Skeletal myoblasts overexpressing relaxin improve differentiation and communication of primary murine cardiomyocyte cell cultures

Formigli, Lucia; Francini, Fabio; Nistri, Silvia; Margheri, Martina; Luciani, Giorgia; Naro, Fabio; Silvertown, Josh D.; Orlandini, Sandra Zecchi; Meacci, Elisabetta; Bani, Danièle

doi:10.1016/j.yjmcc.2009.05.008

Cited by 42 publications

(50 citation statements)

References 41 publications

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“…Heterologous expression of TRPC1 has provided controversial data concerning the activation of TRPC1-supported currents by stretch (24,57). In skeletal muscle, however, other studies suggest that TRPC1 also contributes to MS channels in differentiated muscle cells (58) and in C2C12 myoblasts (59). Moreover, stretch-activated currents share similar electrophysiological properties with store-operated currents when recorded at the surface membrane of skeletal fibers (23).…”

Section: Discussionmentioning

confidence: 99%

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

Sabourin

Lamiche

Vandebrouck

et al. 2009

Journal of Biological Chemistry

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The dystrophin-associated protein complex (DAPC) is essential for skeletal muscle, and the lack of dystrophin in Duchenne muscular dystrophy results in a reduction of DAPC components such as syntrophins and in fiber necrosis. By anchoring various molecules, the syntrophins may confer a role in cell signaling to the DAPC. Calcium disorders and abnormally elevated cation influx in dystrophic muscle cells have suggested that the DAPC regulates some sarcolemmal cationic channels. We demonstrated previously that minidystrophin and ␣1-syntrophin restore normal cation entry in dystrophin-deficient myotubes and that sarcolemmal TRPC1 channels associate with dystrophin and the bound PDZ domain of ␣1-syntrophin. This study shows that small interfering RNA (siRNA) silencing of ␣1-syntrophin dysregulated cation influx in myotubes. Moreover, deletion of the PDZcontaining domain prevented restoration of normal cation entry by ␣1-syntrophin transfection in dystrophin-deficient myotubes. TRPC1 and TRPC4 channels are expressed at the sarcolemma of muscle cells; forced expression or siRNA silencing showed that cation influx regulated by ␣1-syntrophin is supported by TRPC1 and TRPC4. A molecular association was found between TRPC1 and TRPC4 channels and the ␣1-syntrophin-dystrophin complex. TRPC1 and TRPC4 channels may form sarcolemmal channels anchored to the DAPC, and ␣1-syntrophin is necessary to maintain the normal regulation of TRPC-supported cation entry in skeletal muscle. Cation channels with DAPC form a signaling complex that modulates cation entry and may be crucial for normal calcium homeostasis in skeletal muscles.

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Section: Discussionmentioning

confidence: 99%

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

Sabourin

Lamiche

Vandebrouck

et al. 2009

Journal of Biological Chemistry

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“…This postinfarction fibrosis-modulating effect could also assist stem cell-based reparative therapies that appear to be promoted by the peptide. Mouse C2C12 skeletal myoblasts engineered to overexpress human relaxin demonstrate growth and functional maturation of neonatal immature cardiomyocytes assessed by the expression of myocardiumspecific structural genes (connexin 43, troponin T, and HCN4 ion channel) (Formigli et al, 2009). Coronary infusion of C2C12 skeletal myoblasts overexpressing relaxin in conjunction with administration of exogenous relaxin starting at day 30 after infarction in rats improves myocardial viability in the infarcted area compared with myoblast therapy alone (Bonacchi et al, 2009).…”

Section: Physiologic Roles Of Relaxin Family Peptide Receptors Andmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. XCV. Recent Advances in the Understanding of the Pharmacology and Biological Roles of Relaxin Family Peptide Receptors 1–4, the Receptors for Relaxin Family Peptides

Halls¹,

Bathgate²,

Sutton³

et al. 2015

Pharmacol Rev

115

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“…Hearts from 0-to 1-day-old newborn mice were used to obtain primary cultures of ventricular cardiac muscle and stromal cells, according to the previously described method [17] few and scattered and tended to increase in number thereafter (Fig. 1H-K).…”

Section: In Vitro Studiesmentioning

confidence: 99%

Telocytes as supporting cells for myocardial tissue organization in developing and adult heart

Bani¹,

Formigli²,

Gherghiceanu³

et al. 2010

Journal of Cellular and Molecular Medicine

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its morphogenesis. This study is designed to investigate the occurrence of telocytes in the developing heart and provide clues to better understand their role as supporting cells involved in the architectural organization of the myocardium during heart development. Our results showed that stromal cells with the immunophenotypical (vimentin, CD34) and ultrastructural features of telocytes were present in the mouse heart since early embryonic to adult life, as well as in primary cultures of neonatal mouse cardiac cells. These cells formed an extended network of telopodes which closely embraced the growing cardiomyocytes and appeared to contribute to the aggregation of cardiomyocyte clusters in vitro.In conclusion, the present findings strongly suggest that, during heart development, stromal cells identifiable as telocytes could play a nursing and guiding role for myocardial precursors to form the correct three-dimensional tissue pattern and contribute to compaction of the embryonic myocardial trabeculae. It is tempting to speculate that telocytes could be a novel, possible target for therapeutic strategies aimed at potentiating cardiac repair and regeneration after ischemic injury.

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Skeletal myoblasts overexpressing relaxin improve differentiation and communication of primary murine cardiomyocyte cell cultures

Cited by 42 publications

References 41 publications

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

International Union of Basic and Clinical Pharmacology. XCV. Recent Advances in the Understanding of the Pharmacology and Biological Roles of Relaxin Family Peptide Receptors 1–4, the Receptors for Relaxin Family Peptides

Telocytes as supporting cells for myocardial tissue organization in developing and adult heart

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