Kulozik M, Hogg A, Lankat-Buttgereit B, Krieg T
Dermatologische Klinik und Poliklinik, Ludwig-Maximilians-Universität München, Federal Republic of Germany.
J Clin Invest. 1990 Sep;86(3):917-22. doi: 10.1172/JCI114793.
The role of transforming growth factor beta 2 (TGF-beta 2) in the pathogenesis of systemic sclerosis (SSc) was investigated by in situ hybridization of skin biopsies from six patients with SSc. Two patients with acute systemic lupus erythematosis (SLE), one with acute dermatomyositis (DM), and three healthy individuals were used as controls. TGF-beta 2 mRNA was found to be co-localized with pro alpha 1(I) collagen expression around dermal blood vessels in all patients with the inflammatory stage of SSc, whereas there was no expression of either gene in the dermis of patients in the fibrotic stage, the SLE patients or the normal controls. These findings provide evidence that TGF-beta 2 released by inflammatory cells around blood vessels may play a role in mediating the collagen gene disregulation in fibrosis.
通过对6例系统性硬化症(SSc)患者的皮肤活检组织进行原位杂交,研究了转化生长因子β2(TGF-β2)在SSc发病机制中的作用。选取2例急性系统性红斑狼疮(SLE)患者、1例急性皮肌炎(DM)患者和3名健康个体作为对照。发现所有处于SSc炎症期的患者中,TGF-β2 mRNA与真皮血管周围的α1(I)型前胶原表达共定位,而在纤维化期患者、SLE患者或正常对照的真皮中,这两种基因均无表达。这些发现证明,血管周围炎症细胞释放的TGF-β2可能在介导纤维化过程中胶原基因失调方面发挥作用。