Rescue of excitation-contraction coupling in dysgenic muscle by addition of fibroblasts in vitro

Courbin, P.; Koenig, Jeanine; Ressouches, Annie; Beam, Kurt G.; Powell, Jeanne A.

doi:10.1016/0896-6273(89)90072-x

Cited by 35 publications

(27 citation statements)

References 24 publications

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“…5C, note the clusters near the periphery). These clusters near the surface membrane may correspond to sites of peripheral couplings between the SR and surface plasmalemma, which are relatively plentiful early during myogenesis (18,19). The midlevel section also revealed clusters that appeared to be far from the surface and that may represent nascent junctions between the SR and T-tubules (19).…”

Section: Resultsmentioning

confidence: 99%

“…Surprisingly, in dysgenic myotubes expressing the brain N-type (16) or P͞Q-type (17) Ca 2ϩ channels, Ca 2ϩ influx-dependent contractile activity (i.e., cardiac-type EC coupling) is almost never observed even though the Ca 2ϩ current density is comparable to that for the cardiac DHPR. The inability of large, non-L-type Ca 2ϩ currents to trigger SR Ca 2ϩ release might be because of a lack of targeting of the non-L-type Ca 2ϩ channels into clusters at functional sites of EC coupling, namely, the junctions of the SR with either the surface membrane (peripheral couplings) or the transverse (T) tubules (18)(19)(20). Accordingly, few (or none) of the non-L-type Ca 2ϩ channels would be positioned close enough to RyRs to trigger SR Ca 2ϩ release.…”

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confidence: 99%

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Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca ²⁺ channels expressed in dysgenic myotubes

Grabner

Dirksen

Beam

1998

Proc. Natl. Acad. Sci. U.S.A.

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144

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Expression of cardiac L-type Ca 2؉ channels in dysgenic myotubes results in large Ca 2؉ currents and electrically evoked contractions resulting from Ca 2؉ -entry dependent release of Ca 2؉ from the sarcoplasmic reticulum. By contrast, expression of either P͞Q-type or N-type Ca 2؉ channels in dysgenic myotubes does not result in electrically evoked contractions despite producing comparably large Ca 2؉ currents. In this work we examined the possibility that this discrepancy is caused by the preferential distribution of expressed L-type Ca 2؉ channels in close apposition to sarcoplasmic reticulum Ca 2؉ release channels. We tagged the N termini of different ␣ 1 subunits (classes A, B, C, and S) with a modified green f luorescent protein (GFP) and expressed each of the fusion channels in dysgenic myotubes. Each GFP-tagged ␣ 1 subunit exhibited Ca 2؉ channel activity that was indistinguishable from its wild-type counterpart. In addition, expression of GFP-␣ 1S and GFP-␣ 1C in dysgenic myotubes restored skeletal-and cardiac-type excitationcontraction (EC) coupling, respectively, whereas expression of GFP-␣ 1A and GFP-␣ 1B failed to restore EC coupling of any type. Laser-scanning confocal microscopy revealed a distinct expression pattern for L-type compared with non-L-type channels. After injection of cDNA into a single nucleus, GFP-␣ 1S and GFP-␣ 1C were present in the plasmalemma as small punctate foci along much of the longitudinal extent of the myotube. In contrast, GFP-␣ 1A and GFP-␣ 1B were not concentrated into punctate foci and primarily were found adjacent to the injected nucleus. Thus, L-type channels possess a targeting signal that directs their longitudinal transport and insertion into punctate regions of myotubes that presumably represent functional sites of EC coupling.Excitation-contraction (EC) coupling of striated muscle (skeletal and cardiac) occurs as a close interplay between the L-type Ca 2ϩ channels or dihydropyridine receptors (DHPRs) of the plasma membrane and the Ca 2ϩ release channels or ryanodine receptors (RyRs) of the sarcoplasmic reticulum (SR) (for review see ref.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca ²⁺ channels expressed in dysgenic myotubes

Grabner

Dirksen

Beam

1998

Proc. Natl. Acad. Sci. U.S.A.

