ArticleProceedings of the National Academy of Sciences of the United States of America2008
Ablation of smooth muscle myosin heavy chain SM2 increases smooth muscle contraction and results in postnatal death in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Differential phenotypes in mice with smooth muscle-specific heterozygous versus homozygous deletion of Stk11.Scientific reports · 2025Article
- Netrin 1 directs vascular patterning and maturity in the developing kidney.Development (Cambridge, England) · 2023Article
- Visceral myopathy: clinical syndromes, genetics, pathophysiology, and fall of the cytoskeleton.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- Loss of smooth muscle myosin heavy chain results in the bladder and stomach developing lesion during foetal development in mice.Journal of genetics · 2018Article
- Graded effects of unregulated smooth muscle myosin on intestinal architecture, intestinal motility and vascular function in zebrafish.Disease models & mechanisms · 2016Article
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- Molecular and Cellular Characteristics of the Colonic Pseudo-obstruction in Patients With Intractable Constipation.Journal of neurogastroenterology and motility · 2015Article
- Differential expression of multidrug resistance protein 5 and phosphodiesterase 5 and regulation of cGMP levels in phasic and tonic smooth muscle.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Alterations in the contractile phenotype of the bladder: lessons for understanding physiological and pathological remodelling of smooth muscle.Journal of cellular and molecular medicine · 2012Review
- Article
- Vascular smooth muscle phenotypic diversity and function.Physiological genomics · 2010Review
- Molecular regulation of contractile smooth muscle cell phenotype: implications for vascular tissue engineering.Tissue engineering. Part B, Reviews · 2010Review
- Fibulin-4 deficiency results in ascending aortic aneurysms: a potential link between abnormal smooth muscle cell phenotype and aneurysm progression.Circulation research · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The physiological relevance of smooth muscle myosin isoforms SM1 and SM2 has not been understood. In this study we generated a mouse model specifically deficient in SM2 myosin isoform but expressing SM1, using an exon-specific gene targeting strategy. The SM2 homozygous knockout (SM2(-/-)) mice died within 30 days after birth, showing pathologies including segmental distention of alimentary tract, retention of urine in renal pelvis, distension of bladder, and the development of end-stage hydronephrosis. In contrast, the heterozygous (SM2(+/-)) mice appeared normal and reproduced well. In SM2(-/-) bladder smooth muscle the loss of SM2 myosin was accompanied by a concomitant down-regulation of SM1 and a reduced number of thick filaments. However, muscle strips from SM2(-/-) bladder showed increased contraction to K(+) depolarization or in response to M3 receptor agonist Carbachol. An increase of contraction was also observed in SM2(-/-) aorta. However, the SM2(-/-) bladder was associated with unaltered regulatory myosin light chain (MLC20) phosphorylation. Moreover, other contractile proteins, such as alpha-actin and tropomyosin, were not altered in SM2(-/-) bladder. Therefore, the loss of SM2 myosin alone could have induced hypercontractility in smooth muscle, suggesting that distinctly from SM1, SM2 may negatively modulate force development during smooth muscle contraction. Also, because SM2(-/-) mice develop lethal multiorgan dysfunctions, we propose this regulatory property of SM2 is essential for normal contractile activity in postnatal smooth muscle physiology.
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