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The Systems Biology of Stem Cell Released Molecules—Based Therapeutics

DOI: 10.1155/2013/784541

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Abstract:

Most therapeutics are based on the traditional method of reductionism where a clinically defined condition is broken down into a defined biochemical pathway underlying the condition, then a target in the pathway is identified, followed by developing a drug to interact with the target, modifying the target such that the disease is ameliorated. Biology acts as a system, therefore reductionist approaches to developing therapeutics are limited in therapeutic value because disease or traumatized tissue involves multiple underlying pathways, only a part of the pathways underlying the disease is manipulated by the traditional therapeutic. Much data regarding stem cells shows that their beneficial effects are not restricted to their ability to differentiate, but is more likely due in large part to their ability to release a multitude of molecules. Stem cells release potent combinations of factors that modulate the composition of the cellular milieu to evoke a multitude of responses from neighboring cells. Therefore, stem cells represent a natural systems-based biological factory for the production and release of a multitude of molecules that interact with the system of biomolecular circuits underlying an indication. Current research includes efforts to define, stimulate, enhance, and harness stem cell released molecules (SRM) to develop systems-therapeutics. 1. Introduction In the postgenomic era, where even individual somatic cells display genetic heterogeneity [1], knowing the sequence of the genome has limited predictive value in disease diagnosis and treatment [2, 3]. Thus new diagnostic and therapeutic regimens are needed beyond those that rely on simple genomics [4]. While research and development costs in the pharmaceutical industry continue to increase, the number of new approved drugs is on a steady decline and new paradigms for drug development are being proffered [5–7]. Following the rapid emergence of in vitro and in silico screening tools, including molecular and genetic tools, there have now been advances in systems-based tools necessary to describe the effects of drug candidates within the complex biochemical pathways of intact, fully assembled living networks [8]. The pharmaceutical industry has thus realized the need to develop innovative strategies and new technologies to identify and develop new drug candidates, moving away from the over reliance of nonpredictive genetic tools [4]. One of the newly identified strategies and technologies is systems biology. As an example of a systems biology technique, a new analytical tool has emerged called

References

[1]  J. K. Baillie, M. W. Barnett, and K. R. Upton, “Somatic retrotransposition alters the genetic landscape of the human brain,” Nature, vol. 479, pp. 534–537, 2011.
[2]  J. Kaiser, “Genetic influences on disease remain hidden,” Science, vol. 338, pp. 1016–1017, 2012.
[3]  A. Magi, L. Tattini, M. Benelli, B. Giusti, R. Abbate, and S. Ruffo, “WNP: a novel algorithm for gene products annotation from weighted functional networks,” PLoS ONE, vol. 7, no. 6, Article ID e38767, 2012.
[4]  G. Maguire, “Using a systems-based approach for the development of diagnostics,” Expert Review of Molecular Diagnostics. In press.
[5]  J. A. DiMasi, “Risks in new drug development: approval success rates for investigational drugs,” Clinical Pharmacology & Therapeutics, vol. 69, no. 5, pp. 297–307, 2001.
[6]  B. H. Munos and W. W. Chin, “How to revive breakthrough innovation in the pharmaceutical industry,” Science Translational Medicine, vol. 3, no. 89, Article ID 89cm16, 2011.
[7]  L. M. McNamee and F. D. Ledley, “Patterns of technological innovation in biotech,” Nature Biotechnology, vol. 30, pp. 937–943, 2012.
[8]  M. K. Hellerstein, “Exploiting complexity and the robustness of network architecture for drug discovery,” Journal of Pharmacology and Experimental Therapeutics, vol. 325, no. 1, pp. 1–9, 2008.
[9]  G. Maguire, P. Lee, D. Manheim, and L. Boros, “SiDMAP: a metabolomics approach to assess the effects of drug candidates on the dynamic properties of biochemical pathways,” Expert Opinion Drug Discovery, vol. 4, pp. 351–359, 2006.
[10]  G. Maguire, L. Boros, and P. Lee, “Development of tracer-based metabolomics and its implications for the pharmaceutical industry,” International Journal of Pharmaceutical Medicine, vol. 21, no. 3, pp. 217–224, 2007.
[11]  G. G. Harrigan, G. Maguire, and L. Boros, “Metabolomics in alcohol research and drug development,” Alcohol Research & Health, vol. 31, no. 1, pp. 26–35, 2008.
[12]  K. Akiyama, C. Chen, D. Wang, et al., “Mesenchymal-stem-cell-induced immunoregulation involves FAS-ligand-/FAS-mediated T cell apoptosis,” Cell Stem Cell, vol. 10, no. 5, pp. 544–555, 2012.
