Open Access

Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A 

  • Authors:
    • Hao-Wei Deng
    • Wen-Bin Teng
    • Shao-Dan Zhou
    • Zi-Ming Ye
    • Zi-Mei Dong
    • Rui-Ting Hu
    • Chao Qin
  • View Affiliations

  • Published online on: November 5, 2024     https://doi.org/10.3892/mmr.2024.13385
  • Article Number: 20
  • Copyright: © Deng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Long non‑coding RNAs serve a crucial role in autophagy of vascular smooth muscle cells (VSMCs). The present study aimed to investigate the effect of small nucleolar RNA host gene 1 (SNHG1) on autophagy in VSMCs and the associated underlying mechanisms. Rapamycin was used to induce autophagy in VSMCs and the effects of SNHG1 on the proliferation and migration of VSMCs and the change in phenotype were tested following overexpression and silencing of SNHG1. The target gene of SNHG1 was predicted and validated. SNHG1‑regulated autophagy of VSMCs via C‑type lectin domain family 7 member A (CLEC7A) was determined by combined silencing of SNHG1 and overexpression of CLEC7A. Rapamycin‑induced autophagy in VSMCs changed the cell phenotype from contractile to synthetic, with decreased expression of α‑smooth muscle actin and smooth muscle protein 22a and increased expression of osteopontin. Overexpression of SNHG1 caused the same change in phenotype while the opposite change was observed following SNHG1 silencing. Overexpression of SNHG1 promoted the proliferation and migration of VSMCs. CLEC7A was identified as a target gene of SNHG1 and a direct binding relationship between them was confirmed by RNA immunoprecipitation and RNA pull‑down assays. Overexpression of SNHG1 increased the expression of CLEC7A. The expression of both SNHG1 and CLEC7A was increased during autophagy of VSMCs. Overexpression of SNHG1 promoted autophagy of VSMCs and silencing of CLEC7A reduced this effect of SNHG1. In conclusion, SNHG1 and CLEC7A were increased in VSMCs following autophagy. SNHG1 promotes the conversion of VSMCs from a contractile phenotype to a synthetic phenotype by facilitating CLEC7A expression.
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January-2025
Volume 31 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Copy and paste a formatted citation
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Spandidos Publications style
Deng H, Teng W, Zhou S, Ye Z, Dong Z, Hu R and Qin C: Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A . Mol Med Rep 31: 20, 2025.
APA
Deng, H., Teng, W., Zhou, S., Ye, Z., Dong, Z., Hu, R., & Qin, C. (2025). Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A . Molecular Medicine Reports, 31, 20. https://doi.org/10.3892/mmr.2024.13385
MLA
Deng, H., Teng, W., Zhou, S., Ye, Z., Dong, Z., Hu, R., Qin, C."Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A ". Molecular Medicine Reports 31.1 (2025): 20.
Chicago
Deng, H., Teng, W., Zhou, S., Ye, Z., Dong, Z., Hu, R., Qin, C."Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A ". Molecular Medicine Reports 31, no. 1 (2025): 20. https://doi.org/10.3892/mmr.2024.13385