Mechanisms of pathological scarring: Role of myofibroblasts and current developments
ABSTRACT Myofibroblasts play a key role in the wound‐healing process, promoting wound closure and matrix deposition. These cells normally disappear from granulation tissue by apoptosis after wound closure, but under some circumstances, they persist and may contribute to pathological scar formation....
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| Vydané v: | Wound repair and regeneration Ročník 19; číslo s1; s. s10 - s15 |
|---|---|
| Hlavní autori: | , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
Malden, USA
Blackwell Publishing Inc
01.09.2011
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| ISSN: | 1067-1927, 1524-475X, 1524-475X |
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| Abstract | ABSTRACT
Myofibroblasts play a key role in the wound‐healing process, promoting wound closure and matrix deposition. These cells normally disappear from granulation tissue by apoptosis after wound closure, but under some circumstances, they persist and may contribute to pathological scar formation. Myofibroblast differentiation and apoptosis are both modulated by cytokines, mechanical stress, and, more generally, cell–cell and cell–matrix interactions. Tissue repair allows tissues and organs to recover, at least partially, functional properties that have been lost through trauma or disease. Embryonic skin wounds are repaired without scarring or fibrosis, whereas skin wound repair in adults always leads to scar formation, which may have functional or esthetic consequences, as in the case of hypertrophic scars, for example. Skin wound repair involves a precise remodeling process, particularly in the dermal compartment, during which fibroblasts/myofibroblasts play a central role. This article reviews the origins of myofibroblasts and their role in normal and pathological skin wound healing. This article focuses on traumatic skin wound healing, but largely, the same mechanisms apply in other physiological and pathological settings. Tissue healing in other organs is examined by comparison, as well as the stromal reaction associated with cancer. New approaches to wound/scar therapy are discussed. |
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| AbstractList | Myofibroblasts play a key role in the wound-healing process, promoting wound closure and matrix deposition. These cells normally disappear from granulation tissue by apoptosis after wound closure, but under some circumstances, they persist and may contribute to pathological scar formation. Myofibroblast differentiation and apoptosis are both modulated by cytokines, mechanical stress, and, more generally, cell-cell and cell-matrix interactions. Tissue repair allows tissues and organs to recover, at least partially, functional properties that have been lost through trauma or disease. Embryonic skin wounds are repaired without scarring or fibrosis, whereas skin wound repair in adults always leads to scar formation, which may have functional or esthetic consequences, as in the case of hypertrophic scars, for example. Skin wound repair involves a precise remodeling process, particularly in the dermal compartment, during which fibroblasts/myofibroblasts play a central role. This article reviews the origins of myofibroblasts and their role in normal and pathological skin wound healing. This article focuses on traumatic skin wound healing, but largely, the same mechanisms apply in other physiological and pathological settings. Tissue healing in other organs is examined by comparison, as well as the stromal reaction associated with cancer. New approaches to wound/scar therapy are discussed.Myofibroblasts play a key role in the wound-healing process, promoting wound closure and matrix deposition. These cells normally disappear from granulation tissue by apoptosis after wound closure, but under some circumstances, they persist and may contribute to pathological scar formation. Myofibroblast differentiation and apoptosis are both modulated by cytokines, mechanical stress, and, more generally, cell-cell and cell-matrix interactions. Tissue repair allows tissues and organs to recover, at least partially, functional properties that have been lost through trauma or disease. Embryonic skin wounds are repaired without scarring or fibrosis, whereas skin