Rodemann H P, Binder A, Burger A, Güven N, Löffler H, Bamberg M
Department of Radiotherapy, Eberhard-Karls-University, Tübingen, Germany.
Kidney Int Suppl. 1996 May;54:S32-6.
Fibrosis is a common sequela of various exogenous insults to a variety of parenchymal tissues. The underlying mechanisms of the induction and progression of fibrosis both at the molecular and cellular level have not been clarified so far. In the present study the cellular processes that ultimately may lead to interstitial fibrosis are described using the model of radiation-induced terminal differentiation in the fibroblast/fibrocyte cell system. The data reported herein will provide evidence that exogenously induced changes in the proliferation and differentiation pattern of the fibroblast/fibrocyte cell system based on either autocrine and/or paracrine mediators represent the underlying cellular mechanism of fibrosis. Using co-culture systems of parenchymal cells (fibroblasts and type II pneumocytes), the intercellular communication via cytokines, which may lead to fibrosis have been studied. TGF beta 1 could be described as one key modulator of these cellular processes.
纤维化是各种实质组织受到多种外源性损伤后的常见后遗症。迄今为止，纤维化诱导和进展在分子和细胞水平的潜在机制尚未阐明。在本研究中，使用成纤维细胞/纤维细胞系统中辐射诱导的终末分化模型描述了最终可能导致间质纤维化的细胞过程。本文报道的数据将提供证据表明，基于自分泌和/或旁分泌介质，成纤维细胞/纤维细胞系统增殖和分化模式的外源性诱导变化代表了纤维化的潜在细胞机制。使用实质细胞（成纤维细胞和II型肺细胞）的共培养系统，研究了可能导致纤维化的细胞因子介导的细胞间通讯。转化生长因子β1可被描述为这些细胞过程的一个关键调节因子。
