Histology and histopathology · 2025
Regulation of G Protein Signaling 14 protects against cerebral ischemic reperfusion injury by inhibiting the TAK1-JNK/p38 signaling pathway.
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Zhou Gang, Wang Changquan, Bai Wenyi, Gao Ju, Liao Yugao, Wang Lei, Wu Xiangbo, Tian Yu, Wang Guanglin, Xia Guangming, Wang Jinhua
Аннотация
BACKGROUND: Stroke is a crucial cause of morbidity and mortality worldwide. The regulator of G protein signaling 14 (RGS14) plays important roles in mediating multiple signaling pathways and various pathophysiological processes. However, the function of RGS14 in cerebral ischemic reperfusion injury (CIRI) remains unknown.
METHODS AND RESULTS: In this study, the roles of RGS14 during CIRI were studied in terms of gain- and loss-of-function experiments. Using RT-PCR, western blot, and TCC, HE, TUNEL, immunofluorescence, immunohistochemical staining, etc., we found that RGS14 significantly improved CIRI by reducing inflammation and apoptosis in both a mouse model of transient middle cerebral artery occlusion (t/MCAO) and a primary neuronal model of oxygen-glucose deprivation/reperfusion (OGD/R). In addition, mechanism studies have shown that RGS14 acts by inhibiting the activation of the TAK1-JNK/p38 signaling pathway, which was further confirmed using the TAK1 inhibitor (iTAK1), 5Z-7-oxyzeaenol, during OGD/R treatment of AdshRGS14-infected primary neurons.
CONCLUSIONS: These findings imply that RGS14 is a novel negative regulator and may serve as a potential therapeutic target for CIRI.
METHODS AND RESULTS: In this study, the roles of RGS14 during CIRI were studied in terms of gain- and loss-of-function experiments. Using RT-PCR, western blot, and TCC, HE, TUNEL, immunofluorescence, immunohistochemical staining, etc., we found that RGS14 significantly improved CIRI by reducing inflammation and apoptosis in both a mouse model of transient middle cerebral artery occlusion (t/MCAO) and a primary neuronal model of oxygen-glucose deprivation/reperfusion (OGD/R). In addition, mechanism studies have shown that RGS14 acts by inhibiting the activation of the TAK1-JNK/p38 signaling pathway, which was further confirmed using the TAK1 inhibitor (iTAK1), 5Z-7-oxyzeaenol, during OGD/R treatment of AdshRGS14-infected primary neurons.
CONCLUSIONS: These findings imply that RGS14 is a novel negative regulator and may serve as a potential therapeutic target for CIRI.