title: Trichostatin A inhibits collagen synthesis and induces apoptosis in keloid fibroblasts.
abstract: Keloid, a fibro-proliferative benign tumor of skin, is characterized by an enriched milieu of growth factors and an abundant accumulation of extracellular matrix (ECM). Transforming growth factor (TGF)-β1 is well known as the crucial fibrogenic cytokine promoting ECM production and tissue fibrosis in keloid forming. Epigenetic modifications have been shown to play a role in the pathogenesis of cancer as well as autoimmune and inflammatory disorders. Recent publication reports epigenetic modifications in keloid fibroblasts that include an altered pattern of DNA methylation and histone acetylation. Therefore, the field of epigenetics may provide a new therapeutic idea for keloid treatment strategies. Currently, there is some evidence from experimental studies that histone deacetylase (HDAC) inhibitor Trichostatin A (TSA) causes abrogation of TGF-β1 induced collagen synthesis in skin fibroblasts. Furthermore, TSA could suppress proliferation and induce apoptosis in a broad spectrum of tumor cells both in vitro and in vivo. These findings suggest that TSA could also cause abrogation of TGF-β1 induced collagen synthesis and induce apoptosis of proliferating keloid fibroblasts.
authors.affiliation: Institute of Plastic Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
authors.forename: Jian-Sheng
authors.initials: JS
authors.lastname: Diao
authors.forename: Wen-Sen
authors.initials: WS
authors.lastname: Xia
authors.forename: Cheng-Gang
authors.initials: CG
authors.lastname: Yi
authors.forename: Ying-Mei
authors.initials: YM
authors.lastname: Wang
authors.forename: Bing
authors.initials: B
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Xia
authors.forename: Bei
authors.initials: B
authors.lastname: Liu
authors.forename: Shu-Zhong
authors.initials: SZ
authors.lastname: Guo
authors.forename: Xu-De
authors.initials: XD
authors.lastname: Sun
mesh_terms: D000293:Adolescent; D000328:Adult; D017209:Apoptosis / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002648:Child; D003094:Collagen / Q000378:metabolism*; D005260:Female; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D056572:Histone Deacetylase Inhibitors / Q000494:pharmacology; D006801:Humans; D006877:Hydroxamic Acids / Q000494:pharmacology*; D007627:Keloid / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology; D055815:Young Adult
chemical_list: D056572:Histone Deacetylase Inhibitors; D006877:Hydroxamic Acids; D053773:Transforming Growth Factor beta1; C012589:trichostatin A; D003094:Collagen