Reversal of pathological cardiac hypertrophy via the MEF2-coregulator interface

Wei, Jianqin; Joshi, Shaurya; Speransky, S; Crowley, Catherine; Jayathilaka, Nimanthi; Lei, Xiao; Wu, Yongqing; Gai, David; Jain, Siddharth; Hoosien, Michael; Gao, Yan; Chen, Lin; Bishopric, Nanette H.

doi:10.1172/jci.insight.91068

Cited by 38 publications

(24 citation statements)

References 77 publications

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“…Interestingly, in HCC and in non-small cell lung carcinoma, as in various tumors, MEF2D expression is increased and reported to be required to sustain tumor growth (63)(64)(65). The upregulation of PD-L1 frequently observed in HCC has been correlated to the impairment of CD8-mediated cytotoxicity (66) and could explain the inefficient activation of CD8 + lymphocytes observed in this model in Mef2d -/mice. As MEF2D was found to control the expression of PD-L1 (67), in these cancers a targeted therapy to inhibit MEF2D functions could have a double benefit of decreasing the malignancy of tumor cells and increasing the immunoreactivity of T cells.…”

Section: Foxp3 Controls the Expression And Alternative Splicing Of Mementioning

confidence: 72%

MEF2D sustains activation of effector Foxp3+ Tregs during transplant survival and anticancer immunity

Giorgio

Wang

Xiong

et al. 2020

Journal of Clinical Investigation

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Section: Foxp3 Controls the Expression And Alternative Splicing Of Mementioning

confidence: 72%

MEF2D sustains activation of effector Foxp3+ Tregs during transplant survival and anticancer immunity

Giorgio

Wang

Xiong

et al. 2020

Journal of Clinical Investigation

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“…In fact, haemodynamic stress has been suggested to cause cardiac hypertrophy, resulting in cardiac malfunctioning and abrupt failure. [11][12][13] This process corresponds to the expression of genes The HAT activity could be inhibited pharmacologically to increase or decrease related gene expression accordingly. [17][18][19] HAT inhibitors tion.…”

Section: Discussionmentioning

confidence: 99%

Anacardic acid attenuates pressure‐overload cardiac hypertrophy through inhibiting histone acetylases

Peng

Luo

et al. 2019

J Cellular Molecular Medi

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Cardiac hypertrophy has become a major cardiovascular problem wordwide and is considered the early stage of heart failure. Treatment and prevention strategies are needed due to the suboptimal efficacy of current treatment methods. Recently, many studies have demonstrated the important role of histone acetylation in myocardium remodelling along with cardiac hypertrophy. A Chinese herbal extract containing anacardic acid (AA) is known to possess strong histone acetylation inhibitory effects. In previous studies, we demonstrated that AA could reverse alcohol‐induced cardiac hypertrophy in an animal model at the foetal stage. Here, we investigated whether AA could attenuate cardiac hypertrophy through the modulation of histone acetylation and explored its potential mechanisms in the hearts of transverse aortic constriction (TAC) mice. This study showed that AA attenuated hyperacetylation of acetylated lysine 9 on histone H3 (H3K9ac) by inhibiting the expression of p300 and p300/CBP‐associated factor (PCAF) in TAC mice. Moreover, AA normalized the transcriptional activity of the heart nuclear transcription factor MEF2A . The high expression of cardiac hypertrophy‐linked genes ( ANP, β‐MHC ) was reversed through AA treatment in the hearts of TAC mice. Additionally, we found that AA improved cardiac function and survival rate in TAC mice. The current results further highlight the mechanism by which histone acetylation is controlled by AA treatment, which may help prevent and treat hypertrophic cardiomyopathy.

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“…4b), which induces heart failure-causing gene programs. 20,22,24 Adenovirally expressed ABHD5 led to a significant repression of a MEF2 activity in the presence of HDAC4 upon stimulation with endothelin-1 (ET-1) or fetal calf serum (FCS) ( Fig. 4c; Extended Data Fig.…”

Section: Abhd5 Protects From Heart Failurementioning

confidence: 99%

The lipid-droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4

et al. 2019

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Data availability Statement Raw data of experiments presented in Fig. 3F-G, Suppl. Table 1 and Extended Data Fig. 3d were deposited in the gene expression omnibus (GEO, GSE135662) with NCBI tracking system ID #20253819. Source Data provide all uncut gels of the immunoblotting figures in the manuscript, and all data supporting the findings of the manuscript could be obtained from the corresponding author upon request.

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Reversal of pathological cardiac hypertrophy via the MEF2-coregulator interface

Cited by 38 publications

References 77 publications

MEF2D sustains activation of effector Foxp3+ Tregs during transplant survival and anticancer immunity

MEF2D sustains activation of effector Foxp3+ Tregs during transplant survival and anticancer immunity

Anacardic acid attenuates pressure‐overload cardiac hypertrophy through inhibiting histone acetylases

The lipid-droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4

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