wound repair in adults always leads to scar formation, which may have functional or esthetic consequences, as in the case of hypertrophic scars, for example. Skin wound repair involves a precise remodeling process, particularly in the dermal compartment, during which fibroblasts/myofibroblasts play a central role. This article reviews the origins of myofibroblasts and their role in normal and pathological skin wound healing. This article focuses on traumatic skin wound healing, but largely, the same mechanisms apply in other physiological and pathological settings. Tissue healing in other organs is examined by comparison, as well as the stromal reaction associated with cancer. New approaches to wound/scar therapy are discussed. ABSTRACT Myofibroblasts play a key role in the wound‐healing process, promoting wound closure and matrix deposition. These cells normally disappear from granulation tissue by apoptosis after wound closure, but under some circumstances, they persist and may contribute to pathological scar formation. Myofibroblast differentiation and apoptosis are both modulated by cytokines, mechanical stress, and, more generally, cell–cell and cell–matrix interactions. Tissue repair allows tissues and organs to recover, at least partially, functional properties that have been lost through trauma or disease. Embryonic skin wounds are repaired without scarring or fibrosis, whereas skin wound repair in adults always leads to scar formation, which may have functional or esthetic consequences, as in the case of hypertrophic scars, for example. Skin wound repair involves a precise remodeling process, particularly in the dermal compartment, during which fibroblasts/myofibroblasts play a central role. This article reviews the origins of myofibroblasts and their role in normal and pathological skin wound healing. This article focuses on traumatic skin wound healing, but largely, the same mechanisms apply in other physiological and pathological settings. Tissue healing in other organs is examined by comparison, as well as the stromal reaction associated with cancer. New approaches to wound/scar therapy are discussed. Myofibroblasts play a key role in the wound‐healing process, promoting wound closure and matrix deposition. These cells normally disappear from granulation tissue by apoptosis after wound closure, but under some circumstances, they persist and may contribute to pathological scar formation. Myofibroblast differentiation and apoptosis are both modulated by cytokines, mechanical stress, and, more generally, cell–cell and cell–matrix interactions. Tissue repair allows tissues and organs to recover, at least partially, functional properties that have been lost through trauma or disease. Embryonic skin wounds are repaired without scarring or fibrosis, whereas skin wound repair in adults always leads to scar formation, which may have functional or esthetic consequences, as in the case of hypertrophic scars, for example. Skin wound repair involves a precise remodeling process, particularly in the dermal compartment, during which fibroblasts/myofibroblasts play a central role. This article reviews the origins of myofibroblasts and their role in normal and pathological skin wound healing. This article focuses on traumatic skin wound healing, but largely, the same mechanisms apply in other physiological and pathological settings. Tissue healing in other organs is examined by comparison, as well as the stromal reaction associated with cancer. New approaches to wound/scar therapy are discussed. |
| Author | Coulomb, Bernard Micallef, Ludovic Sarrazy, Vincent Desmoulière, Alexis Billet, Fabrice |
| Author_xml | – sequence: 1 givenname: Vincent surname: Sarrazy fullname: Sarrazy, Vincent organization: EA 3842 and Département de Physiologie, Institut Fédératif de Recherche 145, Faculté de Pharmacie, Université de Limoges, Limoges, France – sequence: 2 givenname: Fabrice surname: Billet fullname: Billet, Fabrice organization: EA 3842 and Département de Physiologie, Institut Fédératif de Recherche 145, Faculté de Pharmacie, Université de Limoges, Limoges, France – sequence: 3 givenname: Ludovic surname: Micallef fullname: Micallef, Ludovic organization: EA 3842 and Département de Physiologie, Institut Fédératif de Recherche 145, Faculté de Pharmacie, Université de Limoges, Limoges, France – sequence: 4 givenname: Bernard surname: Coulomb fullname: Coulomb, Bernard organization: Inserm U970, Réparation Artérielle, Université Paris Descartes, Paris, France – sequence: 5 givenname: Alexis surname: Desmoulière fullname: Desmoulière, Alexis organization: EA 3842 and Département de Physiologie, Institut Fédératif de Recherche 145, Faculté de Pharmacie, Université de Limoges, Limoges, France |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21793960$$D View this record in MEDLINE/PubMed |
