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, Ana F.; Sampaio, Susana F.; Wieckowski, Mariusz R.; Sardão, Vilma A.; Oliveira, Paulo J.

doi:10.1016/j.biocel.2013.08.006

Cited by 19 publications

(23 citation statements)

References 55 publications

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“…- [30], supporting the hypothesis that redox signaling alterations are required for myoblasts differentiation [33]. In the heart, the excitation-contraction coupling (ECC) is a physiological process essential for cardiomyocyte function (contraction and relaxation), and involves redox signaling [34].…”

Section: From Receptor Activation To Cell Fate: the Role Of Calcium Amentioning

confidence: 69%

“…The phosphorylation of p66Shc on serine 36 by protein kinase C increases during cellular stress, leading to an amplification of mitochondrial oxidative stress and apoptotic signaling [59]. In a previous study, we demonstrated that the -AR agonist ISO increases the ratio between Ser36-phosphorylated p66Shc and the total p66Shc content in differentiated cardiac cells [30], suggesting a pro-apoptotic/pro-oxidant effect.…”

Section: Mitochondrial Sources Of Omentioning

confidence: 81%

“…At low levels, ROS generation has an important role in signaling functions in cardiac cells by mediating cell proliferation, differentiation and survival pathways [29]. During cardiomyogenesis, mitochondrial ROS formation has an important role in establishing the metabolic mechanisms that allow undifferentiated myoblasts drive to a cardiac-specific energetic requirement [30][31][32]. Our recent study demonstrated that differentiated H9c2 cells generate higher content of mitochondrial O 2 .…”

Section: From Receptor Activation To Cell Fate: the Role Of Calcium Amentioning

confidence: 99%

“…The interaction between Ca 2+ and oxidative stress regulates other stress pathways involved in cell death, such as the p66Shc pathway [30]. p66Shc is known to regulate oxidative stress responses and apoptosis [58].…”

Section: Mitochondrial Sources Of Omentioning

confidence: 99%

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β-Adrenergic Over-Stimulation and Cardio-Myocyte Apoptosis: Two Receptors, One Organelle, Two Fates?

Branco¹,

Moreira²,

Cunha‐Oliveira³

et al. 2014

CDT

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Neuro-hormonal regulation of cardiac function via cathecol-amines results in increased heart rate and contractility. A persistent adrenergic tone, however, is an insult to the heart, affecting its regular homeostasis, altering morphology and gene expression patterns, as well as inducing apoptosis of cardio-myocytes. At the same time as being the main oxygen consumers, mitochondria are also key to the energy production required for the heart to maintain its vital functions and to integrate a series of signaling pathways that define the life and death of the cell. As α-adrenergic receptors (α-AR) orchestrate multiple biochemical events that can either trigger or inhibit cell death, mitochondria can act as a referee in the entire process. In fact, α-AR subtypes α1 and α2 activate various down-stream pathways which differently modulate intracellular calcium levels and production of mitochondrial reactive oxygen species (ROS). The delicate balance between an adaptive (cardio-protective) response resulting in increased contractility and activation of survival pathways, vs. cell death caused by calcium and ROS-induced mitochondrial disruption, along with evidence of their clinical and potential therapeutic translations, are reviewed in this communication.

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Section: From Receptor Activation To Cell Fate: the Role Of Calcium Amentioning

confidence: 69%

Section: Mitochondrial Sources Of Omentioning

confidence: 81%

Section: From Receptor Activation To Cell Fate: the Role Of Calcium Amentioning

confidence: 99%

Section: Mitochondrial Sources Of Omentioning

confidence: 99%

See 2 more Smart Citations

β-Adrenergic Over-Stimulation and Cardio-Myocyte Apoptosis: Two Receptors, One Organelle, Two Fates?

