Mitochondrial superoxide anion radicals mediate induction of apoptosis in cardiac myoblasts exposed to chronic hypoxia

Kolamunne, Rajitha T.; Clare, Michelle; Griffiths, Helen R.

doi:10.1016/j.abb.2010.10.015

Cited by 26 publications

(28 citation statements)

References 48 publications

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“…Several previous studies used HL-1 cells to investigate the cardiologic effects of physiological and pathological conditions in vitro, including oxidative stress, ischemia, hypoxia, hyperglycemia and hyperinsulinemia [33]. Similarly, H9c2 cells were widely used to study the effects, mechanisms, and therapeutic interventions of hypoxia/reoxygenation, autophagy, hypertrophy, insulin resistance, apoptosis, endoplasmic reticulum-mitochondria interactions and cellular signaling [6,13,14,16,34–36], as well as various differentiation aspects [37–39]. …”

Section: Discussionmentioning

confidence: 99%

H9c2 and HL-1 cells demonstrate distinct features of energy metabolism, mitochondrial function and sensitivity to hypoxia-reoxygenation

Kuznetsov

Javadov

Sickinger

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

198

159

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Dysfunction of cardiac energy metabolism plays a critical role in many cardiac diseases, including heart failure, myocardial infarction and ischemia–reperfusion injury and organ transplantation. The characteristics of these diseases can be elucidated in vivo, though animal-free in vitro experiments, with primary adult or neonatal cardiomyocytes, the rat ventricular H9c2 cell line or the mouse atrial HL-1 cells, providing intriguing experimental alternatives. Currently, it is not clear how H9c2 and HL-1 cells mimic the responses of primary cardiomyocytes to hypoxia and oxidative stress. In the present study, we show that H9c2 cells are more similar to primary cardiomyocytes than HL-1 cells with regard to energy metabolism patterns, such as cellular ATP levels, bioenergetics, metabolism, function and morphology of mitochondria. In contrast to HL-1, H9c2 cells possess beta-tubulin II, a mitochondrial isoform of tubulin that plays an important role in mitochondrial function and regulation. We demonstrate that H9c2 cells are significantly more sensitive to hypoxia-reoxygenation injury in terms of loss of cell viability and mitochondrial respiration, whereas HL-1 cells were more resistant to hypoxia as evidenced by their relative stability. In comparison to HL-1 cells, H9c2 cells exhibit a higher phosphorylation (activation) state of AMP-activated protein kinase, but lower peroxisome proliferator-activated receptor gamma coactivator 1-alpha levels, suggesting that each cell type is characterized by distinct regulation of mitochondrial biogenesis. Our results provide evidence that H9c2 cardiomyoblasts are more energetically similar to primary cardiomyocytes than are atrial HL-1 cells. H9c2 cells can be successfully used as an in vitro model to simulate cardiac ischemia–reperfusion injury.

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Section: Discussionmentioning

confidence: 99%

H9c2 and HL-1 cells demonstrate distinct features of energy metabolism, mitochondrial function and sensitivity to hypoxia-reoxygenation

Kuznetsov

Javadov

Sickinger

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

198

159

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“…While ROS appears to exert some regulatory function on HIF-1, there is still debate as to whether ROS levels are increased [62,66,67] or decreased [68][69][70] during hypoxia. Contradictory results may occur due to differences in cell type, mode of generating hypoxia, oxygen levels and assays used to measure ROS.…”

Section: Regulation Of the Hif-1 System By Rosmentioning

confidence: 99%

The Interaction Between Redox and Hypoxic Signalling Pathways in the Dynamic Oxygen Environment of Cancer Cells

Bhatia¹,

Karlenius²,

Trapani³

et al. 2013

Carcinogenesis

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“…Hypoxia is an important factor in the pathology of a number of human diseases, including cancer, diabetes, aging, and stroke/ischemia (Melvin and Rocha, 2012;Semenza, 2012). Hypoxia can also lead to the production of oxygen radicals in a variety of experimental systems via electron attack of molecular oxygen in the inactive mitochondria (Favaro et al, 2010;Kolamunne et al, 2011;Selivanov et al, 2011). The roles of these mitochondrial-generated free radicals are especially important in hypoxia signaling pathways, which have important implications for cancer, inflammation, and a variety of other diseases (Poyton et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Molecular Responses to Hypoxia-Inducible Factor 1α and Beyond

2014

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Cellular response to changes in oxygen tension during normal development or pathologic processes is, in part, regulated by hypoxia-inducible factor (HIF), an oxygen-sensitive transcription factor. HIF activity is primarily controlled through post-translational modifications and stabilization of HIF-1a and HIF-2a proteins and is regulated by a number of cellular pathways involving both oxygen-dependent and -independent mechanisms. Stabilization of HIF-1a activates transcription of genes that participate in key pathways in carcinogenesis, such as angiogenesis, dedifferentiation, and invasion. Since its discovery more than two decades ago, HIF-1a has become a hot topic in molecular research and has been implicated not only in disease pathology but also in prognosis. In this review, we will focus on recent insights into HIF-1a regulation, function, and gene expression. We will also discuss emerging data on the involvement of HIF in cancer prognosis and therapeutic interventions.

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Mitochondrial superoxide anion radicals mediate induction of apoptosis in cardiac myoblasts exposed to chronic hypoxia

Cited by 26 publications

References 48 publications

H9c2 and HL-1 cells demonstrate distinct features of energy metabolism, mitochondrial function and sensitivity to hypoxia-reoxygenation

H9c2 and HL-1 cells demonstrate distinct features of energy metabolism, mitochondrial function and sensitivity to hypoxia-reoxygenation

The Interaction Between Redox and Hypoxic Signalling Pathways in the Dynamic Oxygen Environment of Cancer Cells

Molecular Responses to Hypoxia-Inducible Factor 1α and Beyond

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