Regulation of type I collagen and interstitial collagenase mRNA expression in human dermal fibroblasts by colchicine and D-penicillamine | Zendy

Kee Yang Chung | Zendy; Dong Seung Kang | Zendy

Open Access

Regulation of type I collagen and interstitial collagenase mRNA expression in human dermal fibroblasts by colchicine and D-penicillamine

Author(s) -

Kee Yang Chung,

Dong Seung Kang

Publication year - 1999

Publication title -

yonsei medical journal

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.702

H-Index - 63

eISSN - 1976-2437

pISSN - 0513-5796

DOI - 10.3349/ymj.1999.40.5.490

Subject(s) - colchicine , penicillamine , type i collagen , collagenase , messenger rna , northern blot , interstitial collagenase , keloid , chemistry , endocrinology , collagen, type i, alpha 1 , medicine , fibroblast , transforming growth factor , microbiology and biotechnology , biology , extracellular matrix , biochemistry , pathology , in vitro , enzyme , gene

Sclerosis is a disease process in which idiopathic hardening occurs in the skin and/or internal organs as a result of the accumulation of type I collagen, induced mainly by transforming growth factor-beta. Colchicine and D-penicillamine are widely used for its treatment. Their effects are known to be due to post-translational down-regulation of type I collagen synthesis, with colchicine also up-regulating interstitial collagenase. To determine whether or not they have any pre-translational effect on type I collagen and MMP-1, and also to observe their effects on the action of TGF-beta, cultured neonatal foreskin fibroblasts were treated with colchicine and D-penicillamine, singly and together. The amount of type I collagen and MMP-1 mRNA were quantitated by Northern blot hybridization. Colchicine suppresses the basal level of type I collagen mRNA but minimally stimulates the mRNA expression of MMP-1, whereas D-penicillamine does not have any significant effects on either. Colchicine was also able to significantly suppress the TGF-beta-induced up-regulation of type I collagen mRNA expression.

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