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Science China Life Sciences

, Volume 59, Issue 11, pp 1123–1130 | Cite as

Depletion of Kindlin-2 induces cardiac dysfunction in mice

  • Lihua Qi
  • Yu Yu
  • Xiaochun Chi
  • Danyu Lu
  • Yao Song
  • Youyi Zhang
  • Hongquan Zhang
Open Access
Research Paper
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  • 289 Downloads

Abstract

Kindlin-2, a member of the Kindlin family focal adhesion proteins, plays an important role in cardiac development. It is known that defects in the Z-disc proteins lead to hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM). Our previous investigation showed that Kindlin-2 is mainly localized at the Z-disc and depletion of Kindlin-2 disrupts the structure of the Z-Disc. Here, we reported that depletion of Kindlin-2 leads to the disordered myocardial fibers, fractured and vacuolar degeneration in myocardial fibers. Interestingly, depletion of Kindlin-2 in mice induced cardiac myocyte hypertrophy and increased the heart weight. Furthermore, decreased expression of Kindlin-2 led to cardiac dysfunction and also markedly impairs systolic function. Our data indicated that Kindlin-2 not only maintains the cardiac structure but also is required for cardiac function.

Keywords

Kindlin-2 depletion myocardial hypertrophy cardiac dysfunction mouse 
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Supplementary material

11427_2016_25_MOESM1_ESM.docx (244 kb)
Figure S1 Depletion of Kindlin-2 in various organs in mouse with tail vein injection of siRNA

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Copyright information

© The Author(s) 2016

Authors and Affiliations

  • Lihua Qi
    • 1
  • Yu Yu
    • 1
  • Xiaochun Chi
    • 1
  • Danyu Lu
    • 1
  • Yao Song
    • 2
  • Youyi Zhang
    • 2
  • Hongquan Zhang
    • 1
  1. 1.Department of Human Anatomy, Histology and Embryology, and Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Peking University Health Science, and State Key Laboratory of Natural and Biomimetic DrugsPeking University Health Science CenterBeijingChina
  2. 2.Institute of Vascular Medicine, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of HealthPeking University Health ScienceBeijingChina

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