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Activation of mTOR coincides with autophagy during ligation-induced atrophy in the rat submandibular gland

Research output: Contribution to journalArticle

Original languageEnglish
Article numbere14
JournalCell Death & Disease
Volume1
Issue number1
DOIs
PublishedJan 2010

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Abstract

Salivary gland atrophy is a common consequence of pathology, including Sjogren's syndrome, irradiation therapy and obstructive sialadenitis. During severe atrophy of the rat submandibular gland caused by excretory duct ligation, the majority of acinar cells disappear through apoptosis, whereas ductal cells proliferate and dedifferentiate; yet, the gland can survive in the atrophic state almost indefinitely, with an ability to fully recover if deligated. The control mechanisms governing these observations are not well understood. We report that similar to 10% of acinar cells survive in ligation-induced atrophy. Microarray and quantitative real-time PCR analysis of ligated glands indicated sustained transcription of acinar cell-specific genes, whereas ductal-specific genes were reduced to background levels. After 3 days of ligation, activation of the mammalian target of rapamycin (mTOR) pathway and autophagy occurred as shown by phosphorylation of 4E-BP1 and expression of autophagy-related proteins. These results suggest that activation of mTOR and the autophagosomal pathway are important mechanisms that may help to preserve acinar cells during atrophy of salivary glands after injury. Cell Death and Disease (2010) 1, e14; doi:10.1038/cddis.2009.12; published online 21 January 2010

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