Differentiation markers of mouse C2C12 and rat L6 myogenic cell lines and the effect of the differentiation medium

Portier, G.; Benders, A.A.G.M.; Oosterhof, Arie; Veerkamp, J.H.; Kuppevelt, A.H.M.S.M. van

doi:10.1007/s11626-999-0030-8

Cited by 48 publications

(32 citation statements)

References 52 publications

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“…Although L6 myotubes express AChRs (37), they exhibit greatly reduced spontaneous AChR clustering activity compared with C2C12 myotubes (38). We hypothesized that the low spontaneous AChR clustering activity of L6 might in part be due to sialic acid capping of VVA-reactive epitopes on L6 myotube ␣-dystroglycan.…”

Section: Figmentioning

confidence: 99%

Differential Vicia villosa Agglutinin Reactivity Identifies Three Distinct Dystroglycan Complexes in Skeletal Muscle

McDearmon¹,

Combs²,

Ervasti³

2001

Journal of Biological Chemistry

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We present evidence for the expression of three ␣-dystroglycan glycoforms in skeletal muscle cells, including two minor glycoforms marked by either patent or latent reactivity with the N-acetylgalactosaminespecific lectin Vicia villosa agglutinin. Both minor glycoforms co-isolated with ␤-dystroglycan, but not with other dystrophin/utrophin-glycoprotein complex components, suggesting that they may perform distinct or modified cellular functions. We also confirmed that both patent and latent V. villosa agglutinin-reactive ␣-dystroglycan glycoforms are expressed in C2C12 myotubes. However, we found that the combined effect of saturating concentrations of V. villosa agglutinin and laminin-1 were strictly additive with respect to acetylcholine receptor cluster formation in C2C12 myotubes, which suggests that laminin-1 and V. villosa agglutinin do not compete for the same binding site on the cell surface. Finally, although ␤-N-acetylhexosaminidase digestion dramatically inhibited agrin-, V. villosa agglutinin-, and laminin-1-induced acetylcholine receptor clustering in C2C12 myotubes, treatment with this enzyme had no effect on the amount of ␣-dystroglycan that was bound to V. villosa agglutininagarose. We conclude that ␣-dystroglycan is not the V. villosa agglutinin receptor implicated in acetylcholine receptor cluster formation. However, our data provide new support for the hypothesis that different glycoforms of ␣-dystroglycan may perform distinct functions even within the same cell.

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Section: Figmentioning

confidence: 99%

Differential Vicia villosa Agglutinin Reactivity Identifies Three Distinct Dystroglycan Complexes in Skeletal Muscle

McDearmon¹,

Combs²,

Ervasti³

2001

Journal of Biological Chemistry

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“…DM contained 2 ml Ultroser G (15950-017, Pall BioSepra S.A., France) as described previously (data submitted). 25 The first day of transfer to DM will be subsequently referred to as Ôs0' (shift day 0) and following days will be numbered in sequence. Experiments were performed on days s6 and s7.…”

Section: Cell and Tissue Culturementioning

confidence: 99%

The Relative Contributions of Compression and Hypoxia to Development of Muscle Tissue Damage: An In Vitro Study

et al. 2006

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Deep pressure ulcers develop in tissues subjected to sustained mechanical loading. Though it has been hypothesized that this damage mechanism results from local tissue ischemia, it has recently been shown with a cell model that sustained compression can cause cell deformation, leading to tissue breakdown. The present study focuses on the assessment of cell viability during compression and ischemia in an in vitro muscle model to determine their relative contributions to damage development. A model system was developed consisting of engineered skeletal muscle produced from the culture of murine muscle cells in a collagen gel. The tissue was subjected to 0, 20, or 40% compression under hypoxic or normoxic conditions. Experiments were performed on the stage of a microscope and cell viability was monitored using fluorescent markers for apoptotic and necrotic cell death. Hypoxia did not lead to significant cell death over a 22 h period. By contrast, compression led to immediate cell death that increased with time. No additional effect of hypoxia on cell death was observed. These data show that contrary to existing theories, compression can cause development of muscle damage and that hypoxia does not contribute to cell death development within 22 h in engineered muscle.

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“…These comparisons therefore suggest that the collagen-coated glass is too stiff and locks stress-fiber-rich nascent myotubes into tightly adherent, early differentiation states. An important role for substrate compliance in the differentiation of contractile cells such as C2C12s (Portier et al, 1999) is understandable. Fully differentiated myotubes in vivo show vinculin organized into striated structures known as costameres (Pardo et al, 1983).…”

Section: Cell Patterning and Ridgidity-inhibited Differentiationmentioning

confidence: 99%

Adhesion-contractile balance in myocyte differentiation

Griffin

Sen

Sweeney

et al. 2004

Journal of Cell Science

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Tissue cells generally pull on their matrix attachments and balance a quasi-static contractility against adequate adhesion, but any correlation with and/or influence on phenotype are not yet understood. Here, we begin to demonstrate how differentiation state couples to actomyosin-based contractility through adhesion and substrate compliance. Myotubes are differentiated from myoblasts on collagen-patterned coverslips that allow linear fusion but prevent classic myotube branching. Post-fusion, myotubes adhere to the micro-strips but lock into a stress fiber-rich state and do not differentiate significantly further. In contrast, myotubes grown on top of such cells do progress through differentiation, exhibiting actomyosin striations within one week. A compliant adhesion to these lower cells is suggested to couple to contractility and accommodate the reorganization needed for upper cell striation. Contractility is assessed in these adherent cells by mechanically detaching one end of the myotubes. All myotubes, whether striated or not, shorten with an exponential decay. The cell-on-cell myotubes relax more, which implies a greater contractile stress. The non-muscle myosin II inhibitor blebbistatin inhibits relaxation for either case. Myotubes in culture are thus clearly prestressed by myosin II, and this contractility couples to substrate compliance and ultimately influences actomyosin striation.

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Differentiation markers of mouse C2C12 and rat L6 myogenic cell lines and the effect of the differentiation medium

Cited by 48 publications

References 52 publications

Differential Vicia villosa Agglutinin Reactivity Identifies Three Distinct Dystroglycan Complexes in Skeletal Muscle

Differential Vicia villosa Agglutinin Reactivity Identifies Three Distinct Dystroglycan Complexes in Skeletal Muscle

The Relative Contributions of Compression and Hypoxia to Development of Muscle Tissue Damage: An In Vitro Study

Adhesion-contractile balance in myocyte differentiation

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