HuR and miR-1192 regulate myogenesis by modulating the translation of HMGB1 mRNA

Virginie Dormoy-Raclet; Anne Cammas; Barbara Celona; Xian Jin Lian; Kate Van Der Giessen; Marija Zivojnovic; Silvia Brunelli; Francesca Riuzzi; Guglielmo Sorci; Brian T. Wilhelm; Sergio Di Marco; Rosario Donato; Marco E. Bianchi; Imed Eddine Gallouzi

doi:10.1038/ncomms3388

HuR and miR-1192 regulate myogenesis by modulating the translation of HMGB1 mRNA

Virginie Dormoy-Raclet, Anne Cammas, Barbara Celona, Xian Jin Lian, Kate Van Der Giessen, Marija Zivojnovic, Silvia Brunelli, Francesca Riuzzi, Guglielmo Sorci, Brian T. Wilhelm, Sergio Di Marco, Rosario Donato, Marco E. Bianchi, Imed Eddine Gallouzi

Research output: Contribution to journal › Article › peer-review

60 Scopus citations

Abstract

Upon muscle injury, the high mobility group box 1 (HMGB1) protein is upregulated and secreted to initiate reparative responses. Here we show that HMGB1 controls myogenesis both in vitro and in vivo during development and after adult muscle injury. HMGB1 expression in muscle cells is regulated at the translational level: the miRNA miR-1192 inhibits HMGB1 translation and the RNA-binding protein HuR promotes it. HuR binds to a cis-element, HuR binding sites (HuRBS), located in the 3′UTR of the HMGB1 transcript, and at the same time miR-1192 is recruited to an adjacent seed element. The binding of HuR to the HuRBS prevents the recruitment of Argonaute 2 (Ago2), overriding miR-1192-mediated translation inhibition. Depleting HuR reduces myoblast fusion and silencing miR-1192 re-establishes the fusion potential of HuR-depleted cells. We propose that HuR promotes the commitment of myoblasts to myogenesis by enhancing the translation of HMGB1 and suppressing the translation inhibition mediated by miR-1192. © 2013 Macmillan Publishers Limited.

Original language	English (US)
Journal	Nature Communications
Volume	4
DOIs	https://doi.org/10.1038/ncomms3388
State	Published - Sep 19 2013
Externally published	Yes

Bibliographical note

Generated from Scopus record by KAUST IRTS on 2022-09-13

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)
Chemistry(all)
Physics and Astronomy(all)

Access to Document

10.1038/ncomms3388

Cite this

@article{9114a8f33cbd4f5ab50b1bc8fbe3fa35,

title = "HuR and miR-1192 regulate myogenesis by modulating the translation of HMGB1 mRNA",

abstract = "Upon muscle injury, the high mobility group box 1 (HMGB1) protein is upregulated and secreted to initiate reparative responses. Here we show that HMGB1 controls myogenesis both in vitro and in vivo during development and after adult muscle injury. HMGB1 expression in muscle cells is regulated at the translational level: the miRNA miR-1192 inhibits HMGB1 translation and the RNA-binding protein HuR promotes it. HuR binds to a cis-element, HuR binding sites (HuRBS), located in the 3′UTR of the HMGB1 transcript, and at the same time miR-1192 is recruited to an adjacent seed element. The binding of HuR to the HuRBS prevents the recruitment of Argonaute 2 (Ago2), overriding miR-1192-mediated translation inhibition. Depleting HuR reduces myoblast fusion and silencing miR-1192 re-establishes the fusion potential of HuR-depleted cells. We propose that HuR promotes the commitment of myoblasts to myogenesis by enhancing the translation of HMGB1 and suppressing the translation inhibition mediated by miR-1192. {\textcopyright} 2013 Macmillan Publishers Limited.",

