Effect of Angiotensin II-Mediated Janus Kinase/Signal Transducers and Activators of Transcription Pathways on Thoracic Aortic Smooth Muscle Cells

At present, the effect of angiotensin II on the biological behavior of smooth muscle cells of thoracic aortic aneurysm is not clear. In this study, thoracic aortic aneurysm rat model (thoracic aortic aneurysm model group) was prepared by applying calcium chloride to blood vessels, and normal rats were taken as a sham operation group (sham group), with 10 rats in each group. The changes of angiotensin II content in plasma and left ventricular myocardial tissue were detected. Normal rat thoracic aortic smooth muscle cells were extracted and divided into the control group, angiotensin II group (1 mu g/ml angiotensin II), and angiotensin II+angiotensin receptor blocker group (1x10-6 mol/l candesartan+1 mu g/ml angiotensin II). The cholecystokinin cell counting kit-8, flow cytometry, Transwell chamber, scratch healing, and Western blot experiments were used to detect cell proliferation, apoptosis, invasion, migration, and the expression changes of Janus kinase/signal transducers and activators of transcription pathway-related proteins. The results showed that angiotensin II content in left ventricular myocardium of thoracic aortic aneurysm group was higher than that of Sham group (p<0.01). Compared with the control group, angiotensin II group showed increased cell proliferative activity, number of invaded cells, mobility, and expression levels of Ras-related C3 botulinum toxin substrate 1, phosphorylated-Janus kinase 2, phosphorylated-signal transducers and activators of transcription 1, and phosphorylated-signal transducers and activators of transcription 3 proteins, and decreased apoptosis rate (p<0.05). Compared with the angiotensin II group, the cell proliferative activity, the number of invaded cells, and mobility as well as the expression levels of Ras-related C3 botulinum toxin substrate 1, phosphorylatedJanus kinase 2, phosphorylated-signal transducers and activators of transcription 1, and phosphorylatedsignal transducers and activators of transcription 3 proteins in the angiotensin II+angiotensin receptor blocker group were decreased, and the apoptosis rate was increased (p<0.05). These results indicated that angiotensin II could induce the proliferation, invasion, and migration of thoracic aortic aneurysm smooth muscle cells, and promote apoptosis.