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| References | Desmoulière A, Redard M, Darby IA, Gabbiani G. Apoptosis mediates the decrease in cellularity during the transition between granulation tissue and scar. Am J Pathol 1995; 146: 55-66. Ng CP, Hinz B, Swartz MA. Interstitial fluid flow induces myofibroblast differentiation and collagen alignment in vitro. J Cell Sci 2005; 118: 4731-9. Verhaegen PDHM, van Zuijlen PPM, Pennings NM, van Marle J, Niessen FB, van der Horst CMAM, Middelkoop E. Differences in collagen architecture between keloid, hypertrophic scar, normotrophic scar, and normal skin: an objective histopathological analysis. Wound Rep Regen 2009; 17: 649-56. Desmoulière A, Geinoz A, Gabbiani F, Gabbiani G. Transforming growth factor-β1 induces α-smooth muscle actin expression in granulation tissue myofibroblasts and in quiescent and growing cultured fibroblasts. J Cell Biol 1993; 122: 103-11. Yang L, Scott PG, Dodd C, Medina A, Jiao H, Shankowsky HA, Ghahary A, Tredget EE. Identification of fibrocytes in postburn hypertrophic scar. Wound Rep Regen 2005; 13: 398-404. Opalenik SR, Davidson JM. Fibroblast differentiation of bone marrow-derived cells during wound repair. FASEB J 2005; 19: 1561-3. Gallant-Behm CL, Mustoe TA. Occlusion regulates epidermal cytokine production and inhibits scar formation. Wound Rep Regen 2010; 18: 235-44. Werner S, Krieg T, Smola H. Keratinocyte-fibroblast interactions in wound healing. J Invest Dermatol 2007; 127: 998-1008. Bellemare J, Roberge CJ, Bergeron D, Lopez-Vallé CA, Roy M, Moulin VJ. Epidermis promotes dermal fibrosis: role in the pathogenesis of hypertrophic scars. J Pathol 2005; 206: 1-8. Noël A, Jost M, Maquoi E. Matrix metalloproteinases at cancer tumor-host interface. Semin Cell Dev Biol 2008; 19: 52-60. Direkze NC, Hodivala-Dilke K, Jeffery R, Hunt T, Poulsom R, Oukrif D, Alison MR, Wright NA. Bone marrow contribution to tumor-associated myofibroblasts and fibroblasts. Cancer Res 2004; 64: 8492-5. Kohan M, Muro AF, White ES, Berkman N. EDA-containing cellular fibronectin induces fibroblast differentiation through binding to α4β7 integrin receptor and MAPK/Erk 1/2-dependent signaling. FASEB J 2010; 24: 4503-12. Schäfer M, Werner S. Cancer as an overhealing wound: an old hypothesis revisited. Nat Rev Mol Cell Biol 2008; 9: 628-38. Forbes SJ, Russo FP, Rey V, Burra P, Rugge M, Wright NA, Alison MR. A significant proportion of myofibroblasts are of bone marrow origin in human liver fibrosis. Gastroenterology 2004; 126: 955-63. Higashiyama R, Nakao S, Shibusawa Y, Ishikawa O, Moro T, Mikami K, Fukumitsu H, Ueda Y, Minakawa K, Tabata Y, Bou-Gharios G, Inagaki Y. Differential contribution of dermal resident and bone marrow-derived cells to collagen production during wound healing and fibrogenesis in mice. J Invest Dermatol 2011; 131: 529-36. Wells RG. The role of matrix stiffness in regulating cell behavior. Hepatology 2008; 47: 1394-400. Lataillade JJ, Doucet C, Bey E, Carsin H, Huet C, Clairand I, Bottollier-Depois JF, Chapel A, Ernou I, Gourven M, Boutin L, Hayden A, Carcamo C, Buglova E, Joussemet M, de Revel T, Gourmelon P. New approach to radiation burn treatment by dosimetry-guided surgery combined with autologous mesenchymal stem cell therapy. Regen Med 2007; 2: 785-94. Rajkumar VS, Howell K, Csiszar K, Denton CP, Black CM, Abraham DJ. Shared expression of phenotypic markers in systemic sclerosis indicates a convergence of pericytes and fibroblasts to a myofibroblast lineage in fibrosis. Arthritis Res Ther 2005; 7: R1113-23. Radisky DC, Kenny PA, Bissell MJ. Fibrosis and cancer: do myofibroblasts come also from epithelial cells via EMT? J Cell Biochem 2007; 101: 830-9. Abe R, Donnelly SC, Peng T, Bucala R, Metz CN. Peripheral blood fibrocytes: differentiation pathway and migration to wound sites. J Immunol 2001; 166: 7556-62. Hakvoort