[13]  S. Massberg, P. Schaerli, I. Knezevic-Maramica et al., “Immunosurveillance by hematopoietic progenitor cells trafficking through blood, lymph, and peripheral tissues,” Cell, vol. 131, no. 5, pp. 994–1008, 2007.
[14]  S. M. Eppler, D. L. Combs, T. D. Henry et al., “A target-mediated model to describe the pharmacokinetics and hemodynamic effects of recombinant human vascular endothelial growth factor in humans,” Clinical Pharmacology and Therapeutics, vol. 72, no. 1, pp. 20–32, 2002.
[15]  R. Krishnamurthy and M. C. Manning, “The stability factor: importance in formulation development,” Current Pharmaceutical Biotechnology, vol. 3, pp. 361–371, 2002.
[16]  G. Maguire and P. Friedman, “Stem Cell-Based Systems Biology Approach For Developing Therapeutics To Manage Peripheral Pain,” Society for Neuroscience Annual Meeting Abstracts, 2011.
[17]  B. Mannini, R. Cascella, M. Zampagni, et al., “Molecular mechanisms used by chaperones to reduce the toxicity of aberrant protein oligomers,” Proceedings of the National Academy of Sciences of the United States of America, vol. 109, no. 31, pp. 12479–12484, 2012.
[18]  A. R. Wyatt, J. J. Yerbury, R. A. Dabbs, and M. R. Wilson, “Roles of extracellular chaperones in amyloidosis,” Journal of Molecular Biology, vol. 421, pp. 499–516, 2012.
[19]  A. I. Caplan, “Why are MSCs therapeutic? New data: new insight,” Journal of Pathology, vol. 217, no. 2, pp. 318–324, 2009.
[20]  G. E. Kilroy, S. J. Foster, X. Wu et al., “Cytokine profile of human adipose-derived stem cells: expression of angiogenic, hematopoietic, and pro-inflammatory factors,” Journal of Cellular Physiology, vol. 212, no. 3, pp. 702–709, 2007.
[21]  B. Mannini, R. Cascella, M. Zampagni, et al., “Molecular mechanisms used by chaperones to reduce the toxicity of aberrant protein oligomers,” Proceedings of the National Academy of Sciences of the United States of America, vol. 109, pp. 12479–12484, 2012.
[22]  H. Sarojini, R. Estrada, H. Lu et al., “PEDF from mouse mesenchymal stem cell secretome attracts fibroblasts,” Journal of Cellular Biochemistry, vol. 104, no. 5, pp. 1793–1802, 2008.
[23]  T. Schink?the, W. Bloch, and A. Schmidt, “In vitro secreting profile of human mesenchymal stem cells,” Stem Cells and Development, vol. 17, no. 1, pp. 199–206, 2008.
[24]  D. Schubert, F. Herrera, R. Cumming et al., “Neural cells secrete a unique repertoire of proteins,” Journal of Neurochemistry, vol. 109, no. 2, pp. 427–435, 2009.
[25]  S. Zvonic, M. Lefevre, G. Kilroy et al., “Secretome of primary cultures of human adipose-derived stem cells: modulation of serpins by adipogenesis,” Molecular & Cellular Proteomics, vol. 6, no. 1, pp. 18–28, 2007.
[26]  E. Prinsloo, M. M. Setati, V. M. Longshaw, and G. L. Blatch, “Chaperoning stem cells: a role for heat shock proteins in the modulation of stem cell self-renewal and differentiation?” BioEssays, vol. 31, no. 4, pp. 370–377, 2009.
[27]  X. M. Xu, J. Wang, Z. Xuan, et al., “Chaperonins facilitate KNOTTED1 cell-to-cell trafficking and stem cell function,” Science, vol. 333, pp. 1141–1144, 2011.
[28]  M. R. Hicks, T. V. Cao, D. H. Campbell, and P. R. Standley, “Mechanical strain applied to human fibroblasts differentially regulates skeletal myoblast differentiation,” Journal of Applied Physiology, vol. 113, pp. 465–472, 2012.
[29]  Y. Dor, J. Brown, O. I. Martinez, and D. A. Melton, “Adult pancreatic β-cells are formed by self-duplication rather than stem-cell differentiation,” Nature, vol. 429, no. 6987, pp. 41–46, 2004.
[30]  I. Chimenti, R. R. Smith, T. S. Li et al., “Relative roles of direct regeneration versus paracrine effects of human cardiosphere-derived cells transplanted into infarcted mice,” Circulation Research, vol. 106, no. 5, pp. 971–980, 2010.
