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Steroid receptor RNA activator affects the development of poststroke depression by regulating the peroxisome proliferator-activated receptor γ signaling pathway

The long noncoding RNA, steroid receptor RNA activator (SRA), has been reported to be involved in the development of many types of disease in humans. The aim of this study was to evaluate whether SRA was associated with poststroke depression (PSD). A PSD rat model was established, and depression-lik...

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Detalles Bibliográficos
Autores principales: Jiang, Baoying, Wang, Hongwei, Xu, Houchi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6903361/
https://www.ncbi.nlm.nih.gov/pubmed/31714481
http://dx.doi.org/10.1097/WNR.0000000000001367
Descripción
Sumario:The long noncoding RNA, steroid receptor RNA activator (SRA), has been reported to be involved in the development of many types of disease in humans. The aim of this study was to evaluate whether SRA was associated with poststroke depression (PSD). A PSD rat model was established, and depression-like behaviors and sucrose consumption in rats with PSD were analyzed. Reverse transcription-quantitative PCR (RT-PCR), western blot and luciferase dual reporter assay analyses were performed to detect the expression of peroxisome proliferator-activated receptor γ (PPARγ) expression following SRA small interfering RNA (siRNA) treatment. Compared with the control, the horizontal and vertical movement scores and consumption of sucrose solution were decreased in the PSD, PSD + LV-SRA and PSD + pioglitazone groups at 7 days post-SRA-siRNA treatment, while they were increased in the PSD + LV-SRA and PSD + pioglitazone groups. Furthermore, SRA expression in the PSD, PSD + LV-SRA and PSD + pioglitazone groups was lowered compared with the control group at 7 days postinjection. SRA increased the reported luciferase activity, but pioglitazone had no effect on the luciferase activity induced by SRA. SRA upregulated PPARγ mRNA and protein expression, whereas SRA siRNA significantly downregulated its expression. No significant differences in characteristics were identified between rats with and without PSD. SRA was more highly expressed in rats with PSD than rats without PSD. Collectively, this study suggests that SRA is associated with PSD through PPARγ signaling, indicating a potential therapeutic target of SRA for controlling PSD.