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.
"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 "
[Show abstract][Hide abstract] 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.
Journal of the American Heart Association 12/2014; 3(1):e000471. DOI:10.1161/JAHA.113.000471 · 4.31 Impact Factor
"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). "
[Show abstract][Hide abstract] ABSTRACT: In the course of plant evolution, there is an obvious trend toward an increased complexity of plant bodies, as well as an increased sophistication of plant behavior and communication. Phenotypic plasticity of plants is based on the polar auxin transport machinery that is directly linked with plant sensory systems impinging on plant behavior and adaptive responses. Similar to the emergence and evolution of eukaryotic cells, evolution of land plants was also shaped and driven by infective and symbiotic microorganisms. These microorganisms are the driving force behind the evolution of plant synapses and other neuronal aspects of higher plants; this is especially pronounced in the root apices. Plant synapses allow synaptic cell-cell communication and coordination in plants, as well as sensory-motor integration in root apices searching for water and mineral nutrition. These neuronal aspects of higher plants are closely linked with their unique ability to adapt to environmental changes.
Frontiers in Cellular and Infection Microbiology 08/2013; 3:44. DOI:10.3389/fcimb.2013.00044 · 3.72 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Multiple sclerosis is a major cause of neurological disability, and particularly occurs in young adults. It is characterised by conspicuous patches of damage throughout the brain and spinal cord, with loss of myelin and myelinating cells (oligodendrocytes), and damage to neurons and axons. Multiple sclerosis is incurable, but stem-cell therapy might offer valuable therapeutic potential. Efforts to develop stem-cell therapies for multiple sclerosis have been conventionally built on the principle of direct implantation of cells to replace oligodendrocytes, and therefore to regenerate myelin. Recent progress in understanding of disease processes in multiple sclerosis include observations that spontaneous myelin repair is far more widespread and successful than was previously believed, that loss of axons and neurons is more closely associated with progressive disability than is myelin loss, and that damage occurs diffusely throughout the CNS in grey and white matter, not just in discrete, isolated patches or lesions. These findings have introduced new and serious challenges that stem-cell therapy needs to overcome; the practical challenges to achieve cell replacement alone are difficult enough, but, to be useful, cell therapy for multiple sclerosis must achieve substantially more than the replacement of lost oligodendrocytes. However, parallel advances in understanding of the reparative properties of stem cells-including their distinct immunomodulatory and neuroprotective properties, interactions with resident or tissue-based stem cells, cell fusion, and neurotrophin elaboration-offer renewed hope for development of cell-based therapies. Additionally, these advances suggest avenues for translation of this approach not only for multiple sclerosis, but also for other common neurological and neurodegenerative diseases.
The Lancet 10/2013; 382(9899):1204-1213. DOI:10.1016/S0140-6736(13)61810-3 · 45.22 Impact Factor
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