[1]魏冠平 张淼黄煜 何庆.肺泡上皮细胞促进肺动脉平滑肌细胞增殖[J].心血管病学进展,2020,(10):1106.[doi:10.16806/j.cnki.issn.1004-3934.2020.10.025]
　WEI GuanpingZHANG MiaoHUANG YuHE Qing.Hypoxia-induced Alveolar Epithelial Cells Triggers Lung Smooth Proliferative Expansion[J].Advances in Cardiovascular Diseases,2020,(10):1106.[doi:10.16806/j.cnki.issn.1004-3934.2020.10.025]
点击复制

肺泡上皮细胞促进肺动脉平滑肌细胞增殖()
分享到：

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2020年10期
页码:
1106
栏目:
论著
出版日期:
2020-10-25

文章信息/Info

Title:
Hypoxia-induced Alveolar Epithelial Cells Triggers Lung Smooth Proliferative Expansion
作者:
魏冠平1 张淼1黄煜2 何庆1; 2
(1.西南交通大学医学院,四川 成都 610036 ;2.西南交通大学附属成都市第三人民医院,四川 成都 610036 )
Author(s):
WEI Guanping1ZHANG Miao1HUANG Yu2HE Qing1; 2
(1.Southwest Jiaotong University College Of Medicine,Chengdu 610036,Sichuan,China;2.Southwest Jiaotong University Affiliated Chengdu Third People’s Hospital,Chengdu 610036,Sichuan,China)
关键词:
低氧; CX3CL1; 肺泡上皮细胞; 肺动脉平滑肌细胞
Keywords:
Hypoxia; CX3CL1; Pulmonary alveolar epithelial cells; Pulmonary artery smooth muscle cells
DOI:
10.16806/j.cnki.issn.1004-3934.2020.10.025
摘要:
目的 观察低氧条件下肺泡上皮细胞对肺动脉平滑肌细胞（PASMCs）的作用。方法 首先，低氧条件下培养肺泡上皮细胞48 h，采用WB法检测细胞中CX3CL1蛋白的表达，Elisa法检测细胞上清液中CX3CL1的浓度；其次，采用Transwell小室共培养肺泡上皮细胞和PASMCs 48 h，采用MTT法检测PASMCs增殖；最后利用siRNA沉默PASMCs的CX3CR1，采用MTT法检测PASMCs增殖。结果 与对照组比较，肺泡上皮细胞在低氧处理48 h后，CX3CL1蛋白表达、细胞上清液中CX3CL1浓度明显增加（P<0.05）；与对照组相比，PASMCs与肺泡上皮细胞共培养48 h后，PASMCs增殖明显增加（P<0.05）；siRNA沉默后的PASMCs与大鼠肺泡上皮细胞共培养48 h后，PASMCs增殖无明显增加（P>0.05）。结论 低氧条件下肺泡上皮细胞通过CX3CL1促进PASMCs增殖。
Abstract:
Objective To investigate the effect of pulmonary alveolar epithelial cells (AECs) on pulmonary artery smooth cells(PASMCs) under hypoxic conditions. Methods First, under hypoxic conditions, rat AECs were cultured for 48h, and the expressi on of CX3CL1 protein in the cells was detected by WB, while the concentration of CX3CL1 in the cell supernatant was detected by Elisa. Second, transwell compartment co-cultured rat AECs and PASMCs for 48 h. MTT assay was used to detect the proliferation of PASMCs. Finally, siRNA was used to silence CX3CR1 PASMCs, and MTT method was used to detect the proliferation of PASMCs. Results Compared with the control group, the expression of CX3CL1 protein and the concentration of CX3CL1 in cell supernatant increase d significantly after hypoxic treatment for 48h in rat AECs(P<0.01).Compared with the control group, the proliferation of PASMCs increased significantly after 48 h co-culture of AECs and PASMCs(P<0.01).After 48 h of co-culture of PASMCs and rat AECs after siRNA silencing, there was no significant increase in the proliferation of PASMCs (P>0.01).Conclusion Hypoxia-induced AECs CX3CL1 triggers lung smooth proliferative expansion

参考文献/References:


[1] 张国振,何庆.活性氧对高原性肺动脉高压的影响[J].心血管病学进展,2018,39(4):576-579.

[2] Amsellem V,Abid S,Poupel L,et al.Roles for the CX3CL1/CX3CR1 and CCL2/CCR2 chemokine systems in hypoxic pulmonary hypertension [J].Am J Respir Cell Mol Biol,2017,56(5):597-608.

