Mitochondrial functions in stem cells

Margineantu, Daciana; Hockenbery, David M.

doi:10.1016/j.gde.2016.05.004

Cited by 26 publications

(15 citation statements)

References 96 publications

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“…Mitochondria are multitasking organelles [28], and many environmental and stress stimuli can cause mitochondrial dysfunction [29,30], thereby affecting spermatogenesis [31][32][33][34]. The present study is a follow-up to our previous works, which showed that Sucla2 expression decreased in testes and GC1 cells with increasing apoptotic cells after exposure to endocrine disruptor BDE47 [8].…”

Section: Discussionsupporting

confidence: 73%

Knockdown of Sucla2 decreases the viability of mouse spermatocytes by inducing apoptosis through injury of the mitochondrial function of cells

Huang

Wang

2016

Folia Histochem Cytobiol.

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Introduction. Sucla2, a b subunit of succinyl coenzyme A synthase, is located in the mitochondrial matrix. Sucla2 catalyzes the reversible synthesis of succinate and adenosine triphosphate (ATP) in the tricarboxylic acid cycle. Sucla2 expression was found to be correlated with the capacitation of boar spermatozoa. We have previously reported that Sucla2 was decreased in the testes of rats with spermatogenesis failure after exposure to endocrine disruptor BDE47. Yet, the expression model of Sucla2 in spermatogenesis and the function of Sucla2 in spermatogenic cells are still unclear. Our objective was to explore the localization of Sucla2 during mouse spermatogenesis and its function in the mouse spermatocyte line (GC2). Material and methods. The localization of Sucla2 in the mouse testis was explored through immunohistochemistry (IHC). Sucla2 was knocked down in GC2 cells and its expression was detected by Western blot (WB) to verify the efficiency of the siRNA transfection. Mitochondrial membrane potential (MMP), apoptosis and ROS of GC2 were detected by flow cytometry. ATP production was measured by the luminometric method and the presence of Bcl2 of GC2 was detected by WB. Results. Sucla2 is highly expressed in all germ cells but not in interstitial cells. Coarse Sucla2 signals are found in spermatocytes in stages VII-XII of mouse spermatogenesis. In GC2 cells, knockdown of Sucla2 decreased cell viability and MMP, induced apoptosis of GC2 cells, decreased ATP production, and Bcl2 expression, and increased ROS levels. Conclusions. Sucla2 is related to the developmental stages of mouse spermatogenesis. Knockdown of Sucla2 decreases the viability of mouse spermatocytes by inducing apoptosis via decreased mitochondrial function of the cells.

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Section: Discussionsupporting

confidence: 73%

Knockdown of Sucla2 decreases the viability of mouse spermatocytes by inducing apoptosis through injury of the mitochondrial function of cells

Huang

Wang

2016

Folia Histochem Cytobiol.

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“…Because ROS (like IIS) promotes cell differentiation [78, 79] , including sexual differentiation, one hypothesis is that decreased mitochondrial turnover and increased ROS may be selected for in part due to favorable effects on sexual differentiation and reproduction [2] . For example, when receptor tyrosine kinases involved in cell differentiation are activated by ligand, this activates membrane-bound NADPH oxidase, which in turn results in a localized burst of hydrogen peroxide (Figure 3) [80] .…”

Section: A Unifying Model For Sex Differences In Aging Involving Mitomentioning

confidence: 99%

Sex-Specific Gene Expression and Life Span Regulation

Tower

2017

Trends in Endocrinology & Metabolism

108

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Aging-related diseases show a marked sex bias. For example, women live longer than men yet have more Alzheimer’s disease and osteoporosis, whereas men have more cancer and Parkinson’s disease. Understanding the role of sex will be important in designing interventions and in understanding basic aging mechanisms. Aging also shows sex differences in model organisms. Dietary restriction (DR), reduced insulin/IGF1-like signaling (IIS) and reduced TOR signaling each increase life span preferentially in females, in both flies and mice. Maternal transmission of mitochondria to offspring may lead to greater control over mitochondrial functions in females, including greater life span and a larger response to diet. Consistent with this idea, males show greater loss of mitochondrial gene expression with age.

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“…Besides generating ATP via oxidative phosphorylation to fuel all energy-consuming processes, mitochondria also participate in myriad cellular processes such as ion homeostasis, oxygen sensing, apoptosis, and specification of cell fate in adult and cancer stem cells [2, 3, 34, 35]. Mitochondria are also the prime sites of endogenous ROS production.…”

Section: Mitochondrial Quality Control: Different Types Of Mitophagymentioning

confidence: 99%

Mitophagy Transcriptome: Mechanistic Insights into Polyphenol‐Mediated Mitophagy

Tan

Wong

2017

Oxidative Medicine and Cellular Longevity

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Mitochondria are important bioenergetic and signalling hubs critical for myriad cellular functions and homeostasis. Dysfunction in mitochondria is a central theme in aging and diseases. Mitophagy, a process whereby damaged mitochondria are selectively removed by autophagy, plays a key homeostatic role in mitochondrial quality control. Upregulation of mitophagy has shown to mitigate superfluous mitochondrial accumulation and toxicity to safeguard mitochondrial fitness. Hence, mitophagy is a viable target to promote longevity and prevent age-related pathologies. Current challenge in modulating mitophagy for cellular protection involves identification of physiological ways to activate the pathway. Till date, mitochondrial stress and toxins remain the most potent inducers of mitophagy. Polyphenols have recently been demonstrated to protect mitochondrial health by facilitating mitophagy, thus suggesting the exciting prospect of augmenting mitophagy through dietary intake. In this review, we will first discuss the different surveillance mechanisms responsible for the removal of damaged mitochondrial components, followed by highlighting the transcriptional regulatory mechanisms of mitophagy. Finally, we will review the functional connection between polyphenols and mitophagy and provide insight into the underlying mechanisms that potentially govern polyphenol-induced mitophagy.

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Mitochondrial functions in stem cells

Cited by 26 publications

References 96 publications

Knockdown of Sucla2 decreases the viability of mouse spermatocytes by inducing apoptosis through injury of the mitochondrial function of cells

Knockdown of Sucla2 decreases the viability of mouse spermatocytes by inducing apoptosis through injury of the mitochondrial function of cells

Sex-Specific Gene Expression and Life Span Regulation

Mitophagy Transcriptome: Mechanistic Insights into Polyphenol‐Mediated Mitophagy

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