| First Author | Tian H | Year | 2019 |
| Journal | Biochem Biophys Res Commun | Volume | 513 |
| Issue | 2 | Pages | 360-367 |
| PubMed ID | 30961932 | Mgi Jnum | J:291672 |
| Mgi Id | MGI:6442429 | Doi | 10.1016/j.bbrc.2019.03.187 |
| Citation | Tian H, et al. (2019) SHP-1 inhibits renal ischemia reperfusion injury via dephosphorylating ASK1 and suppressing apoptosis. Biochem Biophys Res Commun 513(2):360-367 |
| abstractText | Apoptosis of tubular epithelium cells (TECs) plays critical roles in renal ischemia reperfusion (I/R) injury, but the molecular regulatory mechanisms of apoptosis still require further investigation. Recently, phosphatase family members have been suggested to regulate multiple aspects of the injury and regeneration response. However, the roles of SHP-1, an important protein-tyrosine phosphatase, in the regulation of renal I/R injury remain unknown. Here, we found that SHP-1 knockdown in vivo significantly increased renal I/R injury and aggravated the apoptosis of TECs. Consistently, after SHP-1 knockdown in TECs in vitro, a sharp increase of apoptosis induced by cobalt dichloride was found. The protective role of SHP-1 was also validated in a TEC cell line stably overexpressing SHP-1. Mechanistically, the ASK1/MKK4/JNK pro-apoptosis signal was over activated after SHP-1 knockdown, and SHP-1 could bind to and dephosphorylate ASK1 to inhibit its activation, thus repressing apoptosis. |
