PMID- 33970415 OWN - NLM STAT- MEDLINE DCOM- 20211207 LR - 20231213 IS - 1559-0305 (Electronic) IS - 1073-6085 (Linking) VI - 63 IP - 7 DP - 2021 Jul TI - Effect of miR-126 on the Proliferation and Migration of Vascular Smooth Muscle Cells in Aortic Aneurysm Mice Under PI3K/AKT/mTOR Signaling Pathway. PG - 631-637 LID - 10.1007/s12033-021-00327-6 [doi] AB - This paper is to investigate the expression changes of Phosphatidylinositol-3 Kinase (PI3K), protein kinase B (AKT), and Mammalian Target of Rapamycin (mTOR) in Vascular Smooth Muscle Cells (VSMCs) of aortic aneurysm mice, and to analyze the mechanism of VSMCs proliferation and migration. Aortic VSMCs cells were cultured using BALB/c mice as the research object. VSMCs were identified using artificial intelligence-based digital microscopy equipment, and liposome-transfected VSMCs experiments were performed. Real-time PCR was used for the mRNA expression levels of miR-126 and Phosphatase and Tensin Homolog (PTEN). Western blot was used for the protein expression levels of PTEN, PI3K, AKT, and mTOR. The cultured cells were identified as mouse VSMCs using digital microscopes based on artificial intelligence. Compared with the normal group, the expression of miR-126 and PTEN mRNA in the model group were significantly increased and reduced, respectively. Compared with the model group, the expression level of miR-126 and PTEN mRNA in the inhibitor group were significantly reduced and increased, respectively. Compared with the model group, the expression of miR-126 and PTEN mRNA in the ursolic acid group was significantly reduced and increased, respectively. After liposome transfection, compared with the normal group, the expression of PTEN protein in the model group was significantly reduced, and the expression of PI3K protein was significantly increased. Compared with the model group, the expression of PTEN protein was significantly increased and the expression of PI3K protein was significantly decreased in the transfection group. Compared with the control group, the expression of PI3K, AKT and mTOR protein in the model group was significantly increased. Compared with the model group, the expression of PI3K, AKT, and mTOR protein in the ursolic acid group was significantly reduced. The expressions of PI3K, AKT and mTOR protein in PI3K inhibitor group and AKT inhibitor group were significantly reduced. In conclusion, ursolic acid can inhibit the proliferation and migration of VSMCs in aortic aneurysm mice through the miR-126/PTEN/PI3K/AKT/mTOR signaling pathway. Furthermore, PTEN gene and miR-126 negatively regulate PI3K/AKT/mTOR and PTEN/PI3K/AKT/mTOR signaling pathway, respectively . FAU - Huang, Changpin AU - Huang C AD - Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China. FAU - Fang, Xin AU - Fang X AUID- ORCID: 0000-0001-7378-5791 AD - Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China. fangxin111@163.com. FAU - Xie, Xupin AU - Xie X AD - Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China. FAU - Liu, Yongchang AU - Liu Y AD - Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China. FAU - Xu, Dong AU - Xu D AD - Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China. FAU - Meng, Xiaohu AU - Meng X AD - Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China. FAU - Long, Jianyun AU - Long J AD - Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China. LA - eng PT - Journal Article DEP - 20210510 PL - Switzerland TA - Mol Biotechnol JT - Molecular biotechnology JID - 9423533 RN - 0 (Liposomes) RN - 0 (MIRN126 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (Triterpenes) RN - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) RN - EC 3.1.3.67 (PTEN Phosphohydrolase) RN - EC 3.1.3.67 (PTEN protein, human) SB - IM MH - Animals MH - Aortic Aneurysm/etiology/*genetics/metabolism MH - Artificial Intelligence MH - Cell Movement/drug effects MH - Cell Proliferation/drug effects MH - Cells, Cultured MH - Disease Models, Animal MH - Humans MH - Liposomes/metabolism MH - Male MH - Mice MH - Mice, Inbred BALB C MH - MicroRNAs/*genetics MH - Muscle, Smooth, Vascular/*cytology/metabolism MH - Myocytes, Smooth Muscle/cytology/metabolism MH - PTEN Phosphohydrolase/*genetics MH - Phosphatidylinositol 3-Kinase/metabolism MH - Proto-Oncogene Proteins c-akt/metabolism MH - Signal Transduction MH - Triterpenes/*pharmacology MH - Ursolic Acid OTO - NOTNLM OT - Artificial intelligence OT - Infectious aortic aneurysm OT - PI3K/AKT/mTOR OT - VSMCs OT - miR-126 EDAT- 2021/05/11 06:00 MHDA- 2021/12/15 06:00 CRDT- 2021/05/10 12:34 PHST- 2021/03/15 00:00 [received] PHST- 2021/04/09 00:00 [accepted] PHST- 2021/05/11 06:00 [pubmed] PHST- 2021/12/15 06:00 [medline] PHST- 2021/05/10 12:34 [entrez] AID - 10.1007/s12033-021-00327-6 [pii] AID - 10.1007/s12033-021-00327-6 [doi] PST - ppublish SO - Mol Biotechnol. 2021 Jul;63(7):631-637. doi: 10.1007/s12033-021-00327-6. Epub 2021 May 10.