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Regulation of YAP translocation by myeloid Pten deficiency alleviates acute lung injury via inhibition of oxidative stress and inflammation.

Free Radic Biol Med

September 2024

Department of Respiratory and Critical Care Medicine, Affiliated People's Hospital of Jiangsu University, Zhenjiang School of Clinical Medicine with Nanjing Medical University, Zhenjiang, Jiangsu, China. Electronic address:

Background: Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is intricately involved in modulating the inflammatory response in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Nevertheless, the myeloid PTEN governing Hippo-YAP pathway mediated oxidative stress and inflammation in lipopolysaccharide (LPS)-induced ALI remains to be elucidate.

Methods: The floxed Pten (Pten) and myeloid-specific Pten knockout (Pten) mice were intratracheal instill LPS (5 mg/kg) to establish ALI, then Yap siRNA mix with the mannose-conjugated polymers was used to knockdown endogenous macrophage YAP in some Pten mice before LPS challenged.

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