[31]  F. T?gel, Z. Hu, K. Weiss, J. Isaac, C. Lange, and C. Westenfelder, “Administered mesenchymal stem cells protect against ischemic acute renal failure through differentiation-independent mechanisms,” American Journal of Physiology, vol. 289, no. 1, pp. F31–F42, 2005.
[32]  J. Gao, J. E. Dennis, R. F. Muzic, M. Lundberg, and A. I. Caplan, “The dynamic in vivo distribution of bone marrow-derived mesenchymal stem cells after infusion,” Cells Tissues Organs, vol. 169, no. 1, pp. 12–20, 2001.
[33]  Y. Wu and R. C. H. Zhao, “The role of chemokines in mesenchymal stem cell homing to myocardium,” Stem Cell Reviews and Reports, vol. 8, no. 1, pp. 243–250, 2012.
[34]  H. Bonig, G. V. Priestley, M. Wohlfahrt, H. P. Kiem, and T. Papayannopoulou, “Blockade of 6-integrin reveals diversity in homing patterns among human, baboon, and murine cells,” Stem Cells and Development, vol. 18, no. 6, pp. 839–844, 2009.
[35]  M. Z. Ratajczak, C. H. Kim, A. Abdel-Latif, et al., “A novel perspective on stem cell homing and mobilization: review on bioactive lipids as potent chemoattractants and cationic peptides as underappreciated modulators of responsiveness to SDF-1 gradients,” Leukemia, vol. 26, no. 1, pp. 63–72, 2012.
[36]  C. Mias, E. Trouche, M. H. Seguelas et al., “Ex vivo pretreatment with melatonin improves survival, proangiogenic/ mitogenic activity, and efficiency of mesenchymal stem cells injected into ischemic kidney,” Stem Cells, vol. 26, no. 7, pp. 1749–1757, 2008.
[37]  X. Fu and H. Li, “Mesenchymal stem cells and skin wound repair and regeneration: possibilities and questions,” Cell and Tissue Research, vol. 335, no. 2, pp. 317–321, 2009.
[38]  S. Ilancheran, Y. Moodley, and U. Manuelpillai, “Human fetal membranes: a source of stem cells for tissue regeneration and repair?” Placenta, vol. 30, no. 1, pp. 2–10, 2009.
[39]  P. Trivedi and P. Hematti, “Derivation and immunological characterization of mesenchymal stromal cells from human embryonic stem cells,” Experimental Hematology, vol. 36, no. 3, pp. 350–359, 2008.
[40]  W. Zhang, “Mesenchymal stem cells in cancer: friends or foes,” Cancer Biology and Therapy, vol. 7, no. 2, pp. 252–254, 2008.
[41]  G. E. Kilroy, S. J. Foster, X. Wu et al., “Cytokine profile of human adipose-derived stem cells: expression of angiogenic, hematopoietic, and pro-inflammatory factors,” Journal of Cellular Physiology, vol. 212, no. 3, pp. 702–709, 2007.
[42]  I. Bochev, G. Elmadjian, D. Kyurkchiev et al., “Mesenchymal stem cells from human bone marrow or adipose tissue differently modulate mitogen-stimulated B-cell immunoglobulin production in vitro,” Cell Biology International, vol. 32, no. 4, pp. 384–393, 2008.
[43]  B. L. Yen, C. J. Chang, Y. C. Chen, et al., “Brief report—human embryonic stem cell-derived mesenchymal progenitors possess strong immunosuppressive effects toward natural killer cells as well as T lymphocytes,” Stem Cells, vol. 27, no. 2, pp. 451–456, 2009.
[44]  A. Bartholomew, C. Sturgeon, M. Siatskas et al., “Mesenchymal stem cells suppress lymphocyte proliferation in vitro and prolong skin graft survival in vivo,” Experimental Hematology, vol. 30, no. 1, pp. 42–48, 2002.
[45]  S. F. Mause and C. Weber, “Microparticles: protagonists of a novel communication network for intercellular information exchange,” Circulation Research, vol. 107, no. 9, pp. 1047–1057, 2010.
[46]  C. Théry, “Exosomes: secreted vesicles and intercellular communications,” F1000 Biology Reports, vol. 3, no. 1, article 15, 2011.
[47]  S. Mathivanan and R. J. Simpson, “ExoCarta: a compendium of exosomal proteins and RNA,” Proteomics, vol. 9, no. 21, pp. 4997–5000, 2009.
