Deletion of ATG5 shows a role of autophagy in salivary homeostatic control

M. Morgan-Bathke, H. H. Lin, A. M. Chibly, W. Zhang, X. Sun, C. H. Chen, P. Flodby, Z. Borok, R. Wu, D. Arnett, R. R. Klein, D. K. Ann, Kirsten Limesand

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)911-917
Number of pages7
JournalJournal of Dental Research
Volume92
Issue number10
DOIs
StatePublished - Oct 2013

Fingerprint

Aquaporin 5
Autophagy
Acinar Cells
Salivary Glands
Amylases
Homeostasis
Secretory Vesicles
Recycling
Carbachol
Growth and Development
Isoproterenol
Saliva
Electron Microscopy
Neck
Head
Genotype
Radiation
Staining and Labeling
Proteins

Keywords

  • animal models
  • apoptosis
  • isoproterenol
  • proliferation
  • salivary gland

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Morgan-Bathke, M., Lin, H. H., Chibly, A. M., Zhang, W., Sun, X., Chen, C. H., ... Limesand, K. (2013). Deletion of ATG5 shows a role of autophagy in salivary homeostatic control. Journal of Dental Research, 92(10), 911-917. https://doi.org/10.1177/0022034513499350

Deletion of ATG5 shows a role of autophagy in salivary homeostatic control. / 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, Kirsten.

In: Journal of Dental Research, Vol. 92, No. 10, 10.2013, p. 911-917.

Research output: Contribution to journalArticle

Morgan-Bathke, M, Lin, HH, Chibly, AM, Zhang, W, Sun, X, Chen, CH, Flodby, P, Borok, Z, Wu, R, Arnett, D, Klein, RR, Ann, DK & Limesand, K 2013, 'Deletion of ATG5 shows a role of autophagy in salivary homeostatic control', Journal of Dental Research, vol. 92, no. 10, pp. 911-917. https://doi.org/10.1177/0022034513499350
Morgan-Bathke M, Lin HH, Chibly AM, Zhang W, Sun X, Chen CH et al. Deletion of ATG5 shows a role of autophagy in salivary homeostatic control. Journal of Dental Research. 2013 Oct;92(10):911-917. https://doi.org/10.1177/0022034513499350
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, Kirsten. / Deletion of ATG5 shows a role of autophagy in salivary homeostatic control. In: Journal of Dental Research. 2013 ; Vol. 92, No. 10. pp. 911-917.
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