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前列地尔抑制转化生长因子-β1诱导人阴茎海绵体平滑肌中胶原蛋白的合成。

PGE1 suppresses the induction of collagen synthesis by transforming growth factor-beta 1 in human corpus cavernosum smooth muscle.

作者信息

Moreland R B, Traish A, McMillin M A, Smith B, Goldstein I, Saenz de Tejada I

机构信息

Department of Urology, Boston University School of Medicine, Massachusetts.

出版信息

J Urol. 1995 Mar;153(3 Pt 1):826-34.

PMID:7861547
Abstract

Collagen synthesis has been examined in primary cultures of human corpus cavernosum smooth muscle cells (HCCSMC), the major mesenchymal cell type of the corpus cavernosum. These cultures were grown from human surgical specimens and characterized by morphological and biochemical characteristics. These cells express mRNA for transforming growth factor-beta 1 (TGF-beta 1), a major regulator of extracellular matrix synthesis, as well as all three subtypes of TGF-beta receptors. Human corpus cavernosum smooth muscle cells primarily synthesize types I and III fibrillar collagen. Treatment of HCCSMC with exogenous TGF-beta 1 (80 pM.) induced a 2.5- to 4.5-fold increase in the synthesis of types I and III collagen and resulted in detectable levels of type V/XI collagen. Treatment of HCCSMC with the eicosanoid PGE1 in combination with TGF-beta 1 suppressed the induction of collagen synthesis by TGF-beta 1 in a dose-dependent manner with concomitant decreases in types I, III and V/XI collagen. The expression of TGF-beta 1 mRNA as well as types I and II TGF-beta receptors was induced by exogenous TGF-beta 1. Transforming growth factor-beta 1 mRNA induction was suppressed by PGE1. These data suggest that prostaglandins and TGF-beta 1 may play a key role in modulation of collagen synthesis in the corpus cavernosum, and in the regulation of fibrosis of the corpus cavernosum.

摘要

已在人海绵体平滑肌细胞(HCCSMC)的原代培养物中检测了胶原蛋白的合成,HCCSMC是海绵体主要的间充质细胞类型。这些培养物由人类手术标本培养而来,并通过形态学和生化特征进行表征。这些细胞表达转化生长因子-β1(TGF-β1)的mRNA,TGF-β1是细胞外基质合成的主要调节因子,同时还表达TGF-β受体的所有三种亚型。人海绵体平滑肌细胞主要合成I型和III型纤维状胶原蛋白。用外源性TGF-β1(80 pM)处理HCCSMC可使I型和III型胶原蛋白的合成增加2.5至4.5倍,并导致可检测水平的V/XI型胶原蛋白。用类花生酸PGE1与TGF-β1联合处理HCCSMC,可剂量依赖性地抑制TGF-β1诱导的胶原蛋白合成,同时I型、III型和V/XI型胶原蛋白减少。外源性TGF-β1可诱导TGF-β1 mRNA以及I型和II型TGF-β受体的表达。PGE1可抑制转化生长因子-β1 mRNA的诱导。这些数据表明,前列腺素和TGF-β1可能在海绵体胶原蛋白合成的调节以及海绵体纤维化的调节中起关键作用。

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