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Peer-reviewedCC BY-NC-ND 4.0BMC Cardiovascular Disorders

Upregulation of miR-200b-3p serves as a diagnostic biomarker for coronary atherosclerosis and regulates the oxidized low-density lipoprotein cholesterol-induced dysfunction of vascular smooth muscle cells

  • Yuxuan Xia1
  • Yujuan Gao2
  • Fei Chai3
  • Liqiu Yan4,5
  • Yetao Lin6
6 affiliations
  1. 1Outpatient Department, Center for Clinical Pharmacy, Cancer Center, Department of Pharmacy, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital, Hangzhou Medical College, Hangzhou, 310014 China
  2. 2Department of Cardiology, Qingdao Central Hospital, University of Health and Rehabilitation Sciences(Qingdao Central Hospital), Qingdao, 266300 China
  3. 3Department of Anesthesiology, The Affiliated Hospital of Hebei University, Baoding City, 071000 Hebei Province China
  4. 4Department of Cardiology, The Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, Dongguan, 523326 China
  5. 5Dongguan Key Laboratory of Cardiovascular Aging and Myocardial Regeneration, Dongguan Cardiovascular Research Institute, Dongguan, China
  6. 6Department of Cardiovascular Medicine, The Second Affiliated Hospital of Shantou University Medical College, Jinping District, Shantou, 515800 Guangdong Province China
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Abstract

Background: MicroRNAs that are abnormally expressed in coronary atherosclerosis (CAS) have gradually been discovered due to their unique advantages.

Objective: Assessing the value of miR-200b-3p in CAS.

Methods: The level of miR-200b-3p and RAP1B in CAS (n = 103) and healthy (n = 77) subjects was analyzed by RT-qPCR. The role of miR-200b-3p in CAS was determined through the ROC curve, correlation, and multivariate logistic regression analysis. Downstream targets of miR-200b-3p were screened by online databases. A dual-luciferase reporter assay evaluated the regulatory relationship between miR-200b-3p and RAP1B. An ox-LDL-induced human vascular smooth muscle cell (HVSMC) model was used to explore the potential mechanism of the miR-200b-3p/RAP1B axis in CAS progression.

Results: The expression of miR-200b-3p was upregulated in the CAS group compared with the HC group and showed a diagnostic value in distinguishing CAS from healthy participants. The miR-200b-3p expression was correlated with TG, TC, LDL-C, HDL-C, coronary artery stenosis and calcification, and predicted the risk of CAS development. RAP1B was a target of miR-200b-3p and negatively correlated with the level of miR-200b-3p. In ox-LDL-induced HVSMCs, upregulated miR-200b-3p expression and downregulated RAP1B expression were observed. The silence of miR-200b-3p mitigated the ox-LDL-treated HVSMC injury through suppressing cell proliferation, migration, inflammation (IL-6, TNF-α), and calcification (Ca2+, ALP activity) in HVSMCs by targeting RAP1B.

Conclusions: Upregulation of miR-200b-3p served as a biomarker in diagnosing CAS. Upregulated miR-200b-3p expression might be involved in CAS progression through promoting the ox-LDL-stimulated vascular smooth muscle cell (VSMC) injury via regulating RAP1B.

Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12872-026-06289-4.

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Cite

BibTeXRIS
BibTeX
@article{xia2026upregulation,
  title = {{Upregulation of miR-200b-3p serves as a diagnostic biomarker for coronary atherosclerosis and regulates the oxidized low-density lipoprotein cholesterol-induced dysfunction of vascular smooth muscle cells}},
  author = {Yuxuan Xia and Yujuan Gao and Fei Chai and Liqiu Yan and Yetao Lin},
  journal = {BMC Cardiovascular Disorders},
  year = {2026},
  month = jul,
  doi = {10.1186/s12872-026-06289-4},
  url = {https://doi.org/10.1186/s12872-026-06289-4},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Upregulation of miR-200b-3p serves as a diagnostic biomarker for coronary atherosclerosis and regulates the oxidized low-density lipoprotein cholesterol-induced dysfunction of vascular smooth muscle cells
AU  - Yuxuan Xia
AU  - Yujuan Gao
AU  - Fei Chai
AU  - Liqiu Yan
AU  - Yetao Lin
PY  - 2026
DA  - 2026/07/30
JO  - BMC Cardiovascular Disorders
DO  - 10.1186/s12872-026-06289-4
UR  - https://doi.org/10.1186/s12872-026-06289-4
AB  - Background: MicroRNAs that are abnormally expressed in coronary atherosclerosis (CAS) have gradually been discovered due to their unique advantages.  Objective: Assessing the value of miR-200b-3p in CAS.  Methods: The level of miR-200b-3p and RAP1B in CAS (n = 103) and healthy (n = 77) subjects was analyzed by RT-qPCR. The role of miR-200b-3p in CAS was determined through the ROC curve, correlation, and multivariate logistic regression analysis. Downstream targets of miR-200b-3p were screened by online databases. A dual-luciferase reporter assay evaluated the regulatory relationship between miR-200b-3p and RAP1B. An ox-LDL-induced human vascular smooth muscle cell (HVSMC) model was used to explore the potential mechanism of the miR-200b-3p/RAP1B axis in CAS progression.  Results: The expression of miR-200b-3p was upregulated in the CAS group compared with the HC group and showed a diagnostic value in distinguishing CAS from healthy participants. The miR-200b-3p expression was correlated with TG, TC, LDL-C, HDL-C, coronary artery stenosis and calcification, and predicted the risk of CAS development. RAP1B was a target of miR-200b-3p and negatively correlated with the level of miR-200b-3p. In ox-LDL-induced HVSMCs, upregulated miR-200b-3p expression and downregulated RAP1B expression were observed. The silence of miR-200b-3p mitigated the ox-LDL-treated HVSMC injury through suppressing cell proliferation, migration, inflammation (IL-6, TNF-α), and calcification (Ca2+, ALP activity) in HVSMCs by targeting RAP1B.  Conclusions: Upregulation of miR-200b-3p served as a biomarker in diagnosing CAS. Upregulated miR-200b-3p expression might be involved in CAS progression through promoting the ox-LDL-stimulated vascular smooth muscle cell (VSMC) injury via regulating RAP1B.  Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12872-026-06289-4.
SN  - 1471-2261
ER  -