AI Article Synopsis
- CCL8 (C-C motif chemokine ligand 8) is linked to disease progression, but its role in atherosclerosis (AS) is not fully understood.
- In experiments with human aortic smooth muscle cells (HASMCs) stimulated by PDGF-BB, researchers observed increased cell viability and migration, alongside decreased α-SMA levels and increased CCL8 expression.
- Silencing CCL8 reduced HASMC proliferation and migration and altered cell cycle progression, indicating that CCL8 may be a potential therapeutic target for treating atherosclerosis.
Article Abstract
C-C motif Chemokine ligand 8 (CCL8) has been found in diseases' pathogenesis. But its molecular mechanism in atherosclerosis (AS) remains to be elucidated. Human aortic smooth muscle cells (HASMCs) were stimulated by PDGF-BB to establish cell model. α-SMA in PDGF-BB-stimulated HASMCs was measured by immunofluorescence staining. Relative gene expressions in PDGF-BB-stimulated HASMCs were detected by quantitative real-time polymerase chain reaction and western blot. HASMCs proliferation, migration, and cell cycle were assessed by cell counting kit-8, wound-healing assay, and flow cytometry. HASMCs viability was increased after PDGF-BB stimulation, with α-SMA downregulation yet CCL8 upregulation. Silencing CCL8 inhibited PDGF-BB-stimulated HASMCs proliferation and migration, and increased cells percentage in G1 phases but decreased those in S phase. Also, silencing CCL8 decreased OPN and cyclinD1 expressions and AKT and ERK1/2 phosphorylation while increased those of α-SMA and Sm22α. However, upregulating CCL8 led to opposite effects, suggesting CCL8 could be an atherosclerosis therapeutic target.
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| http://dx.doi.org/10.1080/09168451.2020.1762160 | DOI Listing |
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Article Synopsis
- CCL8 (C-C motif chemokine ligand 8) is linked to disease progression, but its role in atherosclerosis (AS) is not fully understood.
- In experiments with human aortic smooth muscle cells (HASMCs) stimulated by PDGF-BB, researchers observed increased cell viability and migration, alongside decreased α-SMA levels and increased CCL8 expression.
- Silencing CCL8 reduced HASMC proliferation and migration and altered cell cycle progression, indicating that CCL8 may be a potential therapeutic target for treating atherosclerosis.
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