Smith P C, Martínez J
Faculty of Odontology, Institute of Nutrition and Food Technology (INTA), University of Chile, Olivos 943, Casilla 1903, Santiago, Chile.
J Dent Res. 2006 Feb;85(2):150-5. doi: 10.1177/154405910608500207.
Transforming Growth Factor-beta1 (TGF-beta1) plays a key role in connective tissue remodeling and inflammation. Under pathological conditions, like periodontal disease, fibroblasts may display an altered response to this growth factor. To investigate this question, we have studied whether TGF-beta1 may differentially regulate the expression of urokinase at the protein level in primary cultures of fibroblasts derived from healthy gingiva, granulation tissue from gingival wounds, and chronic periodontal disease. We observed that TGF-beta1 may repress urokinase expression in healthy gingival fibroblasts and promote its production in granulation-tissue fibroblasts. A significant correlation was found between expression of the myofibroblast marker alpha-smooth-muscle actin and stimulation of urokinase production by TGF-beta1. Immunostaining of gingival wounds showed that myofibroblasts were involved in urokinase production. TGF-beta1-stimulated urokinase expression was blocked after inhibition of the c-jun-NH2 terminal kinase signaling pathway. We propose that stimulation of urokinase production by TGF-beta1 is involved in the responses of activated fibroblasts to tissue injury.
转化生长因子-β1（TGF-β1）在结缔组织重塑和炎症中起关键作用。在病理条件下，如牙周疾病，成纤维细胞对这种生长因子的反应可能会发生改变。为了研究这个问题，我们研究了TGF-β1是否可能在源自健康牙龈、牙龈伤口肉芽组织和慢性牙周疾病的原代成纤维细胞培养物中，在蛋白质水平上差异调节尿激酶的表达。我们观察到，TGF-β1可能会抑制健康牙龈成纤维细胞中尿激酶的表达，并促进肉芽组织成纤维细胞中尿激酶的产生。在肌成纤维细胞标志物α-平滑肌肌动蛋白的表达与TGF-β1对尿激酶产生的刺激之间发现了显著相关性。牙龈伤口的免疫染色显示肌成纤维细胞参与了尿激酶的产生。在抑制c-jun-NH2末端激酶信号通路后，TGF-β1刺激的尿激酶表达被阻断。我们认为，TGF-β1刺激尿激酶的产生与活化的成纤维细胞对组织损伤的反应有关。