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144

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“…T tubules and SR develop normally in dysgenic myotubes in culture (57), but triads with visible feet seemed to be lacking (58,59). Immunocytochemistry showed failure of RyRs and triadin to cluster (39).…”

Section: Development Of Triadsmentioning

confidence: 99%

Formation of junctions involved in excitation-contraction coupling in skeletal and cardiac muscle.

Flucher

Franzini‐Armstrong

1996

Proc. Natl. Acad. Sci. U.S.A.

200

152

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During excitation-contraction (e-c) coupling of striated muscle, depolarization of the surface membrane is converted into Ca2+ release from internal stores. This process occurs at intracellular junctions characterized by a specialized composition and structural organization of membrane proteins. The coordinated arrangement of the two key junctional components-the dihydropyridine receptor (DHPR) in the surface membrane and the ryanodine receptor (RyR) in the sarcoplasmic reticulum-is essential for their normal, tissue-specific function in e-c coupling. The mechanisms involved in the formation of the junctions and a potential participation of DHPRs and RyRs in this process have been subject of intensive studies over the past 5 years. In this review we discuss recent advances in understanding the organization of these molecules in skeletal and cardiac muscle, as well as their concurrent and independent assembly during development of normal and mutant muscle. From this information we derive a model for the assembly of the junctions and the establishment of the precise structural relationship between DHPRs and RyRs that underlies their interaction in e-c coupling.

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“…Fibroblasts, express markers common to mesodermal cells, such as collagens and vimentin. Normal fibroblasts fuse with dysgenic mdg (Restoration of dysgenic murine) myoblasts to restore the expression of the membrane calcium channel in the mutant (Chaudary et al 1989;Courbin et al 1989). It was suggested that fibroblast nuclei would be exposed to muscle transcription factors due to the infrequent random fusion (Blau et al 1985).…”

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confidence: 99%

Effects of stress hormone cortisol on the mRNA expression of myogenenin, MyoD, Myf5, PAX3 and PAX7

Pandurangan

Moorthy²,

Ravikumar

et al. 2013

Cytotechnology

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The present investigation was carried out to evaluate the effect of stress hormone cortisol on the myogenic markers in the C2C12 cells co-cultured with 3T3-L1 preadipocytes. Co-culturing was achieved by transwell inserts with a 0.4 lm porous membrane. C2C12 and 3T3-L1 cells were grown independently on the transwell plates. After differentiation, inserts containing 3T3-L1 cells were transferred to C2C12 plates for co-culturing. 10 lg/ll of cortisol was added to the medium. After 72 h of treatment, C2C12 cells which were in the lower well were harvested for analysis. RT-PCR analysis of myogenic markers such as of myogenin, MyoD, Myf5, PAX3 and PAX7 showed a significant reduction in the mRNA expression of these myogenic markers. In addition, cortisol increased calpain activity, which led to accelerated protein degradation, which in turn reduced the myogenic rate. In conclusion, cortisol treatment reduced mRNA expression of myogenic markers in the cocultured C2C12 cells, which is quite distinct from one dimensional mono-cultured C2C12 cells.

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Rescue of excitation-contraction coupling in dysgenic muscle by addition of fibroblasts in vitro

Cited by 35 publications

References 24 publications

Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca ²⁺ channels expressed in dysgenic myotubes

Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca ²⁺ channels expressed in dysgenic myotubes

Formation of junctions involved in excitation-contraction coupling in skeletal and cardiac muscle.

Effects of stress hormone cortisol on the mRNA expression of myogenenin, MyoD, Myf5, PAX3 and PAX7

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Rescue of excitation-contraction coupling in dysgenic muscle by addition of fibroblasts in vitro

Cited by 35 publications

References 24 publications

Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca 2+ channels expressed in dysgenic myotubes

Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca 2+ channels expressed in dysgenic myotubes

Formation of junctions involved in excitation-contraction coupling in skeletal and cardiac muscle.

Effects of stress hormone cortisol on the mRNA expression of myogenenin, MyoD, Myf5, PAX3 and PAX7

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Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca ²⁺ channels expressed in dysgenic myotubes

Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca ²⁺ channels expressed in dysgenic myotubes