본문 바로가기
HOME> 논문 > 논문 검색상세

논문 상세정보

Biochemical and biophysical research communications v.494 no.3/4, 2017년, pp.534 - 541   SCI SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

Interleukin-6 deficiency attenuates angiotensin II-induced cardiac pathogenesis with increased myocyte hypertrophy

Chen, Fan (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) ; Chen, Dandan (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) ; Zhang, Yubin (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) ; Jin, Liang (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) ; Zhang, Han (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) ; Wan, Miyang (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) ; Pan, Tianshu ; Wang, Xiaochuan ; Su, Yuheng ; Xu, Yitao ; Ye, Junmei ;
  • 초록  

    Abstract Interleukin-6 (IL-6) signaling is critical for cardiomyocyte hypertrophy, while the role of IL-6 in the pathogenesis of myocardium hypertrophy remains controversial. To determine the essential role of IL-6 signaling for the cardiac development during AngII-induced hypertension, and to elucidate the mechanisms, wild-type (WT) and IL-6 knockout (IL-6 KO) mice were infused subcutaneously with either vehicle or AngII (1.5 μg/h/mouse) for 1 week. Immunohistological and serum studies revealed that the extents of cardiac fibrosis, inflammation and apoptosis were reduced in IL-6 KO heart during AngII-stimulation, while cardiac hypertrophy was obviously induced. To investigate the underlying mechanisms, by using myocardial tissue and neonatal cardiomyocytes, we observed that IL-6/STAT3 signaling was activated under the stimulation of AngII both in vivo and in vitro . Further investigation suggested that STAT3 activation enhances the inhibitory effect of EndoG on MEF2A and hampers cardiomyocyte hypertrophy. Our study is the first to show the important role of IL-6 in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6/STAT3 and EndoG/MEF2A pathway that affects cardiac hypertrophy during AngII stimulation. Highlights IL-6 deficiency alleviates cardiac fibrosis during AngII stimulation. IL-6 KO-AngII hearts exhibited decreased inflammation and apoptosis. Cardiac hypertrophy is provoked in IL-6 KO mice under AngII stimulation. IL-6/STAT3 regulates AngII-induced myocyte hypertrophy via EndoG/MEF2A pathway. Graphical abstract Schematic diagram showing the development of cardiomyopathy under the regulation of IL-6 during AngII-stimulation. During AngII stimulation, IL-6 expression increases in cardiomyocytes and activates STAT3. STAT3 phosphorylation promotes its nucleus translocation. On one hand, phosphorylated STAT3 (p-STAT3) facilitates the transcription of genes associated with inflammation; on the other hand, p-STAT3 also strengthens the inhibitory effect of EndoG on MEF2A, resulting in alleviated myocyte hypertrophy. AngII also affects the EndoG-MEF2A signaling pathway by inhibiting EndoG expression, causing increased cardiac hypertrophy. Moreover, AngII promotes myocardium apoptosis via upregulating the ratio of Bax/Bcl-2.Dashed arrows: our hypothesis in the study. [DISPLAY OMISSION]


  • 주제어

    Interluekin-6 (IL-6) .   Signal transducer and activator of transcription 3 (STAT3) .   Endonuclease G (EndoG) .   Myocyte enhancer factor 2A (MEF2A) .   Cardiac hypertrophy.  

 활용도 분석

  • 상세보기

    amChart 영역
  • 원문보기

    amChart 영역

원문보기

무료다운로드
  • 원문이 없습니다.
유료다운로드

유료 다운로드의 경우 해당 사이트의 정책에 따라 신규 회원가입, 로그인, 유료 구매 등이 필요할 수 있습니다. 해당 사이트에서 발생하는 귀하의 모든 정보활동은 NDSL의 서비스 정책과 무관합니다.

원문복사신청을 하시면, 일부 해외 인쇄학술지의 경우 외국학술지지원센터(FRIC)에서
무료 원문복사 서비스를 제공합니다.

NDSL에서는 해당 원문을 복사서비스하고 있습니다. 위의 원문복사신청 또는 장바구니 담기를 통하여 원문복사서비스 이용이 가능합니다.

이 논문과 함께 출판된 논문 + 더보기