[48]  L. Barile, M. Gherghiceanu, L. M. Popescu, T. Moccetti, G. Vassallib, and I. D. Article, “Ultrastructural evidence of exosome secretion by progenitor cells in adult mouse myocardium and adult human cardiospheres,” Journal of Biomedicine and Biotechnology, vol. 2012, Article ID 354605, 10 pages, 2012.
[49]  S. Sahoo, E. Klychko, T. Thorne, et al., “Exosomes from human CD34+ stem cells mediate their proangiogenic paracrine activity,” Circulation Research, vol. 109, pp. 724–728, 2011.
[50]  P. Lu, L. L. Jones, E. Y. Snyder, and M. H. Tuszynski, “Neural stem cells constitutively secrete neurotrophic factors and promote extensive host axonal growth after spinal cord injury,” Experimental Neurology, vol. 181, pp. 115–129, 2003.
[51]  A. Nasef, A. Chapel, C. Mazurier et al., “Identification of IL-10 and TGF-β transcripts involved in the inhibition of T-lymphocyte proliferation during cell contact with human mesenchymal stem cells,” Gene Expression, vol. 13, no. 4-5, pp. 217–226, 2007.
[52]  K. English, F. P. Barry, C. P. Field-Corbett, and B. P. Mahon, “IFN-γ and TNF-α differentially regulate immunomodulation by murine mesenchymal stem cells,” Immunology Letters, vol. 110, no. 2, pp. 91–100, 2007.
[53]  K. Sato, K. Ozaki, I. Oh et al., “Nitric oxide plays a critical role in suppression of T-cell proliferation by mesenchymal stem cells,” Blood, vol. 109, no. 1, pp. 228–234, 2007.
[54]  R. Meisel, A. Zibert, M. Laryea, U. G?bel, W. D?ubener, and D. Dilloo, “Human bone marrow stromal cells inhibit allogeneic T-cell responses by indoleamine 2,3-dioxygenase-mediated tryptophan degradation,” Blood, vol. 103, no. 12, pp. 4619–4621, 2004.
[55]  J. Plumas, L. Chaperot, M. J. Richard, J. P. Molens, J. C. Bensa, and M. C. Favrot, “Mesenchymal stem cells induce apoptosis of activated T cells,” Leukemia, vol. 19, no. 9, pp. 1597–1604, 2005.
[56]  S. Aggarwal and M. F. Pittenger, “Human mesenchymal stem cells modulate allogeneic immune cell responses,” Blood, vol. 105, no. 4, pp. 1815–1822, 2005.
[57]  J. A. Potian, H. Aviv, N. M. Ponzio, J. S. Harrison, and P. Rameshwar, “Veto-like activity of mesenchymal stem cells: functional discrimination between cellular responses to alloantigens and recall antigens,” Journal of Immunology, vol. 171, no. 7, pp. 3426–3434, 2003.
[58]  S. H. Yang, M. J. Park, I. H. Yoon, et al., “Soluble mediators from mesenchymal stem cells suppress T cell proliferation by inducing IL-10,” Experimental & Molecular Medicine, vol. 41, no. 5, pp. 315–324, 2009.
[59]  S. Asari, S. Itakura, K. Ferreri et al., “Mesenchymal stem cells suppress B-cell terminal differentiation,” Experimental Hematology, vol. 37, no. 5, pp. 604–615, 2009.
[60]  I. Rasmusson, K. Le Blanc, B. Sundberg, and O. Ringdén, “Mesenchymal stem cells stimulate antibody secretion in human B cells,” Scandinavian Journal of Immunology, vol. 65, no. 4, pp. 336–343, 2007.
[61]  R. Ramasamy, H. Fazekasova, E. W. F. Lam, I. Soeiro, G. Lombardi, and F. Dazzi, “Mesenchymal stem cells inhibit dendritic cell differentiation and function by preventing entry into the cell cycle,” Transplantation, vol. 83, no. 1, pp. 71–76, 2007.
[62]  F. Djouad, L. M. Charbonnier, C. Bouffi et al., “Mesenchymal stem cells inhibit the differentiation of dendritic cells through an interleukin-6-dependent mechanism,” Stem Cells, vol. 25, no. 8, pp. 2025–2032, 2007.
[63]  G. M. Spaggiari, H. Abdelrazik, F. Becchetti, and L. Moretta, “MSCs inhibit monocyte-derived DC maturation and function by selectively interfering with the generation of immature DCs: central role of MSC-derived prostaglandin E2,” Blood, vol. 113, no. 26, pp. 6576–6583, 2009.