TE, Altun V, Ramrattan RS, van der Kwast TH, Benner R, van Zuijlen PP, Vloemans AF, Prens EP. Epidermal participation in post-burn hypertrophic scar development. Virchows Arch 1999; 434: 221-6. Le Blanc K, Ringdén O. Mesenchymal stem cells: properties and role in clinical bone marrow transplantation. Curr Opin Immunol 2006; 18: 586-91. Hattori N, Mochizuki S, Kishi K, Nakajima T, Takaishi H, D'Armiento J, Okada Y. MMP-13 plays a role in keratinocyte migration, angiogenesis, and contraction in mouse skin wound healing. Am J Pathol 2009; 175: 533-46. Hinz B, Gabbiani G. Mechanisms of force generation and transmission by myofibroblasts. Curr Opin Biotechnol 2003; 14: 538-46. Jahoda C, Reynolds A. Hair follicle dermal sheath cells: unsung participants in wound healing. Lancet 2001; 358: 1445-8. Akaishi S, Ogawa R, Hyakusoku H. Keloid and hypertrophic scar: neurogenic inflammation hypotheses. Med Hypotheses 2008; 71: 32-8. Costa AMA, Peyrol S, Porto LC, Comparin JP, Foyatier JL, Desmoulière A. Mechanical forces induce scar remodeling. Study in non-pressure-treated versus pressure-treated hypertrophic scars. Am J Pathol 1999; 155: 1671-9. Lee JY, Yang CC, Chao SC, Wong TW. Histopathological differential diagnosis of keloid and hypertrophic scar. Am J Dermatopathol 2004; 26: 379-84. Guyot C, Lepreux S, Combe C, Doudnikoff E, Bioulac-Sage P, Balabaud C, Desmoulière A. Hepatic fibrosis and cirrhosis: the (myo)fibroblastic cell subpopulations involved. Int J Biochem Cell Biol 2006; 38: 135-51. Hinz B. The myofibroblast: paradigm for a mechanically active cell. J Biomech 2010; 43: 146-55. Serini G, Bochaton-Piallat ML, Ropraz P, Geinoz A, Borsi L, Zardi L, Gabbiani G. The fibronectin domain ED-A is crucial for myofibroblastic phenotype induction by transforming growth factor-b1. J Cell Biol 1998; 142: 873-81. Ishii G, Sangai T, Oda T, Aoyagi Y, Hasebe T, Kanomata N, Endoh Y, Okumura C, Okuhara Y, Magae J, Emura M, Ochiva T, Ochiai A. Bone-marrow-derived myofibroblasts contribute to the cancer-induced stromal reaction. Biochem Biophys Res Commun 2003; 309: 232-40. Sugimoto H, Mundel TM, Kieran MW, Kalluri R. Identification of fibroblast heterogeneity in the tumor microenvironment. Cancer Biol Ther 2006; 5: 1640-6. Silver J, Miller JH. Regeneration beyond the glial scar. Nat Rev Neurosci 2004; 5: 146-56. Rajkumar VS, Shiwen X, Bostrom M, Leoni P, Muddle J, Ivarsson M, Gerdin B, Denton CP, Bou-Gharios G, Black CM, Abraham DJ. Platelet-derived growth factor-beta receptor activation is essential for fibroblast and pericyte recruitment during cutaneous wound healing. Am J Pathol 2006; 169: 2254-65. Hinz B, Gabbiani G, Chaponnier C. The NH2-terminal peptide of alpha-smooth muscle actin inhibits force generation by the myofibroblast in vitro and in vivo. J Cell Biol 2002; 157: 657-63. Aarabi S, Bhatt KA, Shi Y, Paterno J, Chang EI, Loh SA, Holmes JW, Longaker MT, Yee H, Gurtner GC. Mechanical load initiates hypertrophic scar formation through decreased cellular apoptosis. FASEB J 2007; 21: 3250-61. De Wever O, Demetter P, Mareel M, Bracke M. Stromal myofibroblasts are drivers of invasive cancer growth. Int J Cancer 2008; 123: 2229-38. Orimo A, Weinberg RA. Heterogeneity of stromal fibroblasts in tumors. Cancer Biol Ther 2007; 6: 618-9. Dabiri G, Tumbarello DA, Turner CE, Van de Water L. Hic-5 promotes the hypertrophic scar myofibroblast phenotype by regulating the TGF-beta1 autocrine loop. J Invest Dermatol 2008; 128: 2518-25. Potenta S, Zeisberg E, Kalluri R. The role of endothelial-to-mesenchymal transition in cancer progression. Br J Cancer 2008; 99: 1375-9. Darby IA, Bisucci T, Pittet B, Garbin S, Gabbiani G, Desmoulière A. Skin flap induced regression of granulation tissue correlates with reduced growth factor and increased metalloproteinase expression. J Pathol 2002; 197: 117-27. Hinz B, Mastrangelo D, Iselin CE, Chaponnier C, Gabbiani G. Mechanical tension controls granulation tissue contractile activity and myofibroblast differentiation. Am J Pathol 2001; 159: 1009-20. Gurtner GC, Werner S, Barrandon Y, Longaker MT. Wound repair and regeneration. Nature 2008; 453: 314-21. Ehrlich HP, Desmoulière A, Diegelmann RF, Cohen IK, Compton CC, Garner WL, Kapanci Y, Gabbiani G. Morphological and immunochemical differences between keloid and hypertrophic scar. Am J Pathol 1994; 145: 105-13. van den Bogaerdt AJ, van