MUC1/SEC and MUC1/Y overexpression is associated with inflammation in Sjogren's syndrome
MUC1/SEC and MUC1/Y overexpression is associated with inflammation in Sjogren's syndrome
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DOI：
10.1111/odi.12339
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发表时间：
2015-09-01
期刊：
影响因子：
3.8
通讯作者：
Gonzalez, M-J
中科院分区：
文献类型：
--
作者：
Sung, H. H.;Castro, I.;Gonzalez, M-J
目的探讨干燥综合征患者唇唾液腺MUC1/SEC和MUC1/Y亚型在唇唾液腺（LSG）中的表达、定位及其在细胞因子诱导下的体外表达情况。对象和方法对27例原发性SS患者和22例非SS患者的唇唾液腺进行了研究。qPCR检测MUC1/SEC和MUC1/Y相对mRNA水平，Western blotting检测MUC1/Y蛋白水平。体外检测粘蛋白mrna的诱导作用。采用免疫组织化学进行定位。结果SS患者LSG中MUC1/SEC和MUC1/Y mRNA和蛋白的相对表达水平显著升高。这些mrna是由细胞因子诱导的。在对照组LSGs的腺泡顶端区检测到MUC1/SEC和MUC1/Y，在SS患者的腺泡中观察到明显的细胞质积累。MUC1/Y定位于SS患者LSG炎症细胞的腺泡核和细胞质。细胞MUC1/SEC水平与腺体功能呈显著正相关。结论MUC1/SEC和MUC1/Y在SS患者和非SS患者的LSG中均有表达。观察到的MUC1/SEC和MUC1/Y的过表达和异常定位以及促炎细胞因子的诱导可能有利于炎症环境的延续，从而破坏SS患者的唾液腺稳态。
ObjectivesTo evaluate the expression and localization of MUC1/SEC and MUC1/Y isoforms in labial salivary glands (LSG) from Sjogren's syndrome patients (SS patients), as well as their in vitro expression induced by cytokines.Subjects and methodsLabial salivary gland from 27 primary SS patients and 22 non-SS sicca subjects were studied. Relative MUC1/SEC and MUC1/Y mRNA levels were determined by qPCR and protein levels by Western blotting. Induction of mucin mRNAs was assayed in vitro. Immunohistochemistry was used for localization.ResultsRelative MUC1/SEC and MUC1/Y mRNA and protein levels were significantly higher in LSG from SS patients. These mRNAs were induced by cytokines. MUC1/SEC and MUC1/Y were detected in acini apical region of control LSGs, and significant cytoplasmic accumulation was observed in acini of SS patients. MUC1/Y localized in acinar nuclei and cytoplasm of inflammatory cells of LSG from SS patients. A strong positive correlation was observed between cellular MUC1/SEC levels and glandular function determined by scintigraphy.ConclusionsWe show for the first time that MUC1/SEC and MUC1/Y are expressed in LSG of both SS patients and non-SS sicca subjects. The observed overexpression and aberrant localization of MUC1/SEC and MUC1/Y and their induction by pro-inflammatory cytokines may favor the perpetuation of the inflammatory environment that disrupts the salivary glandular homeostasis in SS patients.