Journal
AGING CELL
Volume 14, Issue 4, Pages 616-624Publisher
WILEY
DOI: 10.1111/acel.12337
Keywords
aging; Bmi-1; homeostasis; p16(Ink4a); stem; progenitor cells; submandibular gland
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Japan Prize Foundation
- Takeda Science Foundation
- Japan Foundation for Aging and Health
- Toyoaki Scholarship Foundation
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Bmi-1 prevents stem cell aging, at least partly, by blocking expression of the cyclin-dependent kinase inhibitor p16(Ink4a). Therefore, dysregulation of the Bmi-1/p16(Ink4a) pathway is considered key to the loss of tissue homeostasis and development of associated degenerative diseases during aging. However, because Bmi-1 knockout (KO) mice die within 20weeks after birth, it is difficult to determine exactly where and when dysregulation of the Bmi-1/p16(Ink4a) pathway occurs during aging in vivo. Using real-time in vivo imaging of p16(Ink4a) expression in Bmi-1-KO mice, we uncovered a novel function of the Bmi-1/p16(Ink4a) pathway in controlling homeostasis of the submandibular glands (SMGs), which secrete saliva into the oral cavity. This pathway is dysregulated during aging in vivo, leading to induction of p16(Ink4a) expression and subsequent declined SMG function. These findings will advance our understanding of the molecular mechanisms underlying the aging-related decline of SMG function and associated salivary gland hypofunction, which is particularly problematic among the elderly.
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