der Veen VC, van Zuijlen PPM, Reijnen L, Verkerk M, Bank RA, Middelkoop E, Ulrich MMW. Collagen cross-linking by adipose-derived mesenchymal stromal cells and scar-derived mesenchymal cells: are mesenchymal stromal cells involved in scar formation? Wound Rep Regen 2009; 17: 548-58. Werner S, Grose R. Regulation of wound healing by growth factors and cytokines. Physiol Rev 2003; 83: 835-70. Ulrich MMW, Verkerk M, Reijnen L, Vlig M, van den Bogaerdt AJ, Middelkoop E. Expression profile of proteins involved in scar formation in the healing process of full-thickness excisional wounds in the porcine model. Wound Rep Regen 2007; 15: 482-90. Nurden AT, Nurden P, Sanchez M, Andia I, Anitua E. Platelets and wound healing. Front Biosci 2008; 13: 3532-48. Xi-Qiao W, Ying-Kai L, Chun Q, Shu-Liang L. Hyperactivity of fibroblasts and functional regression of endothelial cells contribute to microvessel occlusion in hypertrophic scarring. Microvasc Res 2009; 77: 204-11. Sorrell JM, Caplan AI. Fibroblast heterogeneity: more than skin deep. J Cell Sci 2004; 117: 667-75. 2007; 101 2004; 64 2004; 126 2002; 197 2010; 18 2006; 38 2002; 157 2004; 26 2008; 9 2003; 14 2004; 5 2008; 71 1993; 122 1994; 145 2010; 24 2007; 6 2007; 2 2003; 83 2007; 21 2006; 169 2009; 17 2001; 166 2007; 127 2008; 19 2005; 118 2006; 5 2006; 18 2008; 13 2008; 128 2008; 99 2009; 175 2008; 123 2007; 15 2009; 77 2003; 309 2010; 43 2005; 19 2008; 47 2005; 206 2005; 7 1995; 146 1999; 155 2008; 453 1999; 434 2004; 117 2001; 159 1998; 142 2005; 13 2001; 358 Le Blanc K (e_1_2_5_51_2) 2006; 18 e_1_2_5_27_2 e_1_2_5_48_2 e_1_2_5_25_2 e_1_2_5_46_2 Jahoda C (e_1_2_5_21_2) 2001; 358 e_1_2_5_23_2 e_1_2_5_44_2 e_1_2_5_42_2 e_1_2_5_29_2 e_1_2_5_40_2 Guyot C (e_1_2_5_39_2) 2006; 38 Verhaegen PDHM (e_1_2_5_28_2) 2009; 17 e_1_2_5_13_2 e_1_2_5_38_2 e_1_2_5_9_2 e_1_2_5_36_2 Sorrell JM (e_1_2_5_16_2) 2004; 117 e_1_2_5_34_2 e_1_2_5_5_2 e_1_2_5_11_2 e_1_2_5_32_2 Desmoulière A (e_1_2_5_7_2) 1995; 146 e_1_2_5_17_2 e_1_2_5_19_2 van den Bogaerdt AJ (e_1_2_5_22_2) 2009; 17 Radisky DC (e_1_2_5_20_2) 2007; 101 e_1_2_5_30_2 Higashiyama R (e_1_2_5_15_2) e_1_2_5_49_2 e_1_2_5_47_2 e_1_2_5_45_2 Hinz B. (e_1_2_5_4_2) 2010; 43 e_1_2_5_43_2 Nurden AT (e_1_2_5_3_2) 2008; 13 Schäfer M (e_1_2_5_41_2) 2008; 9 Bellemare J (e_1_2_5_35_2) 2005; 206 e_1_2_5_14_2 e_1_2_5_37_2 e_1_2_5_8_2 e_1_2_5_10_2 e_1_2_5_33_2 e_1_2_5_6_2 e_1_2_5_12_2 e_1_2_5_31_2 e_1_2_5_2_2 e_1_2_5_18_2 e_1_2_5_52_2 Abe R (e_1_2_5_24_2) 2001; 166 e_1_2_5_50_2 Ehrlich HP (e_1_2_5_26_2) 1994; 145 |
| References_xml | – reference: Kohan M, Muro AF, White ES, Berkman N. EDA-containing cellular fibronectin induces fibroblast differentiation through binding to α4β7 integrin receptor and MAPK/Erk 1/2-dependent signaling. FASEB J 2010; 24: 4503-12. – reference: Sugimoto H, Mundel TM, Kieran MW, Kalluri R. Identification of fibroblast heterogeneity in the tumor microenvironment. Cancer Biol Ther 2006; 5: 1640-6. – reference: Serini G, Bochaton-Piallat ML, Ropraz P, Geinoz A, Borsi L, Zardi L, Gabbiani G. The fibronectin domain ED-A is crucial for myofibroblastic phenotype induction by transforming growth factor-b1. J Cell Biol 1998; 142: 873-81. – reference: Werner S, Krieg T, Smola H. Keratinocyte-fibroblast interactions in wound healing. J Invest Dermatol 2007; 127: 998-1008. – reference: Jahoda C, Reynolds A. Hair follicle dermal sheath cells: unsung participants in wound healing. Lancet 2001; 358: 1445-8. – reference: van den Bogaerdt AJ, van der Veen VC, van Zuijlen PPM, Reijnen L, Verkerk M, Bank RA, Middelkoop E, Ulrich MMW. Collagen cross-linking by adipose-derived mesenchymal stromal cells and scar-derived mesenchymal cells: are mesenchymal stromal cells involved in scar formation? Wound Rep Regen 2009; 17: 548-58. – reference: Verhaegen PDHM, van Zuijlen PPM, Pennings NM, van Marle J, Niessen FB, van der Horst CMAM, Middelkoop E. Differences in collagen architecture between keloid, hypertrophic scar, normotrophic scar, and normal skin: an objective histopathological analysis. Wound Rep Regen 2009; 17: 649-56. – reference: Direkze NC, Hodivala-Dilke K, Jeffery R, Hunt T, Poulsom R, Oukrif D, Alison MR, Wright NA. Bone marrow contribution to tumor-associated myofibroblasts and fibroblasts. Cancer Res 2004; 64: 8492-5. – reference: Hinz B, Mastrangelo D, Iselin CE, Chaponnier C, Gabbiani G. Mechanical tension controls