Trichostatin A inhibits collagen synthesis and induces apoptosis in keloid fibroblasts.
Arch Dermatol Res
; 303(8): 573-80, 2011 Oct.
Article
en En
| MEDLINE
| ID: mdl-21400246
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)-ß1 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-ß1 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-ß1 induced collagen synthesis and induce apoptosis of proliferating keloid fibroblasts.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Colágeno
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Apoptosis
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Fibroblastos
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Ácidos Hidroxámicos
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Queloide
Límite:
Adolescent
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Adult
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Child
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Female
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Humans
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Male
Idioma:
En
Revista:
Arch Dermatol Res
Año:
2011
Tipo del documento:
Article
País de afiliación:
China