Lu, Jinhua; Lin, Shengyou; Lin, Zechen; Lin, Xianlei; Shen, Yuezhong; Su, Jingyang published the artcile< PPM1A as a key target of the application of Jiawei-Maxing-Shigan decoction for the attenuation of radiation-induced epithelial-mesenchymal transition in type II alveolar epithelial cells>, SDS of cas: 112-63-0, the main research area is type II alveolar epithelial cell mesenchymal transition radiation; Jiawei Maxing Shigan decoction PPM1A; Jiawei‑Maxing‑Shigan decoction; Radiation‑induced injury; TGF‑β1/Smad signaling; epithelial‑mesenchymal transition; protein phosphatase Mg2+/Mn2+‑dependent 1A.
Radiation-induced lung tissue injury is an important reason for the limited application of radiotherapy on thoracic malignancies. Previously, we reported that administration of Jiawei-Maxing-Shigan decoction (JMSD) attenuated the radiation-induced epithelial-mesenchymal transition (EMT) in alveolar epithelial cells (AECs) via TGF-β/Smad signaling. The present study aimed to examine the role of protein phosphatase Mg2+/Mn2+-dependent 1A (PPM1A) in the anti-EMT activity of JMSD on AECs. The components in the aqueous extract of JMSD were identified by high-performance liquid chromatog. coupled with electrospray mass spectrometry. Primary rat type II AECs were treated with radiation (60Co γ-ray at 8 Gy) and JMSD-medicated serum. PPM1A was overexpressed and knocked down in the AECs via lentivirus transduction and the effects of JMSD administration on the key proteins related to TGF-β1/Smad signaling were measured by western blotting. It was found that radiation decreased the PPM1A expression in the AECs and JMSD-medicated serum upregulated the PPM1A expressions in the radiation-induced AECs. PPM1A overexpression increased the E-cadherin level but decreased the phosphorylated (p-)Smad2/3, vimentin and α-smooth muscle actin (α-SMA) levels in the AECs. By contrast, the PPM1A knockdown decreased the E-cadherin level and increased the p-Smad2/3, vimentin and α-SMA levels in the AECs and these effects could be blocked by SB431542 (TGF-β1/Smad signaling inhibitor). JMSD administration increased the E-cadherin level and decreased the p-Smad2/3, vimentin and α-SMA levels in the AECs; however, these effects could be blocked by siPPM1A-2. In conclusion, PPM1A is a key target of JMSD administration for the attenuation of the radiation-induced EMT in primary type II AECs via the TGF-β1/Smad pathway.
Molecular Medicine Reports published new progress about Apricot. 112-63-0 belongs to class esters-buliding-blocks, and the molecular formula is C19H34O2, SDS of cas: 112-63-0.
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