細胞外マトリックスから見たケロイド
ケロイドは，細胞増殖が主体の腫瘍とは異なり，細胞外マトリックスの増殖を主体とした病変と考えられている。皮膚の細胞外マトリックスは，コラーゲン，ヒアルロン酸，プロテオグリカンが主体となっている。ケロイド病変部では，特徴的なコラーゲン線維の束やヒアルロン酸の分布が正常部とは異なることが報告されている。また，プロテオグリカンの構成成分であるグリコサミノグリカン（GAG）の過剰蓄積，弾性線維の減少・消失が報告されているが，ケロイドの病態形成との関連は，いまだ解明されていない。今後細胞外マトリックスの異常そのものが，どのようにケロイドの病態形成にかかわっているかを解明し，細胞外マトリックスの産生・代謝を...
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| Published in | 創傷 Vol. 5; no. 2; pp. 51 - 55 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | Japanese |
| Published |
一般社団法人 日本創傷外科学会
2014
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1884-880X |
| DOI | 10.11310/jsswc.5.51 |
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| Abstract | ケロイドは，細胞増殖が主体の腫瘍とは異なり，細胞外マトリックスの増殖を主体とした病変と考えられている。皮膚の細胞外マトリックスは，コラーゲン，ヒアルロン酸，プロテオグリカンが主体となっている。ケロイド病変部では，特徴的なコラーゲン線維の束やヒアルロン酸の分布が正常部とは異なることが報告されている。また，プロテオグリカンの構成成分であるグリコサミノグリカン（GAG）の過剰蓄積，弾性線維の減少・消失が報告されているが，ケロイドの病態形成との関連は，いまだ解明されていない。今後細胞外マトリックスの異常そのものが，どのようにケロイドの病態形成にかかわっているかを解明し，細胞外マトリックスの産生・代謝を制御することで，ケロイド治療法の開発に発展していく可能性があると考えられる。 |
|---|---|
| AbstractList | ケロイドは，細胞増殖が主体の腫瘍とは異なり，細胞外マトリックスの増殖を主体とした病変と考えられている。皮膚の細胞外マトリックスは，コラーゲン，ヒアルロン酸，プロテオグリカンが主体となっている。ケロイド病変部では，特徴的なコラーゲン線維の束やヒアルロン酸の分布が正常部とは異なることが報告されている。また，プロテオグリカンの構成成分であるグリコサミノグリカン（GAG）の過剰蓄積，弾性線維の減少・消失が報告されているが，ケロイドの病態形成との関連は，いまだ解明されていない。今後細胞外マトリックスの異常そのものが，どのようにケロイドの病態形成にかかわっているかを解明し，細胞外マトリックスの産生・代謝を制御することで，ケロイド治療法の開発に発展していく可能性があると考えられる。 |
| Author | 荒牧, 典子 岡部, 圭介 磯貝, 善蔵 貴志, 和生 |
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| References | 20) Sible JC, Retting WJ, Eriksson E, et al : Gene expression of tenascin is altered in normal scars and keloids. Wound Repair Regen, 1995 ; 3 : 37-48. 11) Phan TT, Lim IJ, Aalami O, et al : Smad3 signaling plays an important role in keloid pathogenesis via epithelial-mesenchymal interaction. J Pathol, 2005 ; 207 : 232-42. 4) Luo S, Benathan M, Raffoul W, et al : Abnormal balance between proliferation and apoptotic cell death in fibroblasts derived from keloid lesions. Plast Reconstr Surg, 2001 ; 107 : 87-96. 14) Ikeda M, Naitoh M, Kubota H, et al : Elastic fiber assembly is disrupted by excessive accumulation of chondroitin sulfate in the human dermal fibrotic disease, keloid. Biochem Biophys Res Commun, 2009 ; 390 : 1221-8. 3) Chodon T, Sugihara T, Igawa HH, et al : Keloid-derived fibroblasts are refractory to Fas-mediated apoptosis and neutralization of autocrine transforming growth factor-β1 can abrogate this resistance. Am J Pathol, 2000 ; 157 : 1661-9. 9) Ulrich D, Ulrich F, Unglaub F, et al : Matrix metalloproteinases and tissue inhibitors of metalloproteinases in patients with different types of scars and keloids. J Plast Reconstr Aesthet Surg, 2010 ; 63 : 1015-21. 1) Smith LT, Holbrook KA, Madri JA : Collagen types I, III, and V in human embryonic and fetal skin. Am J Anat, 1986; 175 : 507-21. 24) 荒牧典子, 磯貝善蔵, 岡部圭介, ほか : ケロイド組織における細胞外マトリックスの産生・分解. 瘢痕・ケロイド治療ジャーナル, 2013 ; 7 : 5-7. 25) Honardoust D, Eslami A, Larjava H, et al : Localization of small leucine-rich proteoglycans and transforming growth factor-beta in human oral mucosal wound healing. Wound Repair Regen, 2008 ; 16 : 814-23. 5) Sasaki T, Majamaa K, Uitto J : Reduction of collagen production in keloid fibroblast cultures by ethyl-3, 4-dihydroxybenzoate. Inhibition of prolyl hydroxylase activity as a mechanism of action. J Biol Chem, 1987 ; 262 : 9397-403. 8) Neely AN, Clendening CE, Gardner J, et al : Gelatinase activity in keloids and hypertrophic scars. Wound Repair Regen, 1999 ; 7 : 166-71. 13) Meyer LJ, Russell SB, Russell JD, et al : Reduced hyaluronan in keloid tissue and cultured keloid fibroblasts. J Invest Dermatol, 2000 ; 114 : 953-9. 21) Yagi Y, Muroga E, Naitoh M, et al : An ex vivo model employing keloid-derived cell-seeded collagen sponges for therapy development. J Invest Dermatol, 2013 ; 133 : 386-93. 