Branco¹,

Moreira²,

Cunha‐Oliveira³

et al. 2014

CDT

Self Cite

View full text Add to dashboard Cite

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“…The role of adrenergic receptors in mitochondrial biogenesis and function has been the subject of many investigations performed on various cell types (Chiang et al 2012, Wills et al 2012, Branco et al 2013, Peterson et al 2013, Pennanen et al 2014. The aim of the present study was to characterize the effect of NE as well as β-and α 1 -adrenergic agonists on mitochondria in pig pinealocytes in organ culture.…”

Section: Introductionmentioning

confidence: 92%

Adrenergic control of pinealocyte chondriome – an in vitro study

Przybylska‐Gornowicz¹,

Lewczuk²,

Ziółkowska³

et al. 2016

Polish Journal of Veterinary Sciences

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Norepinephrine released from sympathetic innervation plays the main role in the regulation of melatonin secretion in mammalian pinealocytes. The present study was conducted for the following reasons: 1) to establish whether the pinealocyte chondriome is controlled by norepinephrine, 2) to determine the effect of adrenergic stimulation on mitochondria, and 3) to characterize adrenoceptors involved in the regulation of the chondriome.The static organ culture of the pineal gland was used. The explants were incubated for 5 consecutive days in control medium and between 20:00 and 08:00 in medium with the presence of 10 μM norepinephrine -adrenergic agonist; isoproterenol -beta-adrenoceptor agonist; cirazoline, methoxamine, M-6364 -alfa 1 -adrenoceptors agonists or PMA -activator of PKC. The explants were then subjected to ultrastructural examination and morphometric analysis.The incubation of explants in the presence of norepinephrine or isoproterenol caused a decrease in the relative volume and the numerical density of mitochondria and induced an increase in the percentage of free mitochondria in pinealocytes. Significant changes in these parameters were not observed after treatment with methoxamine, cirazoline, M-6463 and PMA.The results obtained show that the chondriome of pig pinealocytes is controlled by norepinephrine acting via beta-adrenoceptors. Adrenergic stimulation, repeated for five consecutive days of organ culture, causes a decrease in the number of mitochondria and a shift in the distribution of mitochondria from the form of networks and filaments into the form of single particles. This indicates the intensive remodeling of the mitochondria network, which is closely linked to the metabolic status of the cell.

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Canstatin inhibits isoproterenol-induced apoptosis through preserving mitochondrial morphology in differentiated H9c2 cardiomyoblasts

et al. 2016

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Canstatin, a non-collagenous fragment, is cleaved from type IV collagen α2 chain, an essential component of basement membrane surrounding cardiomyocytes. Although canstatin is known as an endogenous anti-angiogenic factor, its effects on cardiomyocytes have not been clarified. This study examined the effects of canstatin on isoproterenol-induced apoptosis in differentiated H9c2 cardiomyoblasts. Retinoic acid was used to differentiate H9c2 myoblast to cardiomyocyte-like phenotype. Cell viability was determined by a cell counting assay. Western blotting was performed to detect expression of cleaved casepase-3 and phosphorylation of dynamin related protein (Drp)1 at Ser637 which regulates mitochondrial fission. Mito Sox Red staining was performed to examine a mitochondria-dependent production of reactive oxygen species (ROS). Mitochondrial morphology was detected by Mito Tracker Red staining. Isoproterenol (100 μM, 48 h) significantly decreased cell viability and increased cleaved caspase-3 expression, which were inhibited by canstatin (10-250 ng/ml) in a concentration-dependent manner. Canstatin suppressed the isoproterenol-induced mitochondrial fission but not ROS. Canstatin also inhibited the isoproterenol-induced dephosphorylation of Drp1 at Ser637. In conclusion, canstatin inhibits isoproterenol-induced apoptosis through the inhibition of mitochondrial fission via the suppression of dephosphorylation of Drp1 at Ser637 in differentiated H9c2 cardiomyoblasts.

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

Cited by 19 publications

References 55 publications

β-Adrenergic Over-Stimulation and Cardio-Myocyte Apoptosis: Two Receptors, One Organelle, Two Fates?

β-Adrenergic Over-Stimulation and Cardio-Myocyte Apoptosis: Two Receptors, One Organelle, Two Fates?

Adrenergic control of pinealocyte chondriome – an in vitro study

Canstatin inhibits isoproterenol-induced apoptosis through preserving mitochondrial morphology in differentiated H9c2 cardiomyoblasts

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