TSC-36/FRP inhibits vascular smooth muscle cell proliferation and migration
- Resource Type
- Authors
- Hengyi Guo; Jing Han; Wei Wang; Shu Liu; Renyu Sun; Jie Lin; Luya Wang; Qixia Wu; Haiyan Sun
- Source
- Experimental and molecular pathology. 80(2)
- Subject
- Vascular smooth muscle
Follistatin-Related Proteins
Clinical Biochemistry
Muscle, Smooth, Vascular
Pathology and Forensic Medicine
Flow cytometry
Rats, Sprague-Dawley
chemistry.chemical_compound
In vivo
Cell Movement
medicine
Myocyte
Animals
Humans
RNA, Messenger
Molecular Biology
In Situ Hybridization
Cell Proliferation
medicine.diagnostic_test
Cell growth
Chemistry
Daidzein
Matricellular protein
Cell Cycle
Cell migration
Molecular biology
Immunohistochemistry
Isoflavones
Recombinant Proteins
Rats
Carotid Arteries
Immunology
cardiovascular system
- Language
- ISSN
- 0014-4800
Objective : In-stent restenosis is a vascular proliferation/migration disorder characterized by hyperplasia of vascular smooth muscle cells (VSMCs). Because mounting evidence suggests that the therapeutic potential of anti-proliferation and anti-migration therapy, we investigated possible inhibitory effects of the matricellular protein TGF-beta-stimulated clone 36 (TSC-36) on vascular smooth muscle cell proliferation and migration in vitro and in vivo. Methods: : Human umbilical artery smooth muscle cells (SMCs) were treated with inducting agents daidzein or estradiol. TSC-36 expression was detected by nested competitive PCR and in situ hybridization. TSC-36 was expressed in Origami (DE3) cells. The recombinant protein was used to immunize rabbits to produce polyclonal antibodies. VSMCs were treated with various concentrations of recombinant TSC-36 (rTSC-36) protein and daidzein. The MTT assay was used to analyze for cell proliferation. A transwell system was used to detect cell migration. Flow cytometry was used to detect cell phase. A rat carotid artery balloon injury model was duplicated. The rats were treated with daidzein or solvent control. Animals were sacrificed 5 weeks later, and injured arteries were taken for pathology and histology. Results : TSC-36 mRNA and protein expression was induced in SMCs. Cell proliferation and migration were inhibited by rTSC-36. rTSC-36 caused accumulation of SMCs in G2 phase. The inducting agent daidzein decreased neo-intima proliferation. TSC-36 mRNA and protein expression was induced and expressed in the neo-intima. Conclusion : TSC-36 can be induced in VSMCs and inhibits VSMCs proliferation in vitro and in vivo.