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Deletion of ATG5 shows a role of autophagy in salivary homeostatic control
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نویسنده
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morgan-bathke m. ,lin h.h. ,chibly a.m. ,zhang w. ,sun x. ,chen c.-h. ,flodby p. ,borok z. ,wu r. ,arnett d. ,klein r.r. ,ann d.k. ,limesand k.h.
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منبع
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journal of dental research - 2013 - دوره : 92 - شماره : 10 - صفحه:911 -917
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چکیده
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Autophagy is a catabolic pathway utilized to maintain a balance among the synthesis,degradation,and recycling of cellular components,thereby playing a role in cell growth,development,and homeostasis. previous studies revealed that a conditional knockout of essential member(s) of autophagy in a variety of tissues causes changes in structure and function of these tissues. acinar cell-specific expression of knocked-in cre recombinase through control of aquaporin 5 (aqp5) promoter/enhancer (aqp5-cre) allows us to specifically inactivate atg5,a protein necessary for autophagy,in salivary acinar cells of atg5f/f;aqp5-cre mice. there was no difference in apoptotic or proliferation levels in salivary glands of atg5/cre mice from each genotype. however,h&e staining and electron microscopy studies revealed modestly enlarged acinar cells and accumulated secretory granules in salivary glands of atg5f/f;aqp5-cre mice. salivary flow rates and amylase contents of atg5/cre mice indicated that acinar-specific inactivation of atg5 did not alter carbachol-evoked saliva and amylase secretion. conversely,autophagy intersected with salivary morphological and secretory manifestations induced by isoproterenol administration. these results identified a role for autophagy as a homeostasis control in salivary glands. collectively,atg5f/f;aqp5-cre mice would be a useful tool to enhance our understanding of autophagy in adaptive responses following targeted head and neck radiation or sjögren syndrome. © international & american associations for dental research.
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کلیدواژه
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animal models; apoptosis; isoproterenol; proliferation; salivary gland
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آدرس
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department of nutritional sciences,university of arizona,tucson,az 85721, United States, department of molecular pharmacology,beckman research institute,city of hope,duarte,ca 91010, United States, department of nutritional sciences,university of arizona,tucson,az 85721, United States, department of molecular pharmacology,beckman research institute,city of hope,duarte,ca 91010, United States, department of molecular pharmacology,beckman research institute,city of hope,duarte,ca 91010, United States, center of comparative respiratory biology and medicine,university of california,davis,ca 95616, United States, will rogers institute,pulmonary research center,university of southern california,los angeles,ca, United States, will rogers institute,pulmonary research center,university of southern california,los angeles,ca,united states,department of biochemistry and molecular biology,keck school of medicine,university of southern california,los angeles,ca, United States, center of comparative respiratory biology and medicine,university of california,davis,ca 95616, United States, department of nutritional sciences,university of arizona,tucson,az 85721, United States, department of pathology,university of arizona,tucson,az 85721, United States, department of molecular pharmacology,beckman research institute,city of hope,duarte,ca 91010,united states,irell and mandella graduate school of biological sciences,beckman research institute,city of hope,duarte,ca 91010, United States, department of nutritional sciences,university of arizona,tucson,az 85721, United States
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Authors
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