Lactate promotes vascular smooth muscle cell switch to a synthetic phenotype by inhibiting miR-23b expression

Hu Yanchao; Zhang Chunyan; Fan Yajie; Zhang Yan; Wang Yiwen; Wang Congxia

doi:10.4196/kjpp.2022.26.6.519

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자료유형: 학술저널

저자정보: Hu Yanchao (Department of Cardiovascular Medicine The Second Affiliated Hospital of Xi'an Jiaotong University S) Zhang Chunyan (Department of Cardiovascular Medicine The Second Affiliated Hospital of Xi'an Jiaotong University S) Fan Yajie (Department of Cardiovascular Medicine The Second Affiliated Hospital of Xi'an Jiaotong University S) Zhang Yan (Department of Cardiovascular Medicine The Second Affiliated Hospital of Xi'an Jiaotong University S) Wang Yiwen (Department of Cardiovascular Medicine The Second Affiliated Hospital of Xi'an Jiaotong University S) Wang Congxia (Department of Cardiovascular Medicine The Second Affiliated Hospital of Xi'an Jiaotong University S)

저널정보: 대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제26권 제6호

발행연도: 2022.11

수록면: 519 - 530 (12page)

DOI: 10.4196/kjpp.2022.26.6.519

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Recent research indicates that lactate promotes the switching of vascular smooth muscle cells (VSMCs) to a synthetic phenotype, which has been implicated in various vascular diseases. This study aimed to investigate the effects of lactate on the VSMC phenotype switch and the underlying mechanism. The CCK-8 method was used to assess cell viability. The microRNAs and mRNAs levels were evaluated using quantitative PCR. Targets of microRNA were predicted using online tools and confirmed using a luciferase reporter assay. We found that lactate promoted the switch of VSMCs to a synthetic phenotype, as evidenced by an increase in VSMC proliferation, mitochondrial activity, migration, and synthesis but a decrease in VSMC apoptosis. Lactate inhibited miR-23b expression in VSMCs, and miR-23b inhibited VSMC's switch to the synthetic phenotype. Lactate modulated the VSMC phenotype through downregulation of miR-23b expression, suggesting that overexpression of miR-23b using a miR-23b mimic attenuated the effects of lactate on VSMC phenotype modulation. Moreover, we discovered that SMAD family member 3 (SMAD3) was the target of miR-23b in regulating VSMC phenotype. Further findings suggested that lactate promotes VSMC switch to synthetic phenotype by targeting SMAD3 and downregulating miR-23b. These findings suggest that correcting the dysregulation of miR-23b/ SMAD3 or lactate metabolism is a potential treatment for vascular diseases.

#Lactate #miR-23b #Phenotype switch #SMAD3 #Smooth muscle

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