Mitochondria to the rescue

Texas A&M Health Science Center College of Medicine Institute for Regenerative Medicine at Scott & White, Temple, USA.
Nature medicine (Impact Factor: 27.36). 05/2012; 18(5):653-4. DOI: 10.1038/nm.2769
Source: PubMed


A new study using a mouse model of lung diseases is the first demonstration in vivo that bone marrow–derived stromal cells can repair tissue injury through the transfer of mitochondria (pages 759-765). This suggests that rescue of injured cells through mitochondrial transfer may be an important process in many diseases.

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    • "In addition, the limitation of spontaneous BMPC engraftment in the hearts of c‐Kit/CD117‐knockout mice with permanent coronary ligation decreases postinfarction survival and contractile function, compared with wild‐type controls.10 These effects could rely on direct differentiation and/or fusion with adult cardiomyocytes,11 or paracrine mechanisms (including intercellular micro‐RNA12 or mitochondrial13 transfer). The origin of cardiac myofibroblasts is also attributed to circulating precursors that originate in the bone marrow.14–15 "
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    ABSTRACT: The core region of a myocardial infarction is notoriously unsupportive of cardiomyocyte survival. However, there has been less investigation of the potentially beneficial spontaneous recruitment of endogenous bone marrow progenitor cells (BMPCs) within infarcted areas. In the current study we examined the role of tissue oxygenation and derived toxic species in the control of BMPC engraftment during postinfarction heart remodeling. For assessment of cellular origin, local oxygenation, redox status, and fate of cells in the infarcted region, myocardial infarction in mice with or without LacZ(+) bone marrow transplantation was induced by coronary ligation. Sham-operated mice served as controls. After 1 week, LacZ(+) BMPC-derived cells were found inhomogeneously distributed into the infarct zone, with a lower density at its core. Electron paramagnetic resonance (EPR) oximetry showed that pO2 in the infarct recovered starting on day 2 post-myocardial infarction, concomitant with wall thinning and erythrocytes percolating through muscle microruptures. Paralleling this reoxygenation, increased generation of reactive oxygen/nitrogen species was detected at the infarct core. This process delineated a zone of diminished BMPC engraftment, and at 1 week infiltrating cells displayed immunoreactive 3-nitrotyrosine and apoptosis. In vivo treatment with a superoxide dismutase mimetic significantly reduced reactive oxygen species formation and amplified BMPC accumulation. This treatment also salvaged wall thickness by 43% and left ventricular ejection fraction by 27%, with significantly increased animal survival. BMPC engraftment in the infarct inversely mirrored the distribution of reactive oxygen/nitrogen species. Antioxidant treatment resulted in increased numbers of engrafted BMPCs, provided functional protection to the heart, and decreased the incidence of myocardial rupture and death.
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    • "Recent analyses of the available sequence data confirmed the earlier suspicion that Chlamydia bacteria had assisted in this further increase in the complexity of eukaryotic cell (Becker et al., 2008; Price et al., 2012a; Spiegel, 2012; Ball et al., 2013; Baum, 2013). Although both mitochondria and plastids lost their independence during this very long intracellular symbiosis, they still retained some microbial autonomy allowing them even to change their host cells (Spees et al., 2006; Acquistapace et al., 2011; Rebbeck et al., 2011; Islam et al., 2012; Prockop, 2012; Thyssen et al., 2012). Moreover, some microorganism-derived organelles, such as mitosomes and hydrogenosomes, lack a genome and any DNA (Dolezal et al., 2005; Shiflett and Johnson, 2010), suggesting that some other organelles (e.g., peroxisomes) might also have a microbial origin (De Duve, 2007; Duhita et al., 2010). "
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