Volume 19 Issue 8
Aug.  2021
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HE Mingyuan, GE Junfeng, HUANG Ling, WANG Shixiang, YAN Yi. Effect of myosin light chain regulated by cardiac myosin light chain kinase on cardiac hypertrophy[J]. Chinese Journal of General Practice, 2021, 19(8): 1257-1261, 1402. doi: 10.16766/j.cnki.issn.1674-4152.002034
Citation: HE Mingyuan, GE Junfeng, HUANG Ling, WANG Shixiang, YAN Yi. Effect of myosin light chain regulated by cardiac myosin light chain kinase on cardiac hypertrophy[J]. Chinese Journal of General Practice, 2021, 19(8): 1257-1261, 1402. doi: 10.16766/j.cnki.issn.1674-4152.002034

Effect of myosin light chain regulated by cardiac myosin light chain kinase on cardiac hypertrophy

doi: 10.16766/j.cnki.issn.1674-4152.002034
Funds:

 81870320

 81600349

 201803

 201804010008

 TS20190337

 pdjha0413

  • Received Date: 2021-01-16
    Available Online: 2022-02-16
  •   Objective  To investigate the effect of cardiac myosin light chain kinase (cMLCK) on the pathological cardiac hypertrophy induced by AngⅡ.  Methods  The cMLCK was purified and the active sites of cMLCK were explored in vitro. Wild type cMLCK (WT cMLCK) and its N-terminal knockout variants (ΔNT-cMLCK) adenovirus were prepared. The primary cardiomyocytes were infected and randomly divided into 6 groups: control group, AngⅡ group, WT cMLCK group, WT cMLCK+AngⅡ group, Δ NT cMLCK group, Δ NT cMLCK+AngⅡ group, 3 samples in each group. The expression of ANP and β-MHC, which are the heart failure relative factor, was detected by RT-PCR. The expression of cMLCK and MLC2v were detected by western blot. The area of cardiomyocytes was detected by immunofluorescence.  Results  WT-cMLCK could phosphorylated MLC2v effectively, which was abrogated in ΔNT-cMLCK. After treated with AngⅡ, the cell area [(1 787.0±142.6) μm2 vs. (2 458.0±211.3) μm2, P < 0.001] and expression of ANP and β-MHC in neonatal rat cardiomyocyte (NRCM) increased (all P < 0.05). The expression of cMLCK and p-MLC2v were upregulated (all P < 0.05). However, the cardiac hypertrophy induced by AngⅡ was reversed by WT-cMLCK overexpression [(2 527.0±116.4) μm2 vs. (1 775.0±88.5) μm2, P < 0.001], while ΔNT-cMLCK overexpression group lost its protective effect [(1 775.0±88.5) μm2 vs. (2 613.0±118.4) μm2, P < 0.001].  Conclusion  The protective effect of cMLCK to pathological cardiac hypertrophy induced by AngⅡ depends on its N terminal.

     

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