Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions

Abstract The overall objective of the study was to identify mechanisms through which intercellular adhesion molecule-1 (ICAM-1) augments the adhesive and fusogenic properties of myogenic cells. Hypotheses were tested using cultured myoblasts and fibroblasts, which do not constitutively express ICAM-...

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Autores principales:	Francis X. Pizza, Ryan A. Martin, Evan M. Springer, Maxwell S. Leffler, Bryce R. Woelmer, Isaac J. Recker, Douglas W. Leaman
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/78c6672c4e6d4197937075dfb4cc74d0
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spelling	oai:doaj.org-article:78c6672c4e6d4197937075dfb4cc74d02021-12-02T16:07:59ZIntercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions10.1038/s41598-017-05283-32045-2322https://doaj.org/article/78c6672c4e6d4197937075dfb4cc74d02017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05283-3https://doaj.org/toc/2045-2322Abstract The overall objective of the study was to identify mechanisms through which intercellular adhesion molecule-1 (ICAM-1) augments the adhesive and fusogenic properties of myogenic cells. Hypotheses were tested using cultured myoblasts and fibroblasts, which do not constitutively express ICAM-1, and myoblasts and fibroblasts forced to express full length ICAM-1 or a truncated form lacking the cytoplasmic domain of ICAM-1. ICAM-1 mediated myoblast adhesion and fusion were quantified using novel assays and cell mixing experiments. We report that ICAM-1 augments myoblast adhesion to myoblasts and myotubes through homophilic trans-interactions. Such adhesive interactions enhanced levels of active Rac in adherent and fusing myoblasts, as well as triggered lamellipodia, spreading, and fusion of myoblasts through the signaling function of the cytoplasmic domain of ICAM-1. Rac inhibition negated ICAM-1 mediated lamellipodia, spreading, and fusion of myoblasts. The fusogenic property of ICAM-1-ICAM-1 interactions was restricted to myogenic cells, as forced expression of ICAM-1 by fibroblasts did not augment their fusion to ICAM-1+ myoblasts/myotubes. We conclude that ICAM-1 augments myoblast adhesion and fusion through its ability to self-associate and initiate Rac-mediated remodeling of the actin cytoskeleton.Francis X. PizzaRyan A. MartinEvan M. SpringerMaxwell S. LefflerBryce R. WoelmerIsaac J. ReckerDouglas W. LeamanNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-17 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Francis X. Pizza Ryan A. Martin Evan M. Springer Maxwell S. Leffler Bryce R. Woelmer Isaac J. Recker Douglas W. Leaman Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions
description	Abstract The overall objective of the study was to identify mechanisms through which intercellular adhesion molecule-1 (ICAM-1) augments the adhesive and fusogenic properties of myogenic cells. Hypotheses were tested using cultured myoblasts and fibroblasts, which do not constitutively express ICAM-1, and myoblasts and fibroblasts forced to express full length ICAM-1 or a truncated form lacking the cytoplasmic domain of ICAM-1. ICAM-1 mediated myoblast adhesion and fusion were quantified using novel assays and cell mixing experiments. We report that ICAM-1 augments myoblast adhesion to myoblasts and myotubes through homophilic trans-interactions. Such adhesive interactions enhanced levels of active Rac in adherent and fusing myoblasts, as well as triggered lamellipodia, spreading, and fusion of myoblasts through the signaling function of the cytoplasmic domain of ICAM-1. Rac inhibition negated ICAM-1 mediated lamellipodia, spreading, and fusion of myoblasts. The fusogenic property of ICAM-1-ICAM-1 interactions was restricted to myogenic cells, as forced expression of ICAM-1 by fibroblasts did not augment their fusion to ICAM-1+ myoblasts/myotubes. We conclude that ICAM-1 augments myoblast adhesion and fusion through its ability to self-associate and initiate Rac-mediated remodeling of the actin cytoskeleton.
format	article
author	Francis X. Pizza Ryan A. Martin Evan M. Springer Maxwell S. Leffler Bryce R. Woelmer Isaac J. Recker Douglas W. Leaman
author_facet	Francis X. Pizza Ryan A. Martin Evan M. Springer Maxwell S. Leffler Bryce R. Woelmer Isaac J. Recker Douglas W. Leaman
author_sort	Francis X. Pizza
title	Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions
title_short	Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions
title_full	Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions
title_fullStr	Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions
title_full_unstemmed	Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions
title_sort	intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/78c6672c4e6d4197937075dfb4cc74d0
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Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions

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