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A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application
Published on: July 9, 2020
Transient receptor potential canonical 3/5 attenuate endothelial damage-induced neointima formation without affecting
Wenjun Zeng1, Bei Liu2, Lixia Yang2
1Department of Geratology, The first People's Hospital of Yunnan Province; Kunming Medical University, Kunming, Yunnan.
Abstract:
Store-operated calcium channels (SOCCs) are involved in the process of cell proliferation; however, their expression levels differ among cell types and information on their effects in different cells is lacking. This study aimed to compare the differing effects of SOCCs on the proliferation of vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs), and the repair ability of SOCC after vascular endothelial injury. Rat primary coronary VSMCs and VECs were cultured in vitro and expression levels of SOCC molecules were detected by western blotting and quantitative polymerase chain reaction. Various molecules were selected and transfected into VSMCs and VECs using an adenovirus vector, and cell proliferation, the cell cycle, and intracellular Ca2+ were then detected. We also established a rat carotid artery endothelial injury model to verify the results of the in vitro experiments. Expression levels of transient receptor potential canonical (TRPC) 3 and TRPC5 were higher in VSMCs than in VECs. Silencing TRPC3/5 significantly inhibited cell proliferation and Ca2+ influx in VSMCs, but not in VECs. Silencing TRPC3/5 after rat carotid artery endothelial injury inhibited neointima formation, with a better reparative effect on the endothelial cell layer than rapamycin. TRPC3/5 participates in the proliferation of VSMCs via SOCCs, and silencing its expression inhibits the formation of neointima after endothelial injury. However, this effect was not significant in VECs, suggesting that other compensatory pathways may have emerged.
Insights
Store-operated calcium channels (SOCCs), specifically TRPC3/5, drive vascular smooth muscle cell proliferation and neointima formation after injury. Silencing these channels inhibited VSMC proliferation but not endothelial cell repair, suggesting distinct roles in vascular health.
Area of Science:
- Vascular Biology
- Cell Signaling
- Calcium Channels
Background:
- Store-operated calcium channels (SOCCs) regulate cell proliferation, but their specific roles in different vascular cell types remain unclear.
- Vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs) have distinct functions in vascular health and disease.
- Transient receptor potential canonical (TRPC) channels are key components of SOCCs.
Purpose of the Study:
- To compare the effects of SOCCs on VSMC and VEC proliferation.
- To investigate the role of SOCCs in vascular endothelial repair after injury.
- To determine the expression levels and functional significance of TRPC3 and TRPC5 in VSMCs and VECs.
Main Methods:
- Primary rat coronary VSMCs and VECs were cultured and analyzed for SOCC molecule expression using Western blotting and qPCR.
- Adenovirus vectors were used to transfect VSMCs and VECs with various molecules to assess effects on cell proliferation, cell cycle, and intracellular calcium (Ca2+).
- A rat carotid artery endothelial injury model was established to evaluate the in vivo effects of SOCC modulation.
Main Results:
- TRPC3 and TRPC5 expression levels were significantly higher in VSMCs compared to VECs.
- Silencing TRPC3/5 markedly inhibited VSMC proliferation and Ca2+ influx, with no significant effect on VECs.
- In vivo, silencing TRPC3/5 in the injury model reduced neointima formation and improved endothelial repair more effectively than rapamycin.
Conclusions:
- TRPC3/5 channels, acting via SOCCs, are crucial for VSMC proliferation and neointima formation following vascular injury.
- The inhibitory effect of TRPC3/5 silencing on neointima formation highlights its therapeutic potential in vascular disease.
- VECs appear to utilize alternative compensatory pathways, as TRPC3/5 silencing did not significantly impact their repair mechanisms.
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