author = "Virginie Dormoy-Raclet and Anne Cammas and Barbara Celona and Lian, {Xian Jin} and {Van Der Giessen}, Kate and Marija Zivojnovic and Silvia Brunelli and Francesca Riuzzi and Guglielmo Sorci and Wilhelm, {Brian T.} and Marco, {Sergio Di} and Rosario Donato and Bianchi, {Marco E.} and Gallouzi, {Imed Eddine}",

note = "Generated from Scopus record by KAUST IRTS on 2022-09-13",

year = "2013",

month = sep,

day = "19",

doi = "10.1038/ncomms3388",

language = "English (US)",

volume = "4",

journal = "Nature Communications",

issn = "2041-1723",

}

TY - JOUR

T1 - HuR and miR-1192 regulate myogenesis by modulating the translation of HMGB1 mRNA

AU - Dormoy-Raclet, Virginie

AU - Cammas, Anne

AU - Celona, Barbara

AU - Lian, Xian Jin

AU - Van Der Giessen, Kate

AU - Zivojnovic, Marija

AU - Brunelli, Silvia

AU - Riuzzi, Francesca

AU - Sorci, Guglielmo

AU - Wilhelm, Brian T.

AU - Marco, Sergio Di

AU - Donato, Rosario

AU - Bianchi, Marco E.

AU - Gallouzi, Imed Eddine

N1 - Generated from Scopus record by KAUST IRTS on 2022-09-13

PY - 2013/9/19

Y1 - 2013/9/19

N2 - Upon muscle injury, the high mobility group box 1 (HMGB1) protein is upregulated and secreted to initiate reparative responses. Here we show that HMGB1 controls myogenesis both in vitro and in vivo during development and after adult muscle injury. HMGB1 expression in muscle cells is regulated at the translational level: the miRNA miR-1192 inhibits HMGB1 translation and the RNA-binding protein HuR promotes it. HuR binds to a cis-element, HuR binding sites (HuRBS), located in the 3′UTR of the HMGB1 transcript, and at the same time miR-1192 is recruited to an adjacent seed element. The binding of HuR to the HuRBS prevents the recruitment of Argonaute 2 (Ago2), overriding miR-1192-mediated translation inhibition. Depleting HuR reduces myoblast fusion and silencing miR-1192 re-establishes the fusion potential of HuR-depleted cells. We propose that HuR promotes the commitment of myoblasts to myogenesis by enhancing the translation of HMGB1 and suppressing the translation inhibition mediated by miR-1192. © 2013 Macmillan Publishers Limited.

AB - Upon muscle injury, the high mobility group box 1 (HMGB1) protein is upregulated and secreted to initiate reparative responses. Here we show that HMGB1 controls myogenesis both in vitro and in vivo during development and after adult muscle injury. HMGB1 expression in muscle cells is regulated at the translational level: the miRNA miR-1192 inhibits HMGB1 translation and the RNA-binding protein HuR promotes it. HuR binds to a cis-element, HuR binding sites (HuRBS), located in the 3′UTR of the HMGB1 transcript, and at the same time miR-1192 is recruited to an adjacent seed element. The binding of HuR to the HuRBS prevents the recruitment of Argonaute 2 (Ago2), overriding miR-1192-mediated translation inhibition. Depleting HuR reduces myoblast fusion and silencing miR-1192 re-establishes the fusion potential of HuR-depleted cells. We propose that HuR promotes the commitment of myoblasts to myogenesis by enhancing the translation of HMGB1 and suppressing the translation inhibition mediated by miR-1192. © 2013 Macmillan Publishers Limited.

UR - http://www.nature.com/articles/ncomms3388

UR - http://www.scopus.com/inward/record.url?scp=84884126014&partnerID=8YFLogxK

U2 - 10.1038/ncomms3388

DO - 10.1038/ncomms3388

M3 - Article

VL - 4

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

ER -

HuR and miR-1192 regulate myogenesis by modulating the translation of HMGB1 mRNA

Abstract

Bibliographical note

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this