Evidence map›Paper›PMID 39323088›Full record

ArticleJournal of cachexia, sarcopenia and muscle2024

The Innovative Role of Nuclear Receptor Interaction Protein in Orchestrating Invadosome Formation for Myoblast Fusion.

Hsin-Hsiung Chen, Chia-Yang Lin, Ya-Ju Han, Yun-Hsin Huang, Yi-Hsiang Liu, Wan-En Hsu, Li-Kai Tsai, Hsing-Jung Lai, Yeou-Ping Tsao, Hsiang-Po Huang and 1 more

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Article in Journal of cachexia, sarcopenia and muscle, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Hsin-Hsiung ChenGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chia-Yang LinGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ya-Ju HanGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yun-Hsin HuangGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yi-Hsiang LiuGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wan-En HsuGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Li-Kai TsaiDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Hsing-Jung LaiDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Yeou-Ping TsaoDepartment of Ophthalmology, Mackay Memorial Hospital, Taipei, Taiwan.
Hsiang-Po HuangGraduate Institute of Medical Genomics and Proteomics, College of Medicine, National Taiwan University, Taipei, Taiwan.
Show-Li ChenGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.ORCID 0000-0002-6588-8632

Funding

National Science and Technology Council MOST 104-2320-B-002-053-MY3National Science and Technology Council MOST 107-2320-B-002-012-MY3National Science and Technology Council MOST 110-2320-B-002-052-MY3National Science and Technology Council MOST 111-2320-B-002-077-MY3National Science and Technology Council National Health Research InstituteNational Science and Technology Council NHRI-105-1053ISI
6 · The paper itself

Abstract

backgroundNuclear receptor interaction protein (NRIP) is versatile and engages with various proteins to execute its diverse biological function. NRIP deficiency was reported to cause small myofibre size in adult muscle regeneration, indicating a crucial role of NRIP in myoblast fusion.

methodsThe colocalization and interaction of NRIP with actin were investigated by immunofluorescence and immunoprecipitation assay, respectively. The participation of NRIP in myoblast fusion was demonstrated by cell fusion assay and time-lapse microscopy. The NRIP mutants were generated for mechanism study in NRIP-null C2C12 (termed KO19) cells and muscle-specific NRIP knockout (NRIP cKO) mice. A GEO profile database was used to analyse NRIP expression in Duchenne muscular dystrophy (DMD) patients.

resultsIn this study, we found that NRIP directly and reciprocally interacted with actin both in vitro and in cells. Immunofluorescence microscopy showed that the endogenous NRIP colocalized with components of invadosome, such as actin, Tks5, and cortactin, at the tips of cells during C2C12 differentiation. The KO19 cells were generated and exhibited a significant deficit in myoblast fusion compared with wild-type C2C12 cells (3.16% vs. 33.67%, p < 0.005). Overexpressed NRIP in KO19 cells could rescue myotube formation compared with control (3.37% vs. 1.00%, p < 0.01). We further confirmed that NRIP directly participated in cell fusion by using a cell-cell fusion assay. We investigated the mechanism of invadosome formation for myoblast fusion, which depends on NRIP-actin interaction, by analysing NRIP mutants in NRIP-null cells. Loss of actin-binding of NRIP reduced invadosome (enrichment ratio, 1.00 vs. 2.54, p < 0.01) and myotube formation (21.82% vs. 35.71%, p < 0.05) in KO19 cells and forced NRIP expression in KO19 cells and muscle-specific NRIP knockout (NRIP cKO) mice increased myofibre size compared with controls (over 1500 μm

conclusionsNRIP is a novel actin-binding protein for invadosome formation to induce myoblast fusion.

Indexed as

Cell FusionMice, KnockoutMyoblastsPodosomesActinsAnimalsCell DifferentiationCell LineHumansMiceMuscular Dystrophy, DuchenneActinsactininvadosomeIQ domainmyoblast fusionNRIPWD40 domain

Identifiers

PMID39323088
PMCPMC11634477

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.