The histone methyltransferase SETD1A regulates thrombomodulin transcription in vascular endothelial cells

Li, Zilong; Chen, Baoyu; Weng, Xinyu; Yu, Liming; Song, Mingzi; Fang, Mingming; Guo, Junli; Xu, Yong

doi:10.1016/j.bbagrm.2018.06.004

Cited by 40 publications

(20 citation statements)

References 51 publications

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“…Whole cell lysates were obtained by re-suspending cell pellets in RIPA buffer (50 mM Tris pH7.4, 150 mM NaCl, and 1% Triton X-100) with freshly added protease inhibitor (Roche) as previously described (Zeng et al, 2018;Li et al, 2018e;Fan et al, 2019). Nuclear proteins were extracted essentially as described before (Li et al, 2018d). Antibodies were incubated with cell lysates overnight before being absorbed by Protein A/G-plus Agarose beads.…”

Section: Protein Extraction Immunoprecipitation and Western Blotmentioning

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: Protein Extraction Immunoprecipitation and Western Blotmentioning

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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“…RNA was extracted with a commercial RNAprep purification kit (Tiangen) as previously described (Z. Li, B. Chen, X. Weng et al, ). First‐strand synthesis was carried out using a HiScript III RT SuperMix (Vazyme).…”

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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The histone methyltransferase SETD1A regulates thrombomodulin transcription in vascular endothelial cells

Cited by 40 publications

References 51 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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