[64]  Z. Selmani, A. Naji, E. Gaiffe et al., “HLA-G is a crucial immunosuppressive molecule secreted by adult human mesenchymal stem cells,” Transplantation, vol. 87, no. 9, supplement, pp. S62–S66, 2009.
[65]  G. M. Spaggiari, A. Capobianco, S. Becchetti, M. C. Mingari, and L. Moretta, “Mesenchymal stem cell-natural killer cell interactions: evidence that activated NK cells are capable of killing MSCs, whereas MSCs can inhibit IL-2-induced NK-cell proliferation,” Blood, vol. 107, no. 4, pp. 1484–1490, 2006.
[66]  L. A. Ortiz, M. DuTreil, C. Fattman et al., “Interleukin 1 receptor antagonist mediates the antiinflammatory and antifibrotic effect of mesenchymal stem cells during lung injury,” Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 26, pp. 11002–11007, 2007.
[67]  L. Raffaghello, G. Bianchi, M. Bertolotto et al., “Human mesenchymal stem cells inhibit neutrophil apoptosis: a model for neutrophil preservation in the bone marrow niche,” Stem Cells, vol. 26, no. 1, pp. 151–162, 2008.
[68]  G. Ren, L. Zhang, X. Zhao et al., “Mesenchymal stem cell-mediated immunosuppression occurs via concerted action of chemokines and nitric oxide,” Cell Stem Cell, vol. 2, no. 2, pp. 141–150, 2008.
[69]  L. Xu, J. Yan, D. Chen et al., “Human neural stem cell grafts ameliorate motor neuron disease in SOD-1 transgenic rats,” Transplantation, vol. 82, no. 7, pp. 865–875, 2006.
[70]  S. Corti, F. Locatelli, D. Papadimitriou et al., “Neural stem cells LewisX + CXCR4 + modify disease progression in an amyotrophic lateral sclerosis model,” Brain, vol. 130, no. 5, pp. 1289–1305, 2007.
[71]  P. Lu, L. L. Jones, E. Y. Snyder, and M. H. Tuszynski, “Neural stem cells constitutively secrete neurotrophic factors and promote extensive host axonal growth after spinal cord injury,” Experimental Neurology, vol. 181, no. 2, pp. 115–129, 2003.
[72]  J. Yan, A. M. Welsh, S. H. Boka, E. Y. Snyder, and V. E. Koliatsos, “Differentiation and tropic/trophic effects of exogenous neural precursors in the adult spinal cord,” Journal of Comparative Neurology, vol. 480, no. 1, pp. 101–114, 2004.
[73]  L. Crigler, R. C. Robey, A. Asawachaicharn, D. Gaupp, and D. G. Phinney, “Human mesenchymal stem cell subpopulations express a variety of neuro-regulatory molecules and promote neuronal cell survival and neuritogenesis,” Experimental Neurology, vol. 198, no. 1, pp. 54–64, 2006.
[74]  M. H. Tuszynski, “Nerve growth factor gene therapy in Alzheimer disease,” Alzheimer Disease and Associated Disorders, vol. 21, no. 2, pp. 179–189, 2007.
[75]  Y. J. Kim, H. J. Park, G. Lee et al., “Neuroprotective effects of human mesenchymal stem cells on dopaminergic neurons through anti-inflammatory action,” GLIA, vol. 57, no. 1, pp. 13–23, 2009.
[76]  I. Zwart, A. J. Hill, F. Al-Allaf et al., “Umbilical cord blood mesenchymal stromal cells are neuroprotective and promote regeneration in a rat optic tract model,” Experimental Neurology, vol. 216, no. 2, pp. 439–448, 2009.
[77]  H. J. Kim, J. H. Lee, and S. H. Kim, “Therapeutic effects of human mesenchymal stem cells on traumatic brain injury in rats: secretion of neurotrophic factors and inhibition of apoptosis,” Journal of Neurotrauma, vol. 27, no. 1, pp. 131–138, 2010.
[78]  H. Arien-Zakay, S. Lecht, M. M. Bercu et al., “Neuroprotection by cord blood neural progenitors involves antioxidants, neurotrophic and angiogenic factors,” Experimental Neurology, vol. 216, no. 1, pp. 83–94, 2009.
[79]  A. P. Croft and S. A. Przyborski, “Mesenchymal stem cells expressing neural antigens instruct a neurogenic cell fate on neural stem cells,” Experimental Neurology, vol. 216, no. 2, pp. 329–341, 2009.
