 cells were subjected to high-glucose conditions, HSPB8 overexpression, along with upregulated LC3-Ⅱ and Beclin-1 expression, increased the autophagic rate, whereas siRNA-silenced HSPB8 decreased the autophagic rate. Furthermore, in GFP-mRFP-LC3 probe experiments, HSPB8 overexpression p...
Source: International Journal of Medical Sciences - Category: Biomedical Science Tags: Int J Med Sci Source Type: research