15) Amadeu TP, Braune AS, Porto LC, et al : Fibrillin-1 and elastin are differentially expressed in hypertrophic scars and keloids. Wound Repair Regen, 2004 ; 12 : 169-74. 26) Meenakshi J, Vidyameenakshi S, Ananthram D, et al : Low decorin expression along with inherent activation of ERK1, 2 in ear lobe keloids. Burns, 2009 ; 35 : 519-26. 23) Enomoto H, Nelson CM, Somerville RP, et al : Cooperation of two ADAMTS metalloproteases in closure of the mouse palate identifies a requirement for versican proteolysis in regulating palatal mesenchyme proliferation. Development, 2010 ; 137 : 4029-38. 7) Khasigov PZ, Podobed OV, Ktzoeva SA, et al : Matrix metalloproteinases of normal human tissues. Biochemistry (Mosc), 2001 ; 66 : 130-40. 16) Babu M, Diegelmann R, Oliver N : Fibronectin is overproduced by keloid fibroblasts during abnormal wound healing. Mol Cell Biol, 1989 ; 9 : 1642-50. 2) Bran GM, Goessler UR, Hormann K, et al : Keloids : Current concepts of pathogenesis (review). Int J Mol Med, 2009 ; 24 : 283-93. 12) Meran S, Thomas DW, Stephens P, et al : Hyaluronan facilitates transforming growth factor-beta1-mediated fibroblast proliferation. J Biol Chem, 2008 ; 283 : 6530-45. 17) Kischer CW, Hendrix MJ : Fibronectin (FN) in hypertrophic scars and keloids. Cell Tissue Res, 1983 ; 231 : 29-37. 10) Aoki M, Miyake K, Ogawa R, et al : siRNA Knockdown of Tissue Inhibitor of Metalloproteinase-1 in Keloid Fibroblasts Leads to Degradation of Collagen Type I. J Invest Dermatol, 2013 Sep 16. doi : 10. 1038/jid. 2013. 396. 18) Kischer CW, Wagner HN Jr, Pindur J, et al : Increased fibronectin production by cell lines from hypertrophic scar and keloid. Connect Tissue Res, 1989 ; 23 : 279-88. 22) McCulloch DR, Nelson CM, Dixon LJ, et al : ADAMTS metalloproteases generate active versican fragments that regulate interdigital web regression. Dev Cell, 2009 ; 17 : 687-98. 6) Burd A, Huang L : Hypertrophic response and keloid diathesis : two very different forms of scar. Plast Reconstr Surg, 2005 ; 116 : 150e-157e. 19) Dalkowski A, Schuppan D, Orfanos CE, et al : Increased expression of tenascin C by keloids in vivo and in vitro. Br J Dermatol, 1999 ; 141 : 50-6. 27) Sayani K, Dodd CM, Nedelec B, et al : Delayed appearance of decorin in healing burn scars. Histopathology, 2000 ; 36 : 262-72. |
| References_xml | – reference: 10) Aoki M, Miyake K, Ogawa R, et al : siRNA Knockdown of Tissue Inhibitor of Metalloproteinase-1 in Keloid Fibroblasts Leads to Degradation of Collagen Type I. J Invest Dermatol, 2013 Sep 16. doi : 10. 1038/jid. 2013. 396. – reference: 21) Yagi Y, Muroga E, Naitoh M, et al : An ex vivo model employing keloid-derived cell-seeded collagen sponges for therapy development. J Invest Dermatol, 2013 ; 133 : 386-93. – reference: 9) Ulrich D, Ulrich F, Unglaub F, et al : Matrix metalloproteinases and tissue inhibitors of metalloproteinases in patients with different types of scars and keloids. J Plast Reconstr Aesthet Surg, 2010 ; 63 : 1015-21. – reference: 8) Neely AN, Clendening CE, Gardner J, et al : Gelatinase activity in keloids and hypertrophic scars. Wound Repair Regen, 1999 ; 7 : 166-71. – reference: 15) Amadeu TP, Braune AS, Porto LC, et al : Fibrillin-1 and elastin are differentially expressed in hypertrophic scars and keloids. Wound Repair Regen, 2004 ; 12 : 169-74. – reference: 12) Meran S, Thomas DW, Stephens P, et al : Hyaluronan facilitates transforming growth factor-beta1-mediated fibroblast proliferation. J Biol Chem, 2008 ; 283 : 6530-45. – reference: 26) Meenakshi J, Vidyameenakshi S, Ananthram D, et al : Low decorin expression along with inherent activation of ERK1, 2 in ear lobe keloids. Burns, 2009 ; 35 : 