Cardiac differentiation promotes mitochondria development and ameliorates oxidative capacity in H9c2 cardiomyoblasts

Comelli, Marina; Domenis, Rossana; Bisetto, Elena; Contin, Magali; Marchini, Maurizio; Ortolani, Fulvia; Tomasetig, Lara; Mavelli, Irene

doi:10.1016/j.mito.2010.12.007

Cited by 37 publications

(53 citation statements)

References 37 publications

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“…Our results therefore suggest that by producing mitochondria, cardiomyocyte differentiation lays the foundation for enabling beta-oxidation of fatty acids, which indeed was detected at later stages of differentiation by our GO analysis. This reasoning is supported by the observation that mitochondrial mass increases during H9C2 cell differentiation 33 and that increased mitochondrial mass is a prerequisite to address the high energy need of H9C2 CM cells. 34 Similarly, elevation of cardiac-specific ion transporters was suggested to occur at later time points.…”

Section: Discussionmentioning

confidence: 77%

Quantitative proteomics and systems analysis of cultured H9C2 cardiomyoblasts during differentiation over time supports a ‘function follows form’ model of differentiation

et al. 2018

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The rat cardiomyoblast cell line H9C2 has emerged as a valuable tool for studying cardiac development, mechanisms of disease and toxicology. We present here a rigorous proteomic analysis that monitored the changes in protein expression during differentiation of H9C2 cells into cardiomyocyte-like cells over time. Quantitative mass spectrometry followed by gene ontology (GO) enrichment analysis revealed that early changes in H9C2 differentiation are related to protein pathways of cardiac muscle morphogenesis and sphingolipid synthesis. These changes in the proteome were followed later in the differentiation time-course by alterations in the expression of proteins involved in cation transport and beta-oxidation.

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Section: Discussionmentioning

confidence: 77%

Quantitative proteomics and systems analysis of cultured H9C2 cardiomyoblasts during differentiation over time supports a ‘function follows form’ model of differentiation

et al. 2018

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“…Since this sub-type is more associated with pro-apoptotic effect of beta-adrenergic stimulation (Communal et al, 1998), the results obtained in the present and past work suggest than more than the total β-AR sub-type content, the downstream activation of stress and survival pathways determines fate for each cell type. Mitochondrial metabolism alters with H9c2 differentiation (Comelli et al, 2011). An increase reliance on mitochondrial metabolism for ATP production may also imply a remodeling on mitochondrial stress/toxicity responses which impacts mitochondria responses to foreign stresses.…”

Section: Page 21 Of 45mentioning

confidence: 99%

Mitochondrial disruption occurs downstream from β-adrenergic overactivation by isoproterenol in differentiated, but not undifferentiated H9c2 cardiomyoblasts: Differential activation of stress and survival pathways

Branco

Sampaio

Wieckowski

et al. 2013

The International Journal of Biochemistry & Cell Biology

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“…17 The ability of H9c2 to differentiate into cardiomyocytes has prompted its use as a differentiation model in several studies. [18][19][20] The primary interest of this work is to evaluate the potential of CDM, specifically FDM, in cardiac tissue engineering. Biophysical and biochemical properties of FDM were assessed and followed by examination on cell adhesion, proliferation, and differentiation of H9c2 toward cardiomyocytes.…”

Section: Introductionmentioning

confidence: 99%

Cardiomyoblast (H9c2) Differentiation on Tunable Extracellular Matrix Microenvironment

Suhaeri

Subbiah

Van

et al. 2015

Tissue Engineering Part A

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Extracellular matrices (ECM) obtained from in vitro-cultured cells have been given much attention, but its application in cardiac tissue engineering is still limited. This study investigates cardiomyogenic potential of fibroblast-derived matrix (FDM) as a novel ECM platform over gelatin or fibronectin, in generating cardiac cell lineages derived from H9c2 cardiomyoblasts. As characterized through SEM and AFM, FDM exhibits unique surface texture and biomechanical property. Immunofluorescence also found fibronectin, collagen, and laminin in the FDM. Cells on FDM showed a more circular shape and slightly less proliferation in a growth medium. After being cultured in a differentiation medium for 7 days, H9c2 cells on FDM differentiated into cardiomyocytes, as identified by stronger positive markers, such as a-actinin and cTnT, along with more elevated gene expression of Myl2 and Tnnt compared to the cells on gelatin and fibronectin. The gap junction protein connexin 43 was also significantly upregulated for the cells differentiated on FDM. A successive work enabled matrix stiffness tunable; FDM crosslinked by 2wt% genipin increased the stiffness up to 8.5 kPa, 100 times harder than that of natural FDM. The gene expression of integrin subunit a5 was significantly more upregulated on FDM than on crosslinked FDM (X-FDM), whereas no difference was observed for b1 expression. Interestingly, X-FDM showed a much greater effect on the cardiomyoblast differentiation into cardiomyocytes over natural one. This study strongly indicates that FDM can be a favorable ECM microenvironment for cardiomyogenesis of H9c2 and that tunable mechanical compliance induced by crosslinking further provides a valuable insight into the role of matrix stiffness on cardiomyogenesis.

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Cardiac differentiation promotes mitochondria development and ameliorates oxidative capacity in H9c2 cardiomyoblasts

Cited by 37 publications

References 37 publications

Quantitative proteomics and systems analysis of cultured H9C2 cardiomyoblasts during differentiation over time supports a ‘function follows form’ model of differentiation

Quantitative proteomics and systems analysis of cultured H9C2 cardiomyoblasts during differentiation over time supports a ‘function follows form’ model of differentiation

Mitochondrial disruption occurs downstream from β-adrenergic overactivation by isoproterenol in differentiated, but not undifferentiated H9c2 cardiomyoblasts: Differential activation of stress and survival pathways

Cardiomyoblast (H9c2) Differentiation on Tunable Extracellular Matrix Microenvironment

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