Smooth muscle myosin heavy chain isoforms and their role in muscle physiology

Babu, Gopal J.; Warshaw, David M.; Periasamy, Muthu

doi:10.1002/1097-0029(20000915)50:6<532::aid-jemt10>3.0.co;2-e

Cited by 77 publications

(56 citation statements)

References 69 publications

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“…34 -36 To further define the SMC population and to identify the presence of myofibroblasts, antibodies against ␣-SMA and smooth-muscle myosin heavy chain (SM2 or Myh11) were also used. 37,38 Results from the present study demonstrated an increase in the number of DDR2 ϩ cells at 8-and 16-weeks post-TAA induction, suggesting an increase in the number of fibroblasts or fibroblast-derived cells at these time points. Interestingly, this occurred concomitantly with an increase in smooth-muscle myosin staining (Myh11).…”

Section: Analysis Of Taa-induced Cellular Constituentsmentioning

confidence: 48%

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Jones

Beck

Barbour

et al. 2009

The American Journal of Pathology

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The present study tested the hypothesis that changes in the resident endogenous cellular population accompany alterations in aortic collagen and elastin content during thoracic aortic aneurysm (TAA) development in a murine model. Descending thoracic aortas were analyzed at various time points (2, 4, 8, and 16 weeks) post-TAA induction (0.5 M CaCl 2 , 15 minutes). Aortic tissue sections were subjected to histological staining and morphometric analysis for collagen and elastin, as well as immunostaining for cell-type-specific markers to quantify fibroblasts, myofibroblasts, and smoothmuscle cells. Results were compared with reference control mice processed in the same fashion. Aortic dilatation was accompanied by changes in the elastic architecture that included: a decreased number of elastic lamellae (from 6 to 4); altered area fraction of elastin (elevated at 4 weeks and decreased at 16 weeks); and a decreased area between elastic lamellae (minimum reached at 4 weeks). Total collagen content did not change over time. Increased immunoreactivity for fibroblast and myofibroblast markers was observed at 8-and 16-week post-TAA-induction, whereas immunoreactivity for smooth-muscle cell markers peaked at 4 weeks and returned to baseline by 16 weeks. Therefore, this study demonstrated that changes in aortic elastin content were accompanied by the emergence of a subset of fibroblast-derived myofibroblasts whose altered phenotype may play a significant role in TAA development through the enhancement of extracellular matrix proteolysis.

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Section: Analysis Of Taa-induced Cellular Constituentsmentioning

confidence: 48%

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Jones

Beck

Barbour

et al. 2009

The American Journal of Pathology

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“…Among highly downregulated transcripts, there were inhibitors of DNA binding 1 (ID1), cell division cycle 20 (CDC20) and ubiquitin-conjugating enzyme E2C (UBE2C). MYH11 and its isoforms are differentially expressed during muscle cell maturation [45]. It has frequently been reported that CSCs are committed to all cardiac lineages (cardiomyocytes, endothelial, and smooth muscle cells) [29,32,46,47].…”

Section: Discussionmentioning

confidence: 99%

Cellular and Molecular Characterization of Human Cardiac Stem Cells Reveals Key Features Essential for Their Function and Safety

Vahdat

Mousavi

Omrani

et al. 2015

Stem Cells and Development

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“…The reverse regulation pattern of down regulated non-adipogenic gene products (e.g. jagged 1, JAG1 correlated with osteogenesis (Nobta et al, 2005) and angiogenesis (Uyttendaele et al, 2000), CYR61 involved in angiogenesis (Lau and Lam, 1999;Schutze et al, 2005a), muscle-associated tropomyosin 1 (alpha), cysteine and glycine-rich protein 2, CSRP2, myosin heavy polypeptide 11 smooth muscle, and villin 2 A c c e p t e d M a n u s c r i p t -17 -(ezrin), VIL2 (MacLeod and Gooding, 1988;Louis et al, 1997;Babu et al, 2000;Moyen et al, 2004)) and up regulated adipogenesis-related gene products (C/EBPα, LPL and acetyl-CoA carboxylase β (Rosen et al, 2002;Wu et al, 1999;Fried et al, 1993;Spiegelman et al, 1993), and two glucose transporter molecules SLC2A3 and SLC2A14) could contribute to the switch of preosteoblasts into adipocytes during transdifferentiation. Furthermore, the initiation of transdifferentiation could involve other factors and signaling pathways that have not been described in the context of direct differentiation or whose functions have not been revealed so far.…”

Section: Accepted Manuscript -16 -mentioning

confidence: 99%