Mitochondrial dynamics in heart cells: Very low amplitude high frequency fluctuations in adult cardiomyocytes and flow motion in non beating Hl-1 cells

Béraud, Nathalie; Pelloux, Sophie; Usson, Yves; Kuznetsov, Andrey V.; Ronot, Xavier; Tourneur, Yves; Saks, Valdur

doi:10.1007/s10863-009-9214-x

Cited by 90 publications

(54 citation statements)

References 100 publications

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“…Consistent with this notion, rates of mitochondrial fusion and fission have been shown to be very low in adult cardiac myocytes 38,39 compared to that of neonatal cardiac myocytes. 40,41 Thus, loss-of-function of a single mitofusin gene could have a greater impact during periods of intense mitochondrial fusion and fission such as occurs during postnatal myocyte growth and maturation. Accordingly, the full activity of both Mfn1 and Mfn2, driven in part by the “boosting” activity of the PGC-1 coactivators, are likely required during the cardiac postnatal stage, but not in the adult.…”

Section: Discussionmentioning

confidence: 99%

A Role for Peroxisome Proliferator-Activated Receptor γ Coactivator-1 in the Control of Mitochondrial Dynamics During Postnatal Cardiac Growth

Martin

Lai

Soundarapandian

et al. 2014

Circulation Research

187

182

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Rationale Increasing evidence has shown that proper control of mitochondrial dynamics (fusion and fission) is required for high capacity ATP production in heart. The transcriptional coactivators, peroxisome proliferator-activated receptor gamma coactivator 1 (PGC-1) α and β have been shown to regulate mitochondrial biogenesis in heart at the time of birth. The function of the PGC-1 coactivators in heart after birth is incompletely understood. Objective To assess the role of the PGC-1 coactivators during postnatal cardiac development and in the adult heart in mice. Methods and Results Conditional gene targeting was used in mice to explore the role of the PGC-1 coactivators during postnatal cardiac development and in adult heart. Marked mitochondrial structural derangements were observed in hearts of PGC-1α/β-deficient mice during postnatal growth, including fragmentation and elongation, associated with the development of a lethal cardiomyopathy. The expression of genes involved in mitochondrial fusion [mitofusin 1 (Mfn1), optic atrophy 1 (Opa1)] and fission [dynamin-related protein 1 (Drp1), fission protein 1 (Fis1)] was altered in hearts of PGC-1α/β-deficient mice. PGC-lα was shown to directly regulate Mfn1 gene transcription by coactivating the estrogen-related receptor α (ERRα) upon a conserved DNA element. Surprisingly, PGC-1α/β deficiency in the adult heart did not result in evidence of abnormal mitochondrial dynamics or heart failure. However, transcriptional profiling demonstrated that the PGC-1 coactivators are required for high level expression of nuclear- and mitochondrial-encoded genes involved in mitochondrial dynamics and energy transduction in adult heart. Conclusion These results reveal distinct developmental stage-specific programs involved in cardiac mitochondrial dynamics.

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Section: Discussionmentioning

confidence: 99%

A Role for Peroxisome Proliferator-Activated Receptor γ Coactivator-1 in the Control of Mitochondrial Dynamics During Postnatal Cardiac Growth

Martin

Lai

Soundarapandian

et al. 2014

Circulation Research

187

182

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“…More recently, however, mitochondria have been shown to exist as an assortment of shapes including small spheres, short rod shapes, long filamentous entities and networks. In addition the organelle is reported to undergo almost constant displacement by extension, retraction, wriggling, Brownian motion and large directed movements [5,6,24,47]. Substantial networks of electrically coupled mitochondria may also exist; indeed, local depolarisation of the mitochondrial membrane potential (ΔΨ M ) may spread to distant sites [35,38].…”

Section: Positioning Of Mitochondriamentioning

confidence: 99%

Mitochondrial regulation of cytosolic Ca2+ signals in smooth muscle

McCarron

Olson

Chalmers

2012

Pflugers Arch - Eur J Physiol

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The cytosolic Ca²⁺ concentration ([Ca²⁺]c) controls virtually every activity of smooth muscle, including contraction, migration, transcription, division and apoptosis. These processes may be activated by large (>10 μM) amplitude [Ca²⁺]c increases, which occur in small restricted regions of the cell or by smaller (<1 μM) amplitude changes throughout the bulk cytoplasm. Mitochondria contribute to the regulation of these signals by taking up Ca²⁺. However, mitochondria's reported low affinity for Ca²⁺ is thought to require the organelle to be positioned close to ion channels and within a microdomain of high [Ca²⁺]. In cultured smooth muscle, mitochondria are highly dynamic structures but in native smooth muscle mitochondria are immobile, apparently strategically positioned organelles that regulate the upstroke and amplitude of IP₃-evoked Ca²⁺ signals and IP₃ receptor (IP₃R) cluster activity. These observations suggest mitochondria are positioned within the high [Ca²⁺] microdomain arising from an IP₃R cluster to exert significant local control of channel activity. On the other hand, neither the upstroke nor amplitude of voltage-dependent Ca²⁺ entry is modulated by mitochondria; rather, it is the declining phase of the transient that is regulated by the organelle. Control of the declining phase of the transient requires a high mitochondrial affinity for Ca²⁺ to enable uptake to occur over the normal physiological Ca²⁺ range (<1 μM). Thus, in smooth muscle, mitochondria regulate Ca²⁺ signals exerting effects over a large range of [Ca²⁺] (∼200 nM to at least tens of micromolar) to provide a wide dynamic range in the control of Ca²⁺ signals.

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“…41 Nevertheless, an imbalance between fission and fusion is observed in multiple cardiovascular disorders as thoroughly reviewed by Dorn. 42 One example of particular interest is the observation that Opa1 is down-regulated in hearts from both humans with heart failure (HF) and a rat model of HF.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Reactive Oxygen Species at the Heart of the Matter

Kornfeld

Hwang

Disatnik

et al. 2015

Circulation Research

170

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Reactive oxygen species (ROS) have been implicated in a variety of age-related diseases including multiple cardiovascular disorders. However, translation of ROS scavengers (anti-oxidants) into the clinic has not been successful. These anti-oxidants grossly reduce total levels of cellular ROS including ROS that participate in physiological signaling. In this review, we challenge the traditional anti-oxidant therapeutic approach that targets ROS directly with novel approaches that improve mitochondrial functions to more effectively treat cardiovascular diseases.

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Mitochondrial dynamics in heart cells: Very low amplitude high frequency fluctuations in adult cardiomyocytes and flow motion in non beating Hl-1 cells

Cited by 90 publications

References 100 publications

A Role for Peroxisome Proliferator-Activated Receptor γ Coactivator-1 in the Control of Mitochondrial Dynamics During Postnatal Cardiac Growth

A Role for Peroxisome Proliferator-Activated Receptor γ Coactivator-1 in the Control of Mitochondrial Dynamics During Postnatal Cardiac Growth

Mitochondrial regulation of cytosolic Ca2+ signals in smooth muscle

Mitochondrial Reactive Oxygen Species at the Heart of the Matter

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