Salivary gland epithelial cells - A new source of the immunoregulatory hormone adiponectin
Salivary gland epithelial cells - A new source of the immunoregulatory hormone adiponectin
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DOI：
10.1002/art.21944
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发表时间：
2006-07-01
影响因子：
--
通讯作者：
Skopouli, Fotini N.
中科院分区：
文献类型：
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作者：
Katsiougiannis, Stergios;Kapsogeorgou, Efstathia K.;Skopouli, Fotini N.
目标。脂联素是一种脂肪细胞因子，具有胰岛素增敏和免疫调节作用。与纤维化相关的脂肪细胞发育常见于原发干燥综合征皮损，提示有愈合过程。本研究的目的是检测脂联素在原发性SS患者和对照组小涎腺活检标本中的表达。应用免疫组织化学和免疫印迹技术分别检测小涎腺活检标本和长期培养的非肿瘤性涎腺上皮细胞系(SGEC)中脂联素的表达。逆转录-聚合酶链式反应检测脂联素、脂联素受体1(AdipoR1)和AdipoR2信使RNA(MRNA)在SGEC中的表达。脂联素的免疫组织化学分析显示，原发SS皮损的脂肪细胞以及原发SS患者和对照组的导管上皮细胞均呈阳性染色。所有SGEC细胞株均表达脂联素、AdipoR1和AdipoR2，免疫印迹法检测到SS患者SGEC中脂联素蛋白的表达，而对照组SGEC中不表达脂联素蛋白。浓缩培养上清液分析也显示SS患者SGECs脂联素的表达高于对照组。我们的发现提供了新的证据，表明脂联素是由SGEC产生的。原发SS患者SGECs的高结构性脂联素表达可能与这些细胞的异常激活有关。尽管脂联素表达的意义尚不清楚，但相关受体的同时表达提示，脂联素可能以自分泌方式发挥作用。
Objective. Adiponectin is an adipocytokine that displays insulin-sensitizing and immunoregulatory properties. Adipocyte development in association with fibrosis is frequently detected in primary Sjogren's syndrome lesions, connoting a healing process. The aim of this study was to examine the expression of adiponectin in minor salivary gland biopsy specimens obtained from patients with primary SS and controls.Methods. The expression of adiponectin in minor salivary gland biopsy specimens and in long-term-cultured non-neoplastic salivary gland epithelial cell (SGEC) lines obtained from patients with primary SS and control subjects was examined, using immunohistochemistry and immunoblotting, respectively. The expression of adiponectin, adiponectin receptor 1 (AdipoR1), and AdipoR2 messenger RNA (mRNA) by SGECs was investigated by reverse transcription-polymerase chain reaction.Results. Immunohistochemical analysis for adiponectin revealed positive staining of adipocytes from primary SS lesions as well as ductal epithelial cells from both patients with primary SS and controls. All of the SGEC lines tested were shown to express adiponectin, AdipoR1, and AdipoR2 mRNA, whereas adiponectin protein expression was detected by immunoblotting in SGECs from patients with primary SS but not in those from controls. The analysis of concentrated culture supernatants also revealed increased adiponectin expression by SGECs from patients with SS compared with controls.Conclusion. Our findings provide novel evidence that adiponectin is produced by SGECs. The high constitutive expression of adiponectin by SGECs from patients with primary SS is likely attributable to aberrant activation of these cells. Although the significance of adiponectin expression remains unknown, it is possible that adiponectin functions in an autocrine manner, as suggested by concurrent expression of the relevant receptors.