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Ofermanns S.,Max Planck Institute for Heart and Lung Research
Science Translational Medicine | Year: 2012

The antiatherogenic drug nicotinic acid (niacin) has antidyslipidemic ef ects independent of free fatty acid suppression mediated by its receptor HCA2 (GPR109A) (Lauring et al., this issue). Source

Understanding in vivo regeneration of complex structures offers a fascinating perspective for translation into medical applications. Unfortunately, mammals in general lack large-scale regenerative capacity, whereas planarians, newts or Hydra can regenerate complete body parts. Such organisms are, however, poorly annotated because of the lack of sequence information. This leads to limited access for molecular biological investigations. In the last decade, high throughput technologies and new methods enabling the effective generation of transgenic animals have rapidly evolved. These developments have allowed the extensive use of niche model organisms as part of a trend towards the accessibility of a greater panel of model species for scientific research. The case study that follows provides an insight into the impact of high throughput techniques on the landscape of models of regeneration. The cases presented here give evidence of alternative stem cell maintenance pathways, the identification of new protein families and new stem cell markers. Regeneration of complex structures is a capability mastered by a small number of niche model organisms. Although such organisms are poorly annotated, current technologies allow the extensive use of such organisms. Representative studies give evidence of alternative stem cell maintenance pathways, new protein families, and new stem cell markers. © 2014 WILEY Periodicals, Inc. Source

Gunther S.,Max Planck Institute for Heart and Lung Research
Cell stem cell | Year: 2013

Skeletal muscle contains Pax7-expressing muscle stem or satellite cells, enabling muscle regeneration throughout most of adult life. Here, we demonstrate that induced inactivation of Pax7 in Pax7-expressing cells of adult mice leads to loss of muscle stem cells and reduced heterochromatin condensation in rare surviving satellite cells. Inactivation of Pax7 in Myf5-expressing cells revealed that the majority of adult muscle stem cells originate from myogenic lineages, which express the myogenic regulators Myf5 or MyoD. Likewise, the majority of muscle stem cells are replenished from Myf5-expressing myogenic cells during adult life, and inactivation of Pax7 in Myf5-expressing cells after muscle damage leads to a complete arrest of muscle regeneration. Finally, we demonstrate that a relatively small number of muscle stem cells are sufficient for efficient repair of skeletal muscles. We conclude that Pax7 acts at different levels in a nonhierarchical regulatory network controlling muscle-satellite-cell-mediated muscle regeneration. Copyright © 2013 Elsevier Inc. All rights reserved. Source

Kostin S.,Max Planck Institute for Heart and Lung Research
Journal of Cellular and Molecular Medicine | Year: 2010

The existence of a new type of interstitial cells in the heart namely, interstitial Cajal-like cells (ICLC), has been described for the first time by Hinescu and Popescu in 2005. This study was then followed by an ascending trend of publications regarding the morphology, phenotype and distribution of myocardial ICLC in diverse species including human patients. Recently the new term 'telocytes' has been proposed for cells formerly known as ICLC, and the term 'telopodes' has been proposed for the prolongations of these cells. The identification of these cells is based on ultrastructural criteria. In addition, telocyters/telyopodes can be identified by several complementary approaches including methylene blue vital staining, silver impregnation and immunoreactivity against CD117/c-kit, vimentin, etc. This point of view presents critical data existing in literature, as well as own results, which unequivocally provide compelling evidence that telocytes are a new distinct cellular entity of myocardial interstitium. Several presumable functions of the myocardial telocytes are discussed: (i) intercellular signalling, (ii) cardiac repair/remodelling and (iii) stem cell nursing in cardiac renewal. © 2010 The Authors Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. Source

Kostin S.,Max Planck Institute for Heart and Lung Research
Seminars in Cell and Developmental Biology | Year: 2016

Our previous studies suggested that an important variable of the progression of contractile dysfunction to terminal heart failure is the imbalance between myocyte cell death and myocyte renewal. For this reason, preventing myocyte cell death and an increasing generation of new myocytes may represent attractive targets in the treatment of human heart failure. Prospective clues to enhance myocardial regeneration are the newly discovered cells termed telocytes, formerly called interstitial Cajal-like cells, which are believed to nurse or guide the endogenous and exogenous stem cells for activation and commitment, but they also act as supporting cells for progenitor cells migration toward injured myocardium. We have recently found that telocytes are reduced in the diseased and failing myocardium. Importantly, the imbalance between telocyte proliferation and telocyte death is responsible for the telocytes depletion in cardiac diseases leading to heart failure. We have also demonstrated that telocytes are influenced by the extracellular matrix protein composition such that the telocytes are almost absent in areas of severe fibrosis. It is plausible that the reduction in telocytes in diseased human hearts could participate in the abnormal three-dimensional spatial organization and disturbed intercellular signalling of the myocardium. Decreased telocytes in diseased hearts would also be predicted to alter the property of telocytes to maintain cardiac stem cell niche by decreasing the pool of cardiac stem cells and thereby impairing cardiac regeneration. © 2016 Elsevier Ltd. Source

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