Platelet TGF-? 1 inhibits the migration and proliferation of smooth muscle cells in aneurysms

Background: The study explored the role of platelet TGF-fi1 from the perspective of inhibiting the excessive proliferation, migration and invasion of murine aortic vascular smooth muscle cells (MASMCs).Method: The platelets were first extracted from C57BL/6 mice, and the TGF-fi1 protein was obtained after the purification of protein. In vitro, the concentrations of angiotensin II (Ang II) and TGF-fi1 for intervention were screened by testing the viability of MASMCs, followed by the analysis concerning the effects of platelets, Ang II and TGF-fi1 on the proliferation, migration, invasion, and the expressions of pathway-related proteins in MASMCs. In vivo, an Ang II-induced mouse model was established. TGF-fi1 was injected into the tail of mice as a therapeutic agent, and its action mechanism was further verified by the treatment of inhibitor SB505124. The results of the cell experiment were validated by evaluating the maximum diameter of abdominal aorta, the proportion of total weight, the changes of both pathology and the expressions of pathway-related proteins in the mice.Result: 0.5 ng/mL Ang II and 15 ng/mL TGF-fi1 were chosen for treatment. The following results of cell functional experiments and Western blot assay demonstrated that Ang II promoted the proliferation, migration and invasion of MASMCs via regulating related pathways, the effects of which were evidently reversed by TGF-fi1 and platelets. Consistent results were also observed in the animal experiments, where TGF-fi1 effectively alleviated Ang II-induced abdominal aortic injury in mice.Conclusion: TGF-fi1 in platelets inhibits Ang II-induced proliferation, migration and invasion of MASMCs.