Platelet TGF-β1 inhibits the migration and proliferation of smooth muscle cells in aneurysms

Background: The study explored the role of platelet TGF-β1 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-β1 protein was obtained after the purification of protein. In vitro, the concentrations of angiotensin Ⅱ (Ang Ⅱ) and TGF-β1 for intervention were screened by testing the viability of MASMCs, followed by the analysis concerning the effects of platelets, Ang Ⅱ and TGF-β1 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-β1 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-β1 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-β1 and platelets. Consistent results were also observed in the animal experiments, where TGF-β1 effectively alleviated Ang Ⅱ-induced abdominal aortic injury in mice.

Conclusion: TGF-β1 in platelets inhibits Ang Ⅱ-induced proliferation, migration and invasion of MASMCs.