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C1q-tumour necrosis factor-related protein-3 exacerbates cardiac hypertrophy in mice
Zhen-Guo Ma1,2,3, Yu-Pei Yuan1,2,3, Xin Zhang1,2,3
1Department of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, PR China.
Aims:
C1q-tumour necrosis factor-related protein-3 (CTRP3) is an adipokine and a paralog of adiponectin. Our previous study showed that CTRP3 attenuated diabetes-related cardiomyopathy. However, the precise role of CTRP3 in cardiac hypertrophy remains unclear. This study was aimed to clarify the role of CTRP3 involved in cardiac hypertrophy.
Methods And Results:
Cardiomyocyte-specific CTRP3 overexpression was achieved using an adeno-associated virus system, and cardiac CTRP3 expression was knocked down using gene delivery of specific short hairpin RNAs in vivo. CTRP3 expression was upregulated in murine hypertrophic hearts and failing human hearts. Increased CTRP3 was mainly derived from cardiomyocytes and induced by the production of reactive oxygen species (ROS) during the hypertrophic response. CTRP3-overexpressing mice exhibited exacerbated cardiac hypertrophy and cardiac dysfunction in response to pressure overload. Conversely, Ctrp3 deficiency in the heart resulted in an alleviated hypertrophic phenotype. CTRP3 induced hypertrophy in cardiomyocytes, which could be blocked by the addition of CTRP3 antibody in the media. Detection of signalling pathways showed that pressure overload-induced activation of the transforming growth factor β-activated kinase 1 (TAK1)-c-Jun N-terminal kinase (JNK) pathway was enhanced by CTRP3 overexpression and inhibited by CTRP3 disruption. Furthermore, we found that CTRP3 lost its pro-hypertrophic effects in cardiomyocyte-specific Tak1 knockout mice. Protein kinase A (PKA) was involved in the activation of TAK1 by CTRP3.
Conclusion:
In conclusion, our results suggest that CTRP3 promotes pressure overload-induced cardiac hypertrophy via activation of the TAK1-JNK axis.
Insights
C1q-tumour necrosis factor-related protein-3 (CTRP3) promotes cardiac hypertrophy by activating the TAK1-JNK pathway. CTRP3 exacerbates heart dysfunction under pressure overload, while its deficiency alleviates hypertrophy.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Endocrinology
Background:
- C1q-tumour necrosis factor-related protein-3 (CTRP3) is an adipokine and paralog of adiponectin.
- Previous studies indicated CTRP3 attenuates diabetes-related cardiomyopathy.
- The specific role of CTRP3 in cardiac hypertrophy remained unclear.
Purpose of the Study:
- To elucidate the role of CTRP3 in the development of cardiac hypertrophy.
- To investigate the molecular mechanisms by which CTRP3 influences cardiac hypertrophy.
Main Methods:
- Adeno-associated virus system for cardiomyocyte-specific CTRP3 overexpression and short hairpin RNA-mediated knockdown in vivo.
- Analysis of CTRP3 expression in murine hypertrophic and human failing hearts.
- Assessment of cardiac hypertrophy and function in CTRP3-manipulated mice under pressure overload.
- Investigation of signaling pathways, including TAK1-JNK and PKA, and use of cardiomyocyte-specific Tak1 knockout mice.
Main Results:
- CTRP3 expression was upregulated in hypertrophic and failing hearts, primarily in cardiomyocytes, and induced by reactive oxygen species (ROS).
- CTRP3 overexpression exacerbated cardiac hypertrophy and dysfunction, while CTRP3 deficiency alleviated these phenotypes.
- CTRP3 promoted cardiomyocyte hypertrophy, dependent on the TAK1-JNK pathway, with PKA involvement in TAK1 activation.
Conclusions:
- CTRP3 acts as a pro-hypertrophic factor in the heart.
- CTRP3 promotes pressure overload-induced cardiac hypertrophy through the activation of the TAK1-JNK signaling axis.
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