Publication: Regulation of G protein signaling 14 protects against cerebral ischemic reperfusion injury by inhibiting the TAK1-JNK/p38 signaling pathway
Authors
Changquan Wang ; Wenyi Bai ; Ju Gao ; Yugao Liao ; Lei Wang ; Xiangbo Wu ; Yu Tian ; Guanglin Wang ; Guangming Xia ; Jinhua Wang ; Gang Zhou
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Publisher
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Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-25-018
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info:eu-repo/semantics/article
Description
Abstract
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.
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