granulation tissue contractile activity and myofibroblast differentiation. Am J Pathol 2001; 159: 1009-20. – reference: Ishii G, Sangai T, Oda T, Aoyagi Y, Hasebe T, Kanomata N, Endoh Y, Okumura C, Okuhara Y, Magae J, Emura M, Ochiva T, Ochiai A. Bone-marrow-derived myofibroblasts contribute to the cancer-induced stromal reaction. Biochem Biophys Res Commun 2003; 309: 232-40. – reference: Aarabi S, Bhatt KA, Shi Y, Paterno J, Chang EI, Loh SA, Holmes JW, Longaker MT, Yee H, Gurtner GC. Mechanical load initiates hypertrophic scar formation through decreased cellular apoptosis. FASEB J 2007; 21: 3250-61. – reference: Sorrell JM, Caplan AI. Fibroblast heterogeneity: more than skin deep. J Cell Sci 2004; 117: 667-75. – reference: Ng CP, Hinz B, Swartz MA. Interstitial fluid flow induces myofibroblast differentiation and collagen alignment in vitro. J Cell Sci 2005; 118: 4731-9. – reference: Higashiyama R, Nakao S, Shibusawa Y, Ishikawa O, Moro T, Mikami K, Fukumitsu H, Ueda Y, Minakawa K, Tabata Y, Bou-Gharios G, Inagaki Y. Differential contribution of dermal resident and bone marrow-derived cells to collagen production during wound healing and fibrogenesis in mice. J Invest Dermatol 2011; 131: 529-36. – reference: Darby IA, Bisucci T, Pittet B, Garbin S, Gabbiani G, Desmoulière A. Skin flap induced regression of granulation tissue correlates with reduced growth factor and increased metalloproteinase expression. J Pathol 2002; 197: 117-27. – reference: Ehrlich HP, Desmoulière A, Diegelmann RF, Cohen IK, Compton CC, Garner WL, Kapanci Y, Gabbiani G. Morphological and immunochemical differences between keloid and hypertrophic scar. Am J Pathol 1994; 145: 105-13. – reference: Hinz B, Gabbiani G. Mechanisms of force generation and transmission by myofibroblasts. Curr Opin Biotechnol 2003; 14: 538-46. – reference: Dabiri G, Tumbarello DA, Turner CE, Van de Water L. Hic-5 promotes the hypertrophic scar myofibroblast phenotype by regulating the TGF-beta1 autocrine loop. J Invest Dermatol 2008; 128: 2518-25. – reference: Silver J, Miller JH. Regeneration beyond the glial scar. Nat Rev Neurosci 2004; 5: 146-56. – reference: Hinz B. The myofibroblast: paradigm for a mechanically active cell. J Biomech 2010; 43: 146-55. – reference: De Wever O, Demetter P, Mareel M, Bracke M. Stromal myofibroblasts are drivers of invasive cancer growth. Int J Cancer 2008; 123: 2229-38. – reference: Bellemare J, Roberge CJ, Bergeron D, Lopez-Vallé CA, Roy M, Moulin VJ. Epidermis promotes dermal fibrosis: role in the pathogenesis of hypertrophic scars. J Pathol 2005; 206: 1-8. – reference: Rajkumar VS, Howell K, Csiszar K, Denton CP, Black CM, Abraham DJ. Shared expression of phenotypic markers in systemic sclerosis indicates a convergence of pericytes and fibroblasts to a myofibroblast lineage in fibrosis. Arthritis Res Ther 2005; 7: R1113-23. – reference: Xi-Qiao W, Ying-Kai L, Chun Q, Shu-Liang L. Hyperactivity of fibroblasts and functional regression of endothelial cells contribute to microvessel occlusion in hypertrophic scarring. Microvasc Res 2009; 77: 204-11. – reference: Radisky DC, Kenny PA, Bissell MJ. Fibrosis and cancer: do myofibroblasts come also from epithelial cells via EMT? J Cell Biochem 2007; 101: 830-9. – reference: Rajkumar VS, Shiwen X, Bostrom M, Leoni P, Muddle J, Ivarsson M, Gerdin B, Denton CP, Bou-Gharios G, Black CM, Abraham DJ. Platelet-derived growth factor-beta receptor activation is essential for fibroblast and pericyte recruitment during cutaneous wound healing. Am J Pathol 2006; 169: 2254-65. – reference: Opalenik SR, Davidson JM. Fibroblast differentiation of bone marrow-derived cells during wound repair. FASEB J 2005; 19: 1561-3. – reference: Nurden AT, Nurden P, Sanchez M, Andia I, Anitua E. Platelets and wound healing. Front Biosci 2008; 13: 3532-48. – reference: Guyot C, Lepreux S, Combe C, Doudnikoff E, Bioulac-Sage P, Balabaud C, Desmoulière A. Hepatic fibrosis and cirrhosis: the (myo)fibroblastic cell subpopulations involved. Int J Biochem Cell Biol 2006; 38: 135-51. – reference: Abe R, Donnelly SC, Peng T, Bucala R, Metz CN. Peripheral blood fibrocytes: differentiation pathway and migration to wound sites. J Immunol 2001; 166: 7556-62. – reference: Costa AMA, Peyrol S, Porto LC, Comparin JP, Foyatier JL, Desmoulière A. Mechanical forces induce scar remodeling. Study in