Nr4a1 promotes cell adhesion and fusion by regulating Zeb1 transcript levels in myoblasts
Nuclear receptor subfamily 4 group A member 1 (NR4A1) acts as a myogenic factor in muscle development and regeneration; however, it remains unclear how Nr4a1 regulates myoblast physiology. In this study, report a role for Nr4a1-mediated regulation of cell adhesion in myoblast and muscle tissue. Nr4a...
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Published in | Biochemical and biophysical research communications Vol. 556; pp. 127 - 133 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
04.06.2021
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Subjects | |
Online Access | Get full text |
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Summary: | Nuclear receptor subfamily 4 group A member 1 (NR4A1) acts as a myogenic factor in muscle development and regeneration; however, it remains unclear how Nr4a1 regulates myoblast physiology. In this study, report a role for Nr4a1-mediated regulation of cell adhesion in myoblast and muscle tissue. Nr4a1-overexpression myoblast, Nr4a1-konckdown myoblast and mice gastrocnemius muscle following an injection with an adenovirus vector expression Nr4a1 (Nr4a1-AAV) were used to observe the changes in cell adhesion. Nr4a1 was found to enhance cell-cell contact and adhesion molecule expression in myoblasts. In contrast, the deletion of Nr4a1 expression inhibited junction and adhesion between myoblasts. Moreover, Nr4a1 increased myoblast adhesion via directly binding to an upstream site of zinc finger E-box binding homeobox 1 (Zeb1), which is required for myogenesis in myoblasts. In mice, Zeb1 induced increased cadherin and integrin expression in the gastrocnemius muscle following an injection with an adenovirus vector expressing Nr4a1(Nr4a1-AAV). These data indicate that Nr4a1 regulates myoblast adhesion via Zeb1 expression.
•Nr4a1 overexpression enhances myoblast contact and cell adhesion molecule levels.•Nr4a1 silencing decreases myoblast contact and cell adhesion molecule expression.•The effect of Nr4a1 on myoblast adhesion and fusion involves Zeb1. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2021.03.153 |