Epigenetic activation of PERP transcription by MKL1 contributes to ROS-induced apoptosis in skeletal muscle cells

Li, Zilong; Chen, Baoyu; Dong, Wenhui; Xu, Wenping; Song, Mingzi; Fang, Mingming; Guo, Junli; Xu, Yong

doi:10.1016/j.bbagrm.2018.07.011

Cited by 44 publications

(21 citation statements)

References 44 publications

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“…Hypoxia-reoxygenation (HR) was performed as previously described (Ren et al, 2013;Yu et al, 2018). Briefly, macrophages were exposed to 1% O 2 in a hypoxia chamber (Pro-Ox Model C21, BioSpherix, Parish, NY, United States) for 3 h followed by reoxygenation in a regular cell-culture incubator with ambient 21% O 2 for 9 h. MRTF-A expression constructs (Li et al, 2018c), iNOS promoter-luciferase construct (Crosby et al, 2005), ASH2 expression construct (Wu et al, 2008), and TIP60 expression construct (Lin et al, 2012) have been previously described. Small interfering RNAs were purchased from Dharmacon.…”

Section: Methodsmentioning

confidence: 99%

An Interplay Between MRTF-A and the Histone Acetyltransferase TIP60 Mediates Hypoxia-Reoxygenation Induced iNOS Transcription in Macrophages

Yang

et al. 2020

Front. Cell Dev. Biol.

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Cardiac ischemia-reperfusion injury (IRI) represents a major pathophysiological event associated with permanent loss of heart function. Several interdependent processes contribute to cardiac IRI that include accumulation of reactive oxygen species (ROS), aberrant inflammatory response, and depletion of energy supply. Inducible nitric oxide synthase (iNOS) is a pro-inflammatory mediator and a major catalyst of ROS generation. In the present study we investigated the epigenetic mechanism whereby iNOS transcription is up-regulated in macrophages in the context of cardiac IRI. We report that germline deletion or systemic inhibition of myocardin-related transcription factor A (MRTF-A) in mice attenuated up-regulation of iNOS following cardiac IRI in the heart. In cultured macrophages, depletion or inhibition of MRTF-A suppressed iNOS induction by hypoxia-reoxygenation (HR). In contrast, MRTF-A over-expression potentiated activation of the iNOS promoter by HR. MRTF-A directly binds to the iNOS promoter in response to HR stimulation. MRTF-A binding to the iNOS promoter was synonymous with active histone modifications including trimethylated H3K4, acetylated H3K9, H3K27, and H4K16. Further analysis revealed that MRTF-A interacted with H4K16 acetyltransferase TIP60 to synergistically activate iNOS transcription. TIP60 depletion or inhibition achieved equivalent effects as MRTF-A depletion/inhibition in terms of iNOS repression. Of interest, TIP60 appeared to form a crosstalk with the H3K4 trimethyltransferase complex to promote iNOS trans-activation. In conclusion, we data suggest that the MRTF-A-TIP60 axis may play a critical role in iNOS transcription in macrophages and as such be considered as a potential target for the intervention of cardiac IRI.

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Section: Methodsmentioning

confidence: 99%

An Interplay Between MRTF-A and the Histone Acetyltransferase TIP60 Mediates Hypoxia-Reoxygenation Induced iNOS Transcription in Macrophages

Yang

et al. 2020

Front. Cell Dev. Biol.

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“…MKL1 expression constructs (Z. Li, B. Chen, W. Dong et al, ), CTGF promoter constructs (Li et al, ), and ACTA2 promoter construct (Fan et al, ) have been described previously. Primary renal tubular epithelial cells were isolated and maintained in William's E media supplemented with 10% fetal bovine serum as previously described (Xu et al, ).…”

Section: Methodsmentioning

confidence: 99%

MKL1 mediates TGF‐β‐induced CTGF transcription to promote renal fibrosis

Mao

Liu

Zhang

et al. 2019

Journal Cellular Physiology

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“…Chromatin immunoprecipitation (ChIP) assays were performed essentially as described previously . In brief, chromatin in control and treated cells was cross‐linked with 1% formaldehyde.…”

Section: Methodsmentioning

confidence: 99%

“…Chromatin immunoprecipitation (ChIP) assays were performed essentially as described previously. [34][35][36][37][38][39][40][41][42] In brief, chromatin in control and treated cells was cross-linked with 1% formaldehyde. Cells were incubated in lysis buffer (150 mM NaCl, 25 mM Tris-HCl pH 7Á5, 1% Triton-X-100, 0Á1% SDS, 0Á5% deoxycholate) supplemented with protease inhibitor tablet and phenylmethylsulphonyl fluoride.…”

Section: Chromatin Immunoprecipitationmentioning

confidence: 99%

Forkhead transcription factor FOXO3a mediates interferon‐γ‐induced MHC II transcription in macrophages

Fan

Chen

et al. 2019

Immunology

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Summary Macrophages are professional antigen‐presenting cells relying on the expression of class II major histocompatibility complex (MHC II) genes. Interferon‐γ (IFN‐γ) activates MHC II transcription via the assembly of an enhanceosome centred on class II trans‐activator (CIITA). In the present study, we investigated the role of the forkhead transcription factor FOXO3a in IFN‐ γ‐induced MHC II transcription in macrophages. Knockdown of FOXO3a, but not FOXO1 or FOXO4, diminished IFN‐γ‐induced MHC II expression in RAW cells. On the contrary, over‐expression of FOXO3a, but neither FOXO1 nor FOXO4, enhanced CIITA‐mediated trans‐activation of the MHC II promoter. IFN‐γ treatment promoted the recruitment of FOXO3a to the MHC II promoter. Co‐immunoprecipitation and RE‐ChIP assays showed that FOXO3a was a component of the MHC II enhanceosome forming interactions with CIITA, RFX5, RFXB and RFXAP. FOXO3a contributed to MHC II transcription by altering histone modifications surrounding the MHC II promoter. Of interest, FOXO3a was recruited to the type IV CIITA promoter and directly activated CIITA transcription by interacting with signal transducer of activation and transcription 1 in response to IFN‐γ stimulation. In conclusion, our data unveil a novel role for FOXO3a in the regulation of MHC II transcription in macrophages.

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Epigenetic activation of PERP transcription by MKL1 contributes to ROS-induced apoptosis in skeletal muscle cells

Cited by 44 publications

References 44 publications

An Interplay Between MRTF-A and the Histone Acetyltransferase TIP60 Mediates Hypoxia-Reoxygenation Induced iNOS Transcription in Macrophages

An Interplay Between MRTF-A and the Histone Acetyltransferase TIP60 Mediates Hypoxia-Reoxygenation Induced iNOS Transcription in Macrophages

MKL1 mediates TGF‐β‐induced CTGF transcription to promote renal fibrosis

Forkhead transcription factor FOXO3a mediates interferon‐γ‐induced MHC II transcription in macrophages

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