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Clitocybin B inhibits rat aortic smooth muscle cell proliferation through suppressing PDGF-Rβ phosphorylation
Kyu-Dong Yoo1, Eun-Seok Park, Yong Lim
1College of Pharmacy, CBITRC, Chungbuk National University, Cheongju, Republic of Korea.
Abstract:
The increased proliferation of vascular smooth muscle cells (VSMCs) in the arterial wall is a critical pathogenic factor for vascular diseases such as atherosclerosis and restenosis after angioplasty. Clitocybin B was reported to have either a potent free radical scavenging effect or effects that were isolated from the culture broth of mushroom Clitocybe aurantiaca. The present study was designed to investigate the effects of clitocybin B on VSMC proliferation and its possible molecular mechanism. Clitocybin B significantly inhibited the proliferation and the DNA synthesis of PDGF-BB-stimulated VSMCs in a concentration-dependent manner. In agreement with these findings, clitocybin B suppressed the PDGF-BB-induced progression through G0/G1 to S phase of cell cycle. Clitocybin B also down-regulated the expressions of cell cycle-related proteins, including cyclin-dependent kinase (CDK)2, cyclin E, CDK4, cyclin D1, and proliferative cell nuclear antigen in PDGF-BB-stimulated VSMCs. Clitocybin B significantly inhibited the phosphorylation of Akt, extracellular signal-regulated kinase 1/2, and phospholipase C-γ1, in the PDGF-BB signaling pathway. Clitocybin B suppressed the PDGF-Rβ activation in PDGF-BB signaling cascade. These results suggested that the inhibitory effect of clitocybin B on the proliferation of VSMCs may be associated with suppressing PDGF-Rβ phosphorylation. Thus, clitocybin B may be an effective antiproliferative agent for the prevention of atherosclerosis and restenosis.
Insights
Clitocybin B effectively inhibits vascular smooth muscle cell proliferation by blocking key cell cycle proteins and signaling pathways. This compound shows potential as an antiproliferative agent for preventing vascular diseases like atherosclerosis.
Area of Science:
- Pharmacology
- Cell Biology
- Vascular Medicine
Background:
- Vascular smooth muscle cell (VSMC) proliferation is a key factor in vascular diseases such as atherosclerosis and restenosis.
- Clitocybin B, isolated from Clitocybe aurantiaca, has shown potential biological activities.
Purpose of the Study:
- To investigate the effects of Clitocybin B on VSMC proliferation.
- To elucidate the molecular mechanisms underlying Clitocybin B's action on VSMCs.
Main Methods:
- Assessed VSMC proliferation and DNA synthesis in response to PDGF-BB stimulation.
- Analyzed cell cycle progression using flow cytometry.
- Examined the expression of cell cycle-related proteins (e.g., CDK2, cyclin E, CDK4, cyclin D1, PCNA).
- Investigated the impact of Clitocybin B on PDGF-BB signaling pathways (Akt, ERK1/2, PLC-γ1, PDGF-Rβ phosphorylation).
Main Results:
- Clitocybin B significantly inhibited PDGF-BB-induced VSMC proliferation and DNA synthesis in a dose-dependent manner.
- Clitocybin B suppressed cell cycle progression from G0/G1 to S phase.
- Down-regulation of key cell cycle proteins (cyclin E, cyclin D1, CDK2, CDK4, PCNA) was observed.
- Inhibition of PDGF-BB signaling pathway components, including Akt, ERK1/2, PLC-γ1, and notably PDGF-Rβ phosphorylation, was demonstrated.
Conclusions:
- Clitocybin B exhibits potent antiproliferative effects on VSMCs.
- The mechanism involves the suppression of PDGF-Rβ phosphorylation and downstream signaling pathways.
- Clitocybin B holds promise as a therapeutic agent for preventing vascular diseases like atherosclerosis and restenosis.
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