EconPapers    
Economics at your fingertips  
 

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 and Imed-Eddine Gallouzi ()
Additional contact information
Virginie Dormoy-Raclet: McGill University, Goodman Cancer Center
Anne Cammas: McGill University, Goodman Cancer Center
Barbara Celona: San Raffaele University and Scientific Institute
Xian Jin Lian: McGill University, Goodman Cancer Center
Kate van der Giessen: McGill University, Goodman Cancer Center
Marija Zivojnovic: McGill University, Goodman Cancer Center
Silvia Brunelli: University of Milan-Bicocca
Francesca Riuzzi: University of Perugia
Guglielmo Sorci: University of Perugia
Brian T. Wilhelm: Institute for Research in Immunology and Cancer (IRIC), Université de Montréal
Sergio Di Marco: McGill University, Goodman Cancer Center
Rosario Donato: University of Perugia
Marco E. Bianchi: San Raffaele University and Scientific Institute
Imed-Eddine Gallouzi: McGill University, Goodman Cancer Center

Nature Communications, 2013, vol. 4, issue 1, 1-15

Abstract: 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.

Date: 2013
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms3388 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3388

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms3388

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().

 
Page updated 2025-03-19
Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3388