{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhu M"],"funding":["Priority Speciality of Shanghai Huangpu District Commission Health and Family Planning Commission","National Natural Science Foundation of China"],"pagination":["14175-14187"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9342149"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(6)"],"pubmed_abstract":["Diabetic retinopathy (DR) represents an important microvascular complication of diabetes, which is the top etiology of vision impairment worldwide. Although interleukin (IL)-17A is increasingly implicated in DR development, the underlying cellular mechanisms remain poorly defined. This work aims to evaluate IL-17A levels in the retina of streptozotocin (STZ)-induced diabetic mice and elucidate their potential roles. We found IL-17A was upregulated in diabetic retina after intraperitoneal injection of STZ and high-glucose (HG)-cultured primary Müller cells. IL-17A knockout (IL-17A<sup>-/-</sup>) downregulated glial fibrillary acidic protein (GFAP) and inhibited the conversion of proneurotrophin-3 (proNT-3) to mature NT-3 in retinal specimens from diabetic mice as well as in Müller cells cultured under HG conditions. Induced apoptosis and upregulated Bax and cleaved caspase-3 were observed in retinal specimens from IL-17A<sup>-/-</sup> diabetic mice and photoreceptor (661 W) cells after co-culture with IL-17A<sup>-/-</sup> Müller cells. Moreover, RNA interference-induced gene silencing of tyrosine kinase C receptor (TrkC) in 661 W cells reversed the anti-apoptotic effect of IL-17A under HG conditions. Taken together, our findings suggest that IL-17A/NT-3/TrkC axis regulation suppresses apoptosis in photoreceptor cells, providing a new treatment strategy for DR."],"journal":["Bioengineered"],"pubmed_title":["Interleukin-17A attenuates photoreceptor cell apoptosis in streptozotocin-induced diabetic mouse model."],"pmcid":["PMC9342149"],"funding_grant_id":["81970805","HWZFK201803"],"pubmed_authors":["Zhu M","Wang Y","Shen X","Gao S","Li N"],"additional_accession":[]},"is_claimable":false,"name":"Interleukin-17A attenuates photoreceptor cell apoptosis in streptozotocin-induced diabetic mouse model.","description":"Diabetic retinopathy (DR) represents an important microvascular complication of diabetes, which is the top etiology of vision impairment worldwide. Although interleukin (IL)-17A is increasingly implicated in DR development, the underlying cellular mechanisms remain poorly defined. This work aims to evaluate IL-17A levels in the retina of streptozotocin (STZ)-induced diabetic mice and elucidate their potential roles. We found IL-17A was upregulated in diabetic retina after intraperitoneal injection of STZ and high-glucose (HG)-cultured primary Müller cells. IL-17A knockout (IL-17A<sup>-/-</sup>) downregulated glial fibrillary acidic protein (GFAP) and inhibited the conversion of proneurotrophin-3 (proNT-3) to mature NT-3 in retinal specimens from diabetic mice as well as in Müller cells cultured under HG conditions. Induced apoptosis and upregulated Bax and cleaved caspase-3 were observed in retinal specimens from IL-17A<sup>-/-</sup> diabetic mice and photoreceptor (661 W) cells after co-culture with IL-17A<sup>-/-</sup> Müller cells. Moreover, RNA interference-induced gene silencing of tyrosine kinase C receptor (TrkC) in 661 W cells reversed the anti-apoptotic effect of IL-17A under HG conditions. Taken together, our findings suggest that IL-17A/NT-3/TrkC axis regulation suppresses apoptosis in photoreceptor cells, providing a new treatment strategy for DR.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2025-04-21T22:28:15.092Z","creation":"2025-04-05T18:48:13.914Z"},"accession":"S-EPMC9342149","cross_references":{"pubmed":["35730427"],"doi":["10.1080/21655979.2022.2084241"]}}