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STAT3 activation in microglia increases pericyte apoptosis in diabetic retinas through TNF-ɑ/AKT/p70S6 kinase signaling

Cited 0 time in Web of Science Cited 11 time in Scopus
Authors

Yun, Jang-Hyuk; Lee, Da-Hye; Jeong, Han-Seok; Kim, Seung-Hoon; Ye, Sang-Kyu; Cho, Chung-Hyun

Issue Date
2022-07
Publisher
Elsevier B.V.
Citation
Biochemical and Biophysical Research Communications, Vol.613, pp.133-139
Abstract
© 2022 Elsevier Inc.Diabetic retinopathy (DR) is one of the vascular complications associated with diabetes mellitus. Pericyte loss is an early characteristic phenomenon in DR. However, the mechanism by which pericyte apoptosis occurs in DR is not fully understood. We have focused on the increased STAT3 activation in diabetic retinas because STAT3 activation is associated with inflammation, and persistent chronic inflammation is closely related to retinal lesions. In this study, we demonstrated that STAT3 was activated by IFN-γ and IL-6 that highly expressed in diabetic retinas. We identified TNF-α as a potent inducer of pericyte apoptosis in diabetic retinas from the gene expression analysis and found that STAT3 activation in microglia increased TNF-α expression in the diabetic retinas. We also demonstrated that increased TNF-α expression in microglia caused pericyte apoptosis through downregulating AKT/p70S6 kinase signaling. Moreover, we took advantage of mice lacking STAT3 in microglia and demonstrated that STAT3 ablation in microglia reduced the pericyte apoptosis and TNF-α expression in the diabetic retinas. These results suggest that STAT3 activation in microglia plays an important role in pericyte apoptosis in the diabetic retinas through increased TNF-α expression and provide STAT3 activation in microglia as a potential therapeutic target for preventing pericyte loss in DR.
ISSN
0006-291X
URI
https://hdl.handle.net/10371/185334
DOI
https://doi.org/10.1016/j.bbrc.2022.05.004
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