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Galectin-3 Mediates Thrombin-Induced Vascular Smooth Muscle Cell Migration
Lei Tian1, Chun-Kai Huang1, Fenghua Ding1
1Department of Cardiovascular Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Frontiers in Cardiovascular Medicine
|November 8, 2021
Summary
Thrombin induces vascular smooth muscle cell migration via galectin-3, impacting atherosclerosis. Inhibiting galectin-3 or related pathways (MAPK, Src/FAK) prevents this migration, offering new therapeutic targets for plaque instability.
Area of Science:
- Cardiovascular Biology
- Cell Signaling
- Atherosclerosis Research
Background:
- Vascular smooth muscle cell (VSMC) migration is critical in the development of vulnerable atherosclerotic plaques.
- Thrombin plays a significant role in both normal and pathological aspects of atherosclerosis.
- Understanding thrombin's role in VSMC migration is key to preventing plaque instability.
Purpose of the Study:
- To elucidate the mechanisms of thrombin-induced VSMC migration.
- To investigate the role of galectin-3 in this process.
- To identify key signaling pathways involved in thrombin-mediated VSMC migration.
Main Methods:
- Utilized small interfering RNA (siRNA) to knockdown galectin-3.
- Analyzed the activation of MAPK (ERK1/2, p38, JNK) and Src/FAK signaling pathways.
- Assessed VSMC migration and paxillin expression following thrombin stimulation and galectin-3 knockdown or pathway inhibition.
Main Results:
- Thrombin activated MAPK pathways and increased galectin-3 expression.
- Galectin-3 knockdown inhibited thrombin-induced ERK1/2 and p38 MAPK activation and FAK phosphorylation.
- Inhibiting galectin-3, p38 MAPK, or ERK1/2 effectively reduced thrombin-induced VSMC migration and paxillin expression.
Conclusions:
- Galectin-3 regulates thrombin-induced VSMC migration and paxillin expression.
- ERK1/2, p38 MAPK, and Src/FAK signaling pathways are integral to this process.
- Findings provide insights into galectin-3's role in atherosclerosis and potential therapeutic strategies against plaque rupture.
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