| Autor: |
ZHANG Li, WANG Jia, FANG Shizheng, ZHANG Zhongjian, YANG X., WANG Wushua, SUN Xiongshan, YANG Dachun |
| Předmět: |
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| Zdroj: |
Chinese Journal of Pathophysiology; Jun2024, Vol. 40 Issue 6, p971-979, 9p |
| Abstrakt: |
AIM: lo investigate the role of phosphoenolpyruvate carboxykinase 1 ^PCK1) in the proliferation and migration of mouse vascular smooth muscle cells (VSMCs) and the underlying mechanism. METHODS: The proliferation and migration of mouse VSMCs were induced by platelet-derived growth factor (PDGF)-BB. The cells were divided into a vehicle group and a PDGF-BB group. The expression of PCK1 was detected by Western blot and immunofluorescence staining. The mouse Pckl siRNA (siPckl) were transfected into mouse VSMCs to silence PCK1. The cells were divided into the vehicle, siPckl+vehicle, PDGF-BB and siPckl+PDGF-BB groups. The protein level of PCK1 was detected by Western blot. The proliferation was explored by Ki-67 immunofluorescence staining and the viability was detected by CCK-8 assay. The migration was determined by a scratch test. Mitochondrial dynamics were observed via transmission electron microscopy. A lentivirus carrying dynamin-related protein 1 (Drpl) gene (lenti-Drpl) was transfected into VSMCs to induce them to overexpress DRP1. The cells were divided into the PDGF-BB, siPckl +PDGF-BB, lenti-Drpl + PDGF-BB and lenti-Drpl+siPck1+PDGF-BB groups. Proliferation, migration and mitochondrial dynamics were measured as described above. RESULTS: PDGF-BB increased the protein expression of PCK1 and DRP1, cell viability, the percentage of Ki-67-positive cells, the wound healing rate and mitochondrial division in VSMCs. These effects were suppressed when PCK1 protein expression was silenced. After DRP1 was overexpressed, the inhibitory effects of PCK1 silencing on cell viability, the percentage of Ki-67-positive cells, the wound healing rate and mitochondrial division were significantly reversed. CONCLUSION: PCK1 promotes the mitochondrial division, proliferation and migration of VSMCs in mice by upregulating the expression of DRP1. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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