[80]  Y. Li, J. Chen, C. L. Zhang et al., “Gliosis and brain remodeling after treatment of stroke in rats with marrow stromal cells,” GLIA, vol. 49, no. 3, pp. 407–417, 2005.
[81]  Q. Chen, Y. Long, X. Yuan et al., “Protective effects of bone marrow stromal cell transplantation in injured rodent brain: synthesis of neurotrophic factors,” Journal of Neuroscience Research, vol. 80, no. 5, pp. 611–619, 2005.
[82]  S. Wislet-Gendebien, F. Bruyère, G. Hans, P. Leprince, G. Moonen, and B. Rogister, “Nestin-positive mesenchymal stem cells favour the astroglial lineage in neural progenitors and stem cells by releasing active BMP4,” BMC Neuroscience, vol. 5, article 33, 2004.
[83]  R. Barzilay, T. Ben-Zur, O. Sadan, et al., “Intracerebral adult stem cells transplantation increases brain-derived neurotrophic factor levels and protects against phencyclidine-induced social deficit in mice,” Translational Psychiatry, vol. 1, article e61, 2011.
[84]  M. Perez-Ilzarbe, O. Agbulut, B. Pelacho et al., “Characterization of the paracrine effects of human skeletal myoblasts transplanted in infarcted myocardium,” European Journal of Heart Failure, vol. 10, no. 11, pp. 1065–1072, 2008.
[85]  L. B. Balsam, A. J. Wagers, J. L. Christensen, T. Kofidis, I. L. Weissmann, and R. C. Robbins, “Haematopoietic stem cells adopt mature haematopoietic fates in ischaemic myocardium,” Nature, vol. 428, no. 6983, pp. 668–673, 2004.
[86]  C. E. Murry, M. H. Soonpaa, H. Reinecke et al., “Haematopoietic stem cells do not transdifferentiate into cardiac myocytes in myocardial infarcts,” Nature, vol. 428, no. 6983, pp. 664–668, 2004.
[87]  N. Noiseux, M. Gnecchi, M. Lopez-Ilasaca et al., “Mesenchymal stem cells overexpressing Akt dramatically repair infarcted myocardium and improve cardiac function despite infrequent cellular fusion or differentiation,” Molecular Therapy, vol. 14, no. 6, pp. 840–850, 2006.
[88]  M. Takahashi, T. S. Li, R. Suzuki, et al., “Cytokines produced by bone marrow cells can contribute to functional improvement of the infarcted heart by protecting cardiomyocytes from ischemic injury,” American Journal of Physiology, vol. 291, no. 2, pp. H886–H893, 2006.
[89]  R. Uemura, M. Xu, N. Ahmad, and M. Ashraf, “Bone marrow stem cells prevent left ventricular remodeling of ischemic heart through paracrine signaling,” Circulation Research, vol. 98, no. 11, pp. 1414–1421, 2006.
[90]  M. Xu, R. Uemura, Y. Dai, Y. Wang, Z. Pasha, and M. Ashraf, “In vitro and in vivo effects of bone marrow stem cells on cardiac structure and function,” Journal of Molecular and Cellular Cardiology, vol. 42, no. 2, pp. 441–448, 2007.
[91]  C. Kubal, K. Sheth, B. Nadal-Ginard, and M. Galinanes, “Bone marrow cells have a potent anti-ischemic effect against myocardial cell death in humans,” The Journal of Thoracic and Cardiovascular Surgery, vol. 132, no. 5, pp. 1112–1118, 2006.
[92]  M. Korf-Klingebiel, T. Kempf, T. Sauer et al., “Bone marrow cells are a rich source of growth factors and cytokines: implications for cell therapy trials after myocardial infarction,” European Heart Journal, vol. 29, no. 23, pp. 2851–2858, 2008.
[93]  D. K. Singla, G. E. Lyons, and T. J. Kamp, “Transplanted embryonic stem cells following mouse myocardial infarction inhibit apoptosis and cardiac remodeling,” American Journal of Physiology, vol. 293, no. 2, pp. H1308–H1314, 2007.
[94]  C. Huang, H. Gu, Q. Yu, M. C. Manukyan, J. A. Poynter, and M. Wang, “Sca-1+ cardiac stem cells mediate acute cardioprotection via paracrine factor SDF-1 following myocardial ischemia/reperfusion,” PLoS ONE, vol. 6, no. 12, Article ID e29246, 2011.
[95]  H. Hwang, W. Chang, B. Song, et al., “Antiarrhythmic potential of mesenchymal stem cell is modulated by hypoxic environment,” Journal of the American College of Cardiology, vol. 60, no. 17, pp. 1698–1706, 2012.
