ArticleHuman molecular genetics2011
Sarcolemma instability during mechanical activity in Largemyd cardiac myocytes with loss of dystroglycan extracellular matrix receptor function.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- Syntaxin 4-enhanced plasma membrane repair is independent of dysferlin in skeletal muscle.American journal of physiology. Cell physiology · 2025Article
- Dystroglycanopathy: From Elucidation of Molecular and Pathological Mechanisms to Development of Treatment Methods.International journal of molecular sciences · 2021Review
- The role of basement membranes in cardiac biology and disease.Bioscience reports · 2021Review
- Cardiomyopathy in limb girdle muscular dystrophy R9, FKRP related.Muscle & nerve · 2020Article
- Generating a Fractal Microstructure of Laminin-111 to Signal to Cells.Journal of visualized experiments : JoVE · 2020Article
- Dilated cardiomyopathy mutations in δ-sarcoglycan exert a dominant-negative effect on cardiac myocyte mechanical stability.American journal of physiology. Heart and circulatory physiology · 2016Article
- Rationally engineered Troponin C modulates in vivo cardiac function and performance in health and disease.Nature communications · 2016Article
- Article
- Dystrophin-glycoprotein complex regulates muscle nitric oxide production through mechanoregulation of AMPK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Pompe disease results in a Golgi-based glycosylation deficit in human induced pluripotent stem cell-derived cardiomyocytes.The Journal of biological chemistry · 2015Article
- Article
- From stem cells to cardiomyocytes: the role of forces in cardiac maturation, aging, and disease.Progress in molecular biology and translational science · 2014Review
- Muscle-specific expression of LARGE restores neuromuscular transmission deficits in dystrophic LARGE(myd) mice.Human molecular genetics · 2013Article
- Article
- Sustaining cardiac claudin-5 levels prevents functional hallmarks of cardiomyopathy in a muscular dystrophy mouse model.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The abnormal glycosylation and loss of extracellular matrix receptor function of the protein dystroglycan (DG) lead to the development of muscular dystrophy and cardiomyopathy. Dystroglycan is an important receptor for extracellular matrix proteins, such as laminin, in the basement membrane surrounding muscle. Large(myd) mice have a null mutation in a gene encoding the glycosyltransferase LARGE that results in abnormal glycosylation of α-DG and phenotypes similar to those in human α-DG glycosylation-deficient muscular dystrophy. Here, we show that Large(myd) hearts with the loss of DG extracellular matrix receptor function display a cardiomyopathy characterized by myocyte damage in patches of cells positive for membrane impermeant dyes. To examine the cellular mechanisms, we show that isolated adult cardiac myocytes from Large(myd) mice retain normal laminin-dependent cell adhesion, cell surface laminin deposition and basement membrane assembly. However, although isolated adult cardiac myocytes with the loss of α-DG glycosylation adhere normally to laminin substrates both passively and in the presence of mechanical activity, Large(myd) myocytes rapidly take up membrane impermeant dye following cyclical cell stretching. Therefore, while other cell surface laminin receptors are likely responsible for myocardial cell adhesion to the basement membrane, DG has a unique function of stabilizing the cardiac myocyte plasma membrane during repetitive mechanical activity by tightly binding the transmembrane dystrophin-glycoprotein complex to the extracellular matrix. This function of DG to stabilize the myocyte membrane during normal physiologic cell length changes is likely critical for the prevention of the myocardial damage and subsequent remodeling observed in α-DG glycosylation-deficient muscular dystrophies.
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