桩蛋白调控肝肺综合征大鼠血清诱导PASMCs的增殖和迁移
The Regulation of Paxillin on the Proliferation and Migration of PASMCs Induced by the Serum of Rats with HPS
DOI: 10.12677/acm.2025.1572173, PDF,    科研立项经费支持
作者: 文 静*, 鲜俊杰, 陈 杨#：重庆市第七人民医院(重庆理工大学附属中心医院)麻醉科，重庆；陈 林：陆军军医大学第一附属医院麻醉科，重庆
关键词: 肝肺综合征；肺动脉平滑肌细胞；桩蛋白；Hepatopulmonary Syndrome； Pulmonary Arterial Smooth Muscle Cells； Paxillin
摘要: 目的：评价桩蛋白(Paxillin)在肝肺综合征(HPS)大鼠血清诱导肺动脉平滑肌细胞(PASMCs)增殖和迁移中的作用。方法：选取20只雄性Sprague-Dawley大鼠，运用慢性胆总管结扎法构建HPS大鼠模型，并采集腹主动脉血样制备血清。将培养的大鼠PASMCs分别接种于6孔板、24孔板和96孔板，通过随机数字表法均分为2组：对照组(C组)和HPS组。C组添加正常大鼠血清，HPS组加入HPS大鼠血清，使两组血清终浓度均为5%。于细胞孵育24 h (T1)、48 h (T2)和72 h (T3)，采用RT-PCR法和Western blot法测定PASMCs内paxillin mRNA及其蛋白的表达水平；运用3H-TdR法检测PASMCs的增殖水平，借助Transwell小室(T1)及划痕实验(T1~T3)测定PASMCs的迁移水平。结果：与C组相比，HPS组PASMCs的增殖和迁移能力显著增强(P < 0.05)；且HPS组随着刺激时间的延长，paxillin mRNA及其蛋白表达呈现逐渐上调趋势(P < 0.05)。结论：在HPS大鼠血清刺激下，PASMCs中paxillin表达逐渐上调，这可能在HPS相关的PASMCs异常增殖和迁移过程中发挥重要的调节作用。
Abstract: Objective: To explore the mechanism of action of paxillin in the proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs) induced by the serum of rats with hepatopulmonary syndrome (HPS). Methods: Twenty male Sprague-Dawley rats were selected. The HPS rat model was established by chronic common bile duct ligation, and abdominal aortic blood was collected to prepare serum. The cultured rat PASMCs were seeded into 6-well, 24-well, and 96-well plates respectively, and randomly divided into a control group (Group C) and an HPS group using the random number table method. Group C was supplemented with normal rat serum, while the HPS group was added with HPS rat serum, with the final serum concentration adjusted to 5% in both groups. At the time points of 24 h (T1), 48 h (T2), and 72 h (T3) of cell incubation, RT-PCR and Western blot were used to determine the expression levels of paxillin mRNA and protein in PASMCs. The 3H-TdR method was employed to detect the proliferation level of PASMCs, and the Transwell chamber (T1) and scratch assay (T1~T3) were used to measure the migration level of PASMCs. Results: Compared with Group C, the proliferation and migration abilities of PASMCs in the HPS group were significantly enhanced (P < 0.05). In the HPS group, the expression of paxillin mRNA and protein showed a gradually increasing trend with the extension of the stimulation time (P < 0.05). Conclusion: Stimulation by the serum of HPS rats can gradually upregulate the expression of paxillin in PASMCs, which may play a crucial regulatory role in the abnormal proliferation and migration of PASMCs associated with HPS.
文章引用：文静, 鲜俊杰, 陈林, 陈杨. 桩蛋白调控肝肺综合征大鼠血清诱导PASMCs的增殖和迁移[J]. 临床医学进展, 2025, 15(7): 1678-1683. https://doi.org/10.12677/acm.2025.1572173

参考文献

[1] Liu, L., Liu, N., Zhao, Z., Liu, J., Feng, Y., Jiang, H., et al. (2012) TNF‐α Neutralization Improves Experimental Hepatopulmonary Syndrome in Rats. Liver International, 32, 1018-1026. [Google Scholar] [CrossRef] [PubMed]
[2] Morrell, N.W., Adnot, S., Archer, S.L., Dupuis, J., Lloyd Jones, P., MacLean, M.R., et al. (2009) Cellular and Molecular Basis of Pulmonary Arterial Hypertension. Journal of the American College of Cardiology, 54, S20-S31. [Google Scholar] [CrossRef] [PubMed]
[3] Dubrovskyi, O., Tian, X., Poroyko, V., Yakubov, B., Birukova, A.A. and Birukov, K.G. (2012) Identification of Paxilin Domains Interacting with β‐Catenin. FEBS Letters, 586, 2294-2299. [Google Scholar] [CrossRef] [PubMed]
[4] 国斌, 易斌, 徐顺贵, 等. 肝肺综合征大鼠血清对肺微血管内皮细胞Akt表达的影响[J]. 中华麻醉学杂志, 2010, 30(1): 75-78.
[5] Luo, C., Yi, B., Bai, L., Xia, Y., Wang, G., Qian, G., et al. (2010) Suppression of Akt1 Phosphorylation by Adenoviral Transfer of the PTEN Gene Inhibits Hypoxia-Induced Proliferation of Rat Pulmonary Arterial Smooth Muscle Cells. Biochemical and Biophysical Research Communications, 397, 486-492. [Google Scholar] [CrossRef] [PubMed]
[6] Hertzog, J. and Rehwinkel, J. (2023) A Simple Transwell-Based Infection System for Obtaining Pure Populations of VZV-Infected Cells. Journal of Virological Methods, 312, Article ID: 114661. [Google Scholar] [CrossRef] [PubMed]
[7] 王丽平, 李季声, 邓黎, 等. 高迁移率族蛋白B1对体外氧糖剥夺/复氧复糖后大鼠脊髓反应性星形胶质细胞不同亚型的作用[J]. 中国组织工程研究, 2023, 27(24): 3831-3837.
[8] Yi, B., Cui, J., Ning, J., Wang, G., Qian, G. and Lu, K. (2012) Over-Expression of PKGIα Inhibits Hypoxia-Induced Proliferation, Akt Activation, and Phenotype Modulation of Human PASMCs: The Role of Phenotype Modulation of PASMCs in Pulmonary Vascular Remodeling. Gene, 492, 354-360. [Google Scholar] [CrossRef] [PubMed]
[9] Schaller, M.D. (2001) Paxillin: A Focal Adhesion-Associated Adaptor Protein. Oncogene, 20, 6459-6472. [Google Scholar] [CrossRef] [PubMed]
[10] Chen, D., Wang, D., Wu, W., Zeng, Z., Luo, H., Qiu, M., et al. (2012) Overexpression of Paxillin Induced by miR-137 Suppression Promotes Tumor Progression and Metastasis in Colorectal Cancer. Carcinogenesis, 34, 803-811. [Google Scholar] [CrossRef] [PubMed]
[11] Veith, C., Marsh, L.M., Wygrecka, M., Rutschmann, K., Seeger, W., Weissmann, N., et al. (2012) Paxillin Regulates Pulmonary Arterial Smooth Muscle Cell Function in Pulmonary Hypertension. The American Journal of Pathology, 181, 1621-1633. [Google Scholar] [CrossRef] [PubMed]
[12] Kim, M.S., Yoo, N.J. and Lee, S.H. (2011) Absence of Paxillin Gene Mutation in Lung Cancer and Other Common Solid Cancers. Tumori Journal, 97, 211-213. [Google Scholar] [CrossRef] [PubMed]

为你推荐