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Increasing expression of dual-specificity phosphatase 12 mitigates oxygen-glucose deprivation/reoxygenation-induced neuronal apoptosis and inflammation through inactivation of the ASK1-JNK/p38 MAPK pathway.
- Source :
- Autoimmunity; Dec2024, Vol. 57 Issue 1, p1-11, 11p
- Publication Year :
- 2024
-
Abstract
- Dual-specificity phosphatase 12 (DUSP12) is abnormally expressed under various pathological conditions and plays a crucial role in the pathological progression of disorders. however, the role of DUSP12 in cerebral ischaemia/reperfusion injury has not yet been investigated. this study explored the possible link between DUSP12 and cerebral ischaemia/reperfusion injury using an oxygen-glucose deprivation/ reoxygenation (OGD/R) model. Marked decreases in DUSP12 levels have been observed in cultured neurons exposed to OGD/R. DUSP12-overexpressed neurons were resistant to OGD/R-induced apoptosis and inflammation, whereas DUSP12-deficient neurons were vulnerable to OGD/R-evoked injuries. Further investigation revealed that DUSP12 overexpression or deficiency affects the phosphorylation of apoptosis signal-regulating kinase 1 (ASK1), c-Jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) in neurons under OGD/R conditions. Moreover, blockade of ASK1 diminished the regulatory effect of DUSP12 deficiency on JNK and p38 MAPK activation. in addition, DUsP12-deficiency-elicited effects exacerbating neuronal OGD/R injury were reversed by ASK1 blockade. in summary, DUSP12 protects against neuronal OGD/R injury by reducing apoptosis and inflammation through inactivation of the ASK1-JNK/p38 MAPK pathway. these findings imply a neuroprotective function for DUSP12 in cerebral ischaemia/reperfusion injury. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 08916934
- Volume :
- 57
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Autoimmunity
- Publication Type :
- Academic Journal
- Accession number :
- 178523775
- Full Text :
- https://doi.org/10.1080/08916934.2024.2345919