[96]  K. Schenke-Layland, B. M. Strem, M. C. Jordan et al., “Adipose tissue-derived cells improve cardiac function following myocardial infarction,” Journal of Surgical Research, vol. 153, no. 2, pp. 217–223, 2009.
[97]  X. Xu, Z. Xu, Y. Xu, and G. Cui, “Effects of mesenchymal stem cell transplantation on extracellular matrix after myocardial infarction in rats,” Coronary Artery Disease, vol. 16, no. 4, pp. 245–255, 2005.
[98]  S. Ohnishi, T. Yasuda, S. Kitamura, and N. Nagaya, “Effect of hypoxia on gene expression of bone marrow-derived mesenchymal stem cells and mononuclear cells,” Stem Cells, vol. 25, no. 5, pp. 1166–1177, 2007.
[99]  S. Ohnishi, H. Sumiyoshi, S. Kitamura, and N. Nagaya, “Mesenchymal stem cells attenuate cardiac fibroblast proliferation and collagen synthesis through paracrine actions,” FEBS Letters, vol. 581, no. 21, pp. 3961–3966, 2007.
[100]  S. Mureli, C. P. Gans, D. J. Bare, D. L. Geenen, N. M. Kumar, and K. Banach, “Mesenchymal stem cells improve cardiac conduction by upregulation of connexin 43 through paracrine signaling,” American Journal of Physiology, vol. 304, no. 4, pp. 600–609, 2013.
[101]  N. Dib, R. E. Michler, F. D. Pagani et al., “Safety and feasibility of autologous myoblast transplantation in patients with ischemic cardiomyopathy: four-year follow-up,” Circulation, vol. 112, no. 12, pp. 1748–1755, 2005.
[102]  K. Lau, R. Paus, S. Tiede, P. Day, and A. Bayat, “Exploring the role of stem cells in cutaneous wound healing,” Experimental Dermatology, vol. 18, no. 11, pp. 921–933, 2009.
[103]  Y. Wu, L. Chen, P. G. Scott, and E. E. Tredget, “Mesenchymal stem cells enhance wound healing through differentiation and angiogenesis,” Stem Cells, vol. 25, no. 10, pp. 2648–2659, 2007.
[104]  M. P. Zimber, J. N. Mansbridge, M. Taylor et al., “Human cell-conditioned media produced under embryonic-like conditions result in improved healing time after laser resurfacing,” Aesthetic Plastic Surgery, vol. 36, no. 2, pp. 431–437, 2012.
[105]  D. C. Wan, M. D. Kwan, D. M. Gupta, et al., “Global age-dependent differences in gene expression in response to calvarial injury,” Journal of Craniofacial Surgery, vol. 19, no. 5, pp. 1292–1301, 2008.
[106]  Y. Otsuka-Tanaka, S. Oommen, M. Kawasaki, et al., “Oral lining mucosa development depends on mesenchymal microRNAs,” Journal of Dental Research, vol. 92, no. 3, pp. 229–234, 2013.
[107]  P. J. Murray, P. K. Maini, M. V. Plikus, C.-M. Chuong, and R. E. Baker, “Modelling hair follicle growth dynamics as an excitable medium,” vol. 8, no. 12, Article ID e1002804, 2012.
[108]  P. S. Myung, M. Takeo, M. Ito, and R. P. Atit, “Epithelial Wnt ligand secretion is required for adult hair follicle growth and regeneration,” Journal of Investigative Dermatology, vol. 133, no. 1, pp. 31–41, 2012.
[109]  C. Blanpain and E. Fuchs, “Epidermal homeostasis: a balancing act of stem cells in the skin,” Nature Reviews Molecular Cell Biology, vol. 10, no. 3, pp. 207–217, 2009.
[110]  N. Li and H. Clevers, “Coexistence of quiescent and active adult stem cells in mammals,” Science, vol. 327, no. 5965, pp. 542–545, 2010.
[111]  X. Yan and D. M. Owens, “The skin: a home to multiple classes of epithelial progenitor cells,” Stem Cell Reviews, vol. 4, no. 2, pp. 113–118, 2008.
[112]  S. Guo and L. A. DiPietro, “Factors affecting wound healing,” Journal of Dental Research, vol. 89, no. 3, pp. 219–229, 2010.
[113]  Y. D. Teng, D. Yu, A. E. Ropper, et al., “Functional multipotency of stem cells: a conceptual review of neurotrophic factor-based evidence and its role in translational research,” Current Neuropharmacology, vol. 9, no. 4, pp. 574–585, 2011.