[3] 王领,赵一蔚,任培乐,等.FKN浓度对人脐静脉内皮细胞中CX3CR1表达的影响[J].新疆医科大学学报,2018,41(4):468-471.

[4] Liu W,Liang Y,Chan Q,et al.CX3CL1 promotes lung cancer cell migration and invasion via the Src/focal adhesion kinase signaling pathway[J].Oncol Rep,2019,41(3):1911-1917.

[5] Fernandez-Prieto M,Fernandez-Acenero MJ,Lopez-Palacios N,et al.CX3CL1-CX3CR1 axis:a new player in coeliac disease pathogenesis [J].Nutrients,2019,11(11):2551.

[6] Yang XP,Mattagajasingh S,Su S,et al.Fractalkine upregulates intercellular adhesion molecule-1 in endothelial cells through CX3CR1 and the Jak Stat5 pathway [J].Circ Res,2007,101(10):1001-1008.

[7] Zhang J,Hu H,Palma NL,et al.Hypoxia-induced endothelial CX3CL1 triggers lung smooth muscle cell phenotypic switching and proliferative expansion [J].Am J Physiol Lung Cell Mol Physiol,2012,303(10):L912-L922.

[8] 王艳霞.AECs在低氧性肺动脉高压中的作用及机制研究[D].中国人民解放军空军军医大学,2018.

[9] Galie N,McLaughlin VV,Rubin LJ,et al.An overview of the 6th world symposium on pulmonary hypertension[J].Eur Respir J,2019,53(1):1802148.

[10] Strange G,Playford D,Stewart S,et al.Pulmonary hypertension:prevalence and mortality in the armadale echocardiography cohort [J].Heart,2012,98(24):1805-1811.

[11] Simonneau G,Montani D,Celermajer DS,et al.Haemodynamic definitions and updated clinical classification of pulmonary hypertension[J].Eur Respir J,2019,53(1):1801913.

[12] Gall H,Felix JF,Schneck FK,et al.The giessen pulmonary hypertension registry:survival in pulmonary hypertension subgroups[J].J Heart Lung Transplant,2017,36(9):957-967.

[13] Hurdman J,Condliffe R,Elliot CA,et al.Pulmonary hypertension in COPD:results from the ASPIRE registry[J].Eur Respir J,2013,41(6):1292-1301.

[14] Wilkins MR,Ghofrani HA,Weissmann N,et al.Pathophysiology and treatment of high-altitude pulmonary vascular disease[J].Circulation,2015,131(6):582-590.

[15] Mason RJ.Biology of alveolar pulmonary cells[J].Respirology,2006,11 Suppl:S12-15.

[16] Serrano-Mollar A,Gay-Jordi G,Guillamat-Prats R,et al.Safety and tolerability of alveolar pulmonary cell transplantation in idiopathic pulmonary fibrosis [J].Chest,2016,150(3):533-543.

[17] Oczypok EA,Perkins TN,Oury TD.Alveolar epithelial cell-derived mediators:potential direct regulators of large airway and vascular responses [J].Am J Respir Cell Mol Biol,2017,56(6):694-699.

[18] Umehara H,Bloom E,Okazaki T,et al.Fractalkine and vascular injury[J].Trends Immunol,2001,22(11):602-607.

[19] Singh SK,Mishra MK,Singh R.Hypoxia-inducible factor-1alpha induces CX3CR1 expression and promotes the epithelial to mesenchymal transition (EMT) in ovarian cancer cells[J].J Ovarian Res,2019,12(1):42.

[20] McDermott DH,Colla JS,Kleeberger CA,et al.Genetic polymorphism in CX3CR1 and risk of HIV disease [J].Science,2000,290(5499):2031.

[21] Lesnik P,Haskell CA,Charo IF.Decreased atherosclerosis in CX3CR1-/- mice reveals a role for fractalkine in atherogenesis[J].J Clin Invest,2003,111(3):333-340.

[22] Zhang X,Feng X,Cai W,et al.Chemokine CX3CL1 and its receptor CX3CR1 are associated with human atherosclerotic lesion volnerability [J].Thromb Res,2015,135(6):1147-1153.

[23] 陈小菊,程德云,樊莉莉.低氧对大鼠PASMCs和肺微血管内皮细胞表达及分泌Fractalkine的影响[J].四川大学报（医学版）,2012,43(5).661-665.

更新日期/Last Update: 2020-12-22