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Background <p>The role of peripheral vascular smooth muscle cells (VSMCs) in vascular calcification has been overlooked compared with that of the major VSMCs. This study aimed to investigate the differentially expressed genes (DEGs) of peripheral VSMCs in patients with critical limb ischemia (CLI) results from peripheral arterial disease and Chronic Kidney disease (CKD).</p> Methods <p>We isolated peripheral VSMCs from the posterior tibial artery of 6 patients with CKD who underwent below-knee amputation for CLI. Using normal human aortic VSMCs as a control, we cultured all samples in normal and high phosphate media for 10&#xa0;days. Total RNA was extracted and analyzed using mRNA sequencing. Expression levels of genes related to contractile and synthetic phenotypes were examined. Bioinformatics analysis of the DEGs was performed.</p> Results <p>All four genes (<i>ACTA2, CALD1, CNN1,</i> and <i>TAGLN</i>) related to the contractility phenotype increased only in the control group. The expression of all four genes (<i>ICAM1, SPP1, MMP3,</i> and <i>TIMP1</i>) related to the synthetic phenotype showed no significant changes or decreases in all samples. Several genes (<i>SERTAD4, ITGA11, SPRN, IGFBP6, BCL2A1, APOE, TRABD2A,</i> and <i>FAM13B</i>) showed significant changes under calcifying conditions. Only <i>UNC5B</i> expression showed an opposite pattern between normal human aortic VSMC and pathological peripheral VSMCs.</p> Conclusions <p><i>UNC5B</i> was overexpressed only in pathologic peripheral VSMCs under calcifying conditions, whereas downregulated in normal aortic VSMCs. Further research on the effect of <i>UNC5B</i> on peripheral VSMC is warranted. (IRB number: H-1711-022-897).</p>

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Differential gene expression in peripheral vascular smooth muscle cells of patients with peripheral artery disease

  • 期刊论文

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  • 发表日期：

    2025年10月22日

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  • Dongoh Lee,
  • Ji Hye Kim,
  • Dong Yeon Lee

摘要

Background

The role of peripheral vascular smooth muscle cells (VSMCs) in vascular calcification has been overlooked compared with that of the major VSMCs. This study aimed to investigate the differentially expressed genes (DEGs) of peripheral VSMCs in patients with critical limb ischemia (CLI) results from peripheral arterial disease and Chronic Kidney disease (CKD).

Methods

We isolated peripheral VSMCs from the posterior tibial artery of 6 patients with CKD who underwent below-knee amputation for CLI. Using normal human aortic VSMCs as a control, we cultured all samples in normal and high phosphate media for 10 days. Total RNA was extracted and analyzed using mRNA sequencing. Expression levels of genes related to contractile and synthetic phenotypes were examined. Bioinformatics analysis of the DEGs was performed.

Results

All four genes (ACTA2, CALD1, CNN1, and TAGLN) related to the contractility phenotype increased only in the control group. The expression of all four genes (ICAM1, SPP1, MMP3, and TIMP1) related to the synthetic phenotype showed no significant changes or decreases in all samples. Several genes (SERTAD4, ITGA11, SPRN, IGFBP6, BCL2A1, APOE, TRABD2A, and FAM13B) showed significant changes under calcifying conditions. Only UNC5B expression showed an opposite pattern between normal human aortic VSMC and pathological peripheral VSMCs.

Conclusions

UNC5B was overexpressed only in pathologic peripheral VSMCs under calcifying conditions, whereas downregulated in normal aortic VSMCs. Further research on the effect of UNC5B on peripheral VSMC is warranted. (IRB number: H-1711-022-897).