519-26. – reference: 18) Kischer CW, Wagner HN Jr, Pindur J, et al : Increased fibronectin production by cell lines from hypertrophic scar and keloid. Connect Tissue Res, 1989 ; 23 : 279-88. – reference: 23) Enomoto H, Nelson CM, Somerville RP, et al : Cooperation of two ADAMTS metalloproteases in closure of the mouse palate identifies a requirement for versican proteolysis in regulating palatal mesenchyme proliferation. Development, 2010 ; 137 : 4029-38. – reference: 25) Honardoust D, Eslami A, Larjava H, et al : Localization of small leucine-rich proteoglycans and transforming growth factor-beta in human oral mucosal wound healing. Wound Repair Regen, 2008 ; 16 : 814-23. – reference: 11) Phan TT, Lim IJ, Aalami O, et al : Smad3 signaling plays an important role in keloid pathogenesis via epithelial-mesenchymal interaction. J Pathol, 2005 ; 207 : 232-42. – reference: 1) Smith LT, Holbrook KA, Madri JA : Collagen types I, III, and V in human embryonic and fetal skin. Am J Anat, 1986; 175 : 507-21. – reference: 6) Burd A, Huang L : Hypertrophic response and keloid diathesis : two very different forms of scar. Plast Reconstr Surg, 2005 ; 116 : 150e-157e. – reference: 7) Khasigov PZ, Podobed OV, Ktzoeva SA, et al : Matrix metalloproteinases of normal human tissues. Biochemistry (Mosc), 2001 ; 66 : 130-40. – reference: 16) Babu M, Diegelmann R, Oliver N : Fibronectin is overproduced by keloid fibroblasts during abnormal wound healing. Mol Cell Biol, 1989 ; 9 : 1642-50. – reference: 27) Sayani K, Dodd CM, Nedelec B, et al : Delayed appearance of decorin in healing burn scars. Histopathology, 2000 ; 36 : 262-72. – reference: 19) Dalkowski A, Schuppan D, Orfanos CE, et al : Increased expression of tenascin C by keloids in vivo and in vitro. Br J Dermatol, 1999 ; 141 : 50-6. – reference: 22) McCulloch DR, Nelson CM, Dixon LJ, et al : ADAMTS metalloproteases generate active versican fragments that regulate interdigital web regression. Dev Cell, 2009 ; 17 : 687-98. – reference: 17) Kischer CW, Hendrix MJ : Fibronectin (FN) in hypertrophic scars and keloids. Cell Tissue Res, 1983 ; 231 : 29-37. – reference: 4) Luo S, Benathan M, Raffoul W, et al : Abnormal balance between proliferation and apoptotic cell death in fibroblasts derived from keloid lesions. Plast Reconstr Surg, 2001 ; 107 : 87-96. – reference: 2) Bran GM, Goessler UR, Hormann K, et al : Keloids : Current concepts of pathogenesis (review). Int J Mol Med, 2009 ; 24 : 283-93. – reference: 13) Meyer LJ, Russell SB, Russell JD, et al : Reduced hyaluronan in keloid tissue and cultured keloid fibroblasts. J Invest Dermatol, 2000 ; 114 : 953-9. – reference: 20) Sible JC, Retting WJ, Eriksson E, et al : Gene expression of tenascin is altered in normal scars and keloids. Wound Repair Regen, 1995 ; 3 : 37-48. – reference: 14) Ikeda M, Naitoh M, Kubota H, et al : Elastic fiber assembly is disrupted by excessive accumulation of chondroitin sulfate in the human dermal fibrotic disease, keloid. Biochem Biophys Res Commun, 2009 ; 390 : 1221-8. – reference: 5) Sasaki T, Majamaa K, Uitto J : Reduction of collagen production in keloid fibroblast cultures by ethyl-3, 4-dihydroxybenzoate. Inhibition of prolyl hydroxylase activity as a mechanism of action. J Biol Chem, 1987 ; 262 : 9397-403. – reference: 3) Chodon T, Sugihara T, Igawa HH, et al : Keloid-derived fibroblasts are refractory to Fas-mediated apoptosis and neutralization of autocrine transforming growth factor-β1 can abrogate this resistance. Am J Pathol, 2000 ; 157 : 1661-9. – reference: 24) 荒牧典子, 磯貝善蔵, 岡部圭介, ほか : ケロイド組織における細胞外マトリックスの産生・分解. 瘢痕・ケロイド治療ジャーナル, 2013 ; 7 : 5-7. |
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| Title | 細胞外マトリックスから見たケロイド |
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