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腮腺分泌蛋白在实验性糖尿病中的表达及分布

Expression and distribution of parotid secretory proteins in experimental diabetes.

作者信息

Szczepanski A, Mednieks M I, Hand A R

机构信息

Dept. Pediatric Dentistry and Central Electron Microscope Facility, Univ. Connecticut Health Center, Farmington 06030, USA.

出版信息

Eur J Morphol. 1998 Aug;36 Suppl:240-6.

PMID:9825930
Abstract

Previous studies of experimental diabetes have demonstrated changes in the levels of specific salivary proteins. The present study is part of a larger effort aimed at elucidating the mechanism(s) by which insulin regulates salivary protein expression in the rat parotid gland. Diabetes was induced in 2-3-month-old male Fischer 344 rats by injection of streptozotocin (STZ). After 30 days one group of rats was given insulin for 7 days. Untreated rats served as controls. As previously observed, parotid acinar cells from diabetic rats accumulated lipid and contained occasional crystalloid lysosomes. Quantitative immunogold labeling of secretory granules in diabetic glands revealed decreases of 30-60% for proline-rich-proteins (PRPs), amylase and parotid secretory protein (PSP), but labeling for acidic epididymal glycoprotein (AEG) was unchanged. The response to insulin treatment was variable: amylase and PSP labeling were partly restored, but PRP and AEG labeling showed little change. Photoaffinity labeling of cyclic AMP receptor proteins (cARP) showed changes in several tissues including a consistent increase in the diabetic parotid gland. Immunogold labeling of secretory granules with antibody to cARP was similar in control and diabetic parotids, but nuclear and cytoplasmic label was decreased in diabetic acinar cells. These results indicate that STZ-diabetes and insulin reconstitution cause variable changes in the expression of parotid secretory proteins. Changes in cARP levels suggest that the insulin and cyclic AMP pathways may interact in regulating expression of salivary secretory proteins.

摘要

以往对实验性糖尿病的研究已证明特定唾液蛋白水平会发生变化。本研究是一项更大规模研究工作的一部分,旨在阐明胰岛素调节大鼠腮腺唾液蛋白表达的机制。通过注射链脲佐菌素(STZ)诱导2 - 3月龄雄性Fischer 344大鼠患糖尿病。30天后,一组大鼠接受胰岛素治疗7天。未治疗的大鼠作为对照。如先前观察到的,糖尿病大鼠的腮腺腺泡细胞积累脂质并偶尔含有晶体样溶酶体。对糖尿病腺体分泌颗粒进行定量免疫金标记显示,富含脯氨酸蛋白(PRP)、淀粉酶和腮腺分泌蛋白(PSP)减少了30% - 60%,但酸性附睾糖蛋白(AEG)的标记没有变化。对胰岛素治疗的反应各不相同:淀粉酶和PSP的标记部分恢复,但PRP和AEG的标记变化不大。环磷酸腺苷受体蛋白(cARP)的光亲和标记在几个组织中显示出变化,包括糖尿病腮腺中持续增加。用抗cARP抗体对分泌颗粒进行免疫金标记在对照和糖尿病腮腺中相似,但糖尿病腺泡细胞的核和细胞质标记减少。这些结果表明,STZ诱导的糖尿病和胰岛素重建会导致腮腺分泌蛋白表达发生不同变化。cARP水平的变化表明胰岛素和环磷酸腺苷途径可能在调节唾液分泌蛋白表达中相互作用。

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