non-pressure-treated versus pressure-treated hypertrophic scars. Am J Pathol 1999; 155: 1671-9. – reference: Lee JY, Yang CC, Chao SC, Wong TW. Histopathological differential diagnosis of keloid and hypertrophic scar. Am J Dermatopathol 2004; 26: 379-84. – reference: Hattori N, Mochizuki S, Kishi K, Nakajima T, Takaishi H, D'Armiento J, Okada Y. MMP-13 plays a role in keratinocyte migration, angiogenesis, and contraction in mouse skin wound healing. Am J Pathol 2009; 175: 533-46. – reference: Forbes SJ, Russo FP, Rey V, Burra P, Rugge M, Wright NA, Alison MR. A significant proportion of myofibroblasts are of bone marrow origin in human liver fibrosis. Gastroenterology 2004; 126: 955-63. – reference: Lataillade JJ, Doucet C, Bey E, Carsin H, Huet C, Clairand I, Bottollier-Depois JF, Chapel A, Ernou I, Gourven M, Boutin L, Hayden A, Carcamo C, Buglova E, Joussemet M, de Revel T, Gourmelon P. New approach to radiation burn treatment by dosimetry-guided surgery combined with autologous mesenchymal stem cell therapy. Regen Med 2007; 2: 785-94. – reference: Ulrich MMW, Verkerk M, Reijnen L, Vlig M, van den Bogaerdt AJ, Middelkoop E. Expression profile of proteins involved in scar formation in the healing process of full-thickness excisional wounds in the porcine model. Wound Rep Regen 2007; 15: 482-90. – reference: Akaishi S, Ogawa R, Hyakusoku H. Keloid and hypertrophic scar: neurogenic inflammation hypotheses. Med Hypotheses 2008; 71: 32-8. – reference: Potenta S, Zeisberg E, Kalluri R. The role of endothelial-to-mesenchymal transition in cancer progression. Br J Cancer 2008; 99: 1375-9. – reference: Gallant-Behm CL, Mustoe TA. Occlusion regulates epidermal cytokine production and inhibits scar formation. Wound Rep Regen 2010; 18: 235-44. – reference: Wells RG. The role of matrix stiffness in regulating cell behavior. Hepatology 2008; 47: 1394-400. – reference: Hakvoort TE, Altun V, Ramrattan RS, van der Kwast TH, Benner R, van Zuijlen PP, Vloemans AF, Prens EP. Epidermal participation in post-burn hypertrophic scar development. Virchows Arch 1999; 434: 221-6. – reference: Schäfer M, Werner S. Cancer as an overhealing wound: an old hypothesis revisited. Nat Rev Mol Cell Biol 2008; 9: 628-38. – reference: Gurtner GC, Werner S, Barrandon Y, Longaker MT. Wound repair and regeneration. Nature 2008; 453: 314-21. – reference: Noël A, Jost M, Maquoi E. Matrix metalloproteinases at cancer tumor-host interface. Semin Cell Dev Biol 2008; 19: 52-60. – reference: Hinz B, Gabbiani G, Chaponnier C. The NH2-terminal peptide of alpha-smooth muscle actin inhibits force generation by the myofibroblast in vitro and in vivo. J Cell Biol 2002; 157: 657-63. – reference: Desmoulière A, Geinoz A, Gabbiani F, Gabbiani G. Transforming growth factor-β1 induces α-smooth muscle actin expression in granulation tissue myofibroblasts and in quiescent and growing cultured fibroblasts. J Cell Biol 1993; 122: 103-11. – reference: Werner S, Grose R. Regulation of wound healing by growth factors and cytokines. Physiol Rev 2003; 83: 835-70. – reference: Yang L, Scott PG, Dodd C, Medina A, Jiao H, Shankowsky HA, Ghahary A, Tredget EE. Identification of fibrocytes in postburn hypertrophic scar. Wound Rep Regen 2005; 13: 398-404. – reference: Desmoulière A, Redard M, Darby IA, Gabbiani G. Apoptosis mediates the decrease in cellularity during the transition between granulation tissue and scar. Am J Pathol 1995; 146: 55-66. – reference: Le Blanc K, Ringdén O. Mesenchymal stem cells: properties and role in clinical bone marrow transplantation. Curr Opin Immunol 2006; 18: 586-91. – reference: Orimo A, Weinberg RA. Heterogeneity of stromal fibroblasts in tumors. Cancer Biol Ther 2007; 6: 618-9. – volume: 197 start-page: 117 year: 2002 end-page: 27 article-title: Skin flap induced regression of granulation tissue correlates with reduced growth factor and increased metalloproteinase expression publication-title: J Pathol – volume: 47 start-page: 1394 year: 2008 end-page: 400 article-title: The role of matrix stiffness in regulating cell behavior publication-title: Hepatology – volume: 17 start-page: 649 year: 2009 end-page: 56 article-title: Differences in collagen architecture between keloid, hypertrophic scar, normotrophic scar, and normal skin publication-title: an objective histopathological analysis – volume: 453 start-page: 314 year: 2008 