Expression Of Slit3/Robo Single In Mouse Aortic Smooth Muscle Cells And Impact Of Exogenous Slit3on Proliferation And Migration Of Mouse Aortic Smooth Muscle Cells

Background and objectives: Atherosclerosis is a major diseaseaffecting the survival and quality of people’s life. For many years, numerousexperts and scholars had a omnidirectional and multi-level studys about themechanism of atherosclerosis. Although the mechanism has not yet fullyunderstood, however, most scholars believe that abnormal proliferation andmigration of vascular smooth muscle cell is the core pathological changes ofcardiovascular disease. Studies confirm that the proliferation and migration ofVSMCs are a variety of common regulation of inflammatory cytokines andgrowth factors. Recent studies have found that neural axon guidancemolecules Slit3is a novel angiogenic factor, and is closely related to theinflammatory reaction, Slit3may also by paracrine and autocrine mechanismto adjust the function of VSMCs. The purpose of this paper is detectingSlit3/Robo signal expression in mouse aorta smooth muscle cells, clarifingwhether Slit3modulates mouse aorta smooth muscle cells functions,exploreing the molecular mechanism, and laying the theoretical foundationfor clarifing the relationship between Slit3and pathogenesis ofatherosclerosis.Methods: Isolation and culture of mouse aortic smooth muscle cells invitro, identified by immunofluorescence, detect Slit and Robo receptorexpression by RT-PCR and immunohistochemistry. Observation effects ofmouse aorta smooth muscle cell proliferation and migration upon exogenous Slit3stimulation by CCK-8, scratched cells and transwell chambers.Results：1. Cultivation of the primary cell and identification, Slit andRobo detection: Succeeded in producing mouse aortic smooth muscle cells,identified as the target cell, and Slit2, Slit3and Robo1, Robo4genes andproteins were detected in mouse aortic smooth muscle cells.2. Cellproliferation assay：Mouse aorta smooth muscle cells showed mitogenicresponses to exogenous Slit3. The mitogenic activity of40ng/mL Slit3wasthe maximal(P<0.05)．3. Detection of cell migration: Exogenous Slit3couldpromot mouse aorta smooth muscle cells migration. The migration activity of80ng/mL Slit3was maximal (P<0.05).Conclusion:1. Slit2, Slit3and Robo1, Robo4were expresed in mouseaortic smooth muscle cells.2. Exogenous Slit3could promote mouse aortasmooth muscle cells proliferation and migration.