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Increased pericardial fibrosis and cardiac dysfunction in smooth muscle cell-specific SOCS3 deficient mice

Session Poster Session 2

Speaker Toshiyuki YANAI

Event : ESC Congress 2019

  • Topic : basic science
  • Sub-topic : Fibrosis
  • Session type : Poster Session

Authors : T Yanai (Kurume,JP), H Yasukawa (Kurume,JP), K Mawatari (Kurume,JP), T Sasaki (Kurume,JP), J Takahashi (Kurume,JP), S Nohara (Kurume,JP), K Shimozono (Kurume,JP), T Shibata (Kurume,JP), K Okabe (Kurume,JP), M Yamamoto (Kurume,JP), Y Fukumoto (Kurume,JP)

T. Yanai1 , H. Yasukawa1 , K. Mawatari1 , T. Sasaki1 , J. Takahashi1 , S. Nohara1 , K. Shimozono1 , T. Shibata1 , K. Okabe1 , M. Yamamoto2 , Y. Fukumoto1 , 1Kurume University School of Medicine - Kurume - Japan , 2Cardiovascular Research Institute of the Kurume University - Kurume - Japan ,

Basic Science - Cardiac Diseases: Fibrosis

European Heart Journal ( 2019 ) 40 ( Supplement ), 929

Background: Suppressor of cytokine signaling-3 (SOCS3) is an intrinsic negative-feedback regulator of signal transducer and activator of transcription-3 (STAT3) signaling pathway. We have previously shown that myocardial SOCS3 plays an important role in cardiac hypertrophy and survival; however, the role of SOCS3 in smooth muscle cells in cardiovascular pathophysiology remains elusive. In this study, we determined whether STAT3 and SOCS3 in smooth muscle cells would play a role in cardiovascular pathophysiology.

Methods and results: To target inactivation of the SOCS3 gene to smooth muscle cells, SOCS3-flox mice were bred with transgenic mice expressing Cre recombinase under control of the mouse SM22-α promoter (sm-SOCS3-KO mice). Left ventricular weight to body weight ratio was significantly increased in sm-SOCS3-KO mice compared with wild-type mice at 52 weeks of age (p<0.05). Echocardiographic analyses of sm-SOCS3-KOmice showed significantly decreased cardiac function compared with wild-typefrom 52 weeks of age (p<0.05). Interestingly, Sirius-red staining revealed that thickness of pericardium in sm-SOCS3-KOmice was markedly greater compared with wild-typemice at 52 weeks of age (p<0.05). Cardiac interstitial fibrosis in sm-SOCS3-KOmice was also greater compared with wild-typemice (p<0.05). Western blot analyses showed that phosphorylated STAT3 was significantly increased in sm-SOCS3-KOhearts compared with wild-typemice at 52 weeks of age (p<0.05), whereas no significant differences were observed at 7 weeks of age. Immunostaining revealed that phosphorylated STAT3 positive cells were in thickened pericardial area in sm-SOCS3-KOhearts. Some infiltrated inflammatory cells were also found in thickened pericardial area in sm-SOCS3-KOmice hearts.

Conclusion: These results suggest that STAT3 and its negative-feedback regulator SOCS3 in smooth muscle cells play an important role in the pathogenesis of pericardial fibrosis and cardiac dysfunction.

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