end-page: 21 article-title: Wound repair and regeneration publication-title: Nature – volume: 17 start-page: 548 year: 2009 end-page: 58 article-title: Collagen cross‐linking by adipose‐derived mesenchymal stromal cells and scar‐derived mesenchymal cells publication-title: are mesenchymal stromal cells involved in scar formation? – volume: 26 start-page: 379 year: 2004 end-page: 84 article-title: Histopathological differential diagnosis of keloid and hypertrophic scar publication-title: Am J Dermatopathol – volume: 99 start-page: 1375 year: 2008 end-page: 9 article-title: The role of endothelial‐to‐mesenchymal transition in cancer progression publication-title: Br J Cancer – volume: 145 start-page: 105 year: 1994 end-page: 13 article-title: Morphological and immunochemical differences between keloid and hypertrophic scar publication-title: Am J Pathol – volume: 126 start-page: 955 year: 2004 end-page: 63 article-title: A significant proportion of myofibroblasts are of bone marrow origin in human liver fibrosis publication-title: Gastroenterology – volume: 15 start-page: 482 year: 2007 end-page: 90 article-title: Expression profile of proteins involved in scar formation in the healing process of full‐thickness excisional wounds in the porcine model publication-title: Wound Rep Regen – volume: 309 start-page: 232 year: 2003 end-page: 40 article-title: Bone‐marrow‐derived myofibroblasts contribute to the cancer‐induced stromal reaction publication-title: Biochem Biophys Res Commun – volume: 18 start-page: 586 year: 2006 end-page: 91 article-title: Mesenchymal stem cells publication-title: properties and role in clinical bone marrow transplantation – volume: 43 start-page: 146 year: 2010 end-page: 55 article-title: The myofibroblast publication-title: paradigm for a mechanically active cell – volume: 38 start-page: 135 year: 2006 end-page: 51 article-title: Hepatic fibrosis and cirrhosis publication-title: the (myo)fibroblastic cell subpopulations involved – volume: 19 start-page: 52 year: 2008 end-page: 60 article-title: Matrix metalloproteinases at cancer tumor–host interface publication-title: Semin Cell Dev Biol – volume: 157 start-page: 657 year: 2002 end-page: 63 article-title: The NH2‐terminal peptide of alpha‐smooth muscle actin inhibits force generation by the myofibroblast in vitro and in vivo publication-title: J Cell Biol – volume: 9 start-page: 628 year: 2008 end-page: 38 article-title: Cancer as an overhealing wound publication-title: an old hypothesis revisited – volume: 175 start-page: 533 year: 2009 end-page: 46 article-title: MMP‐13 plays a role in keratinocyte migration, angiogenesis, and contraction in mouse skin wound healing publication-title: Am J Pathol – volume: 18 start-page: 235 year: 2010 end-page: 44 article-title: Occlusion regulates epidermal cytokine production and inhibits scar formation publication-title: Wound Rep Regen – volume: 14 start-page: 538 year: 2003 end-page: 46 article-title: Mechanisms of force generation and transmission by myofibroblasts publication-title: Curr Opin Biotechnol – volume: 122 start-page: 103 year: 1993 end-page: 11 article-title: Transforming growth factor‐β1 induces α‐smooth muscle actin expression in granulation tissue myofibroblasts and in quiescent and growing cultured fibroblasts 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Myofibroblasts play a key role in the wound‐healing process, promoting wound closure and matrix deposition. These cells normally disappear from... Myofibroblasts play a key role in the wound‐healing process, promoting wound closure and matrix deposition. These cells normally disappear from granulation... Myofibroblasts play a key role in the wound-healing process, promoting wound closure and matrix deposition. These cells normally disappear from granulation... |
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| SubjectTerms | Cicatrix - physiopathology Cicatrix, Hypertrophic - physiopathology Granulation Tissue - physiology Humans Keloid - physiopathology Liver - physiopathology Myofibroblasts - cytology Myofibroblasts - physiology Neoplasms - physiopathology Stress, Mechanical Transforming Growth Factor beta1 - physiology Wound Healing - physiology |
| Title | Mechanisms of pathological scarring: Role of myofibroblasts and current developments |
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