[114]  N. Rao, S. Evans, D. Stewart et al., “Fibroblasts influence muscle progenitor differentiation and alignment in contact independent and dependent manners in organized co-culture devices,” Biomedical Microdevices, vol. 15, no. 1, pp. 161–169, 2013.
[115]  T. M. Hammoudi, C. A. Rivet, M. L. Kemp, H. Lu, and J. S. Temenoff, “Three-dimensional in vitro tri-culture platform to investigate effects of crosstalk between mesenchymal stem cells, osteoblasts, and adipocytes,” Tissue Engineering A, vol. 18, pp. 1686–1697, 2012.
[116]  V. W. Wong, B. Levi, J. Rajadas, M. T. Longaker, and G. C. Gurtner, “Stem cell niches for skin regeneration,” International Journal of Biomaterials, vol. 2012, Article ID 926059, 8 pages, 2012.
[117]  W. S. Kim, B. S. Park, and J. H. Sung, “The wound-healing and antioxidant effects of adipose-derived stem cells,” Expert Opinion on Biological Therapy, vol. 9, no. 7, pp. 879–887, 2009.
[118]  C. Widmer, J. M. Gebauer, E. Brunstein et al., “Molecular basis for the action of the collagen-specific chaperone Hsp47/SERPINH1 and its structure-specific client recognition,” Proceedings of the National Academy of Sciences of the United States of America, vol. 109, no. 33, pp. 13243–13247, 2012.
[119]  Y. Tamura, T. Torigoe, K. Kukita et al., “Heat-shock proteins as endogenous ligands building a bridge between innate and adaptive immunity,” Immunotherapy, vol. 4, no. 8, pp. 841–852, 2012.
[120]  P. W. Lewis, S. J. Elsaesser, K. M. Noh, S. C. Stadler, and C. D. Allis, “Daxx is an H3.3-specific histone chaperone and cooperates with ATRX in replication-independent chromatin assembly at telomeres,” Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 32, pp. 14075–14080, 2010.
[121]  J. J. Yerbury, E. M. Stewart, A. R. Wyatt, and M. R. Wilson, “Quality control of protein folding in extracellular space,” EMBO Reports, vol. 6, no. 12, pp. 1131–1136, 2005.
[122]  N. E. Sharpless and R. A. DePinho, “How stem cells age and why this makes us grow old,” Nature Reviews Molecular Cell Biology, vol. 8, no. 9, pp. 703–713, 2007.
[123]  A. Waterstrat and G. Van Zant, “Effects of aging on hematopoietic stem and progenitor cells,” Current Opinion in Immunology, vol. 21, no. 4, pp. 408–413, 2009.
[124]  H. Toledano, C. D’Alterio, B. Czech, E. Levine, and D. L. Jones, “The let-7-Imp axis regulates ageing of the Drosophila testis stem-cell niche,” Nature, vol. 485, pp. 605–610, 2012.
[125]  Y. Guo, B. Graham-Evans, and H. E. Broxmeyer, “Murine embryonic stem cells secrete cytokines/growth modulators that enhance cell survival/anti-apoptosis and stimulate colony formation of murine hematopoietic progenitor cells,” Stem Cells, vol. 24, no. 4, pp. 850–856, 2006.
[126]  R. E. Davey and P. W. Zandstra, “Spatial organization of embryonic stem cell responsiveness to autocrine Gp130 ligands reveals an autoregulatory stem cell niche,” Stem Cells, vol. 24, no. 11, pp. 2538–2548, 2006.
[127]  I. Flores, M. L. Cayuela, and M. A. Blasco, “Effects of telomerase and telomere length on epidermal stem cell behavior,” Science, vol. 309, no. 5738, pp. 1253–1256, 2005.
[128]  M. Collins, V. Renault, L. A. Grobler et al., “Athletes with exercise-associated fatigue have abnormally short muscle DNA telomeres,” Medicine and Science in Sports and Exercise, vol. 35, no. 9, pp. 1524–1528, 2003.
[129]  C. He, M. C. Bassik, V. Moresi, et al., “Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis,” Nature, vol. 481, pp. 511–515, 2012.
[130]  M. C. Valero, H. D. Huntsman, J. Liu, K. Zou, and M. D. Boppart, “Eccentric exercise facilitates mesenchymal stem cell appearance in skeletal muscle,” PLoS ONE, vol. 7, no. 1, Article ID e29760, 2012.
[131]  A. Carrel and C. A. Lindbergh, The Culture of Organs, Paul Hoeber, New York, NY, USA, 1938.

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