telomere shortening impairs regeneration of the olfactory epithelium in response to injury but not under homeostatic conditions端粒缩短损害嗅觉上皮的再生反应损伤但不是在稳态条件下.pdf

Telomere Shortening Impairs Regeneration of the Olfactory Epithelium in Response to Injury but Not Under Homeostatic Conditions 1 2 ´ 2 2 Masami Watabe-Rudolph , Yvonne Begus-Nahrmann , Andre Lechel , Harshvardhan Rolyan , Marc- 1 1 3 2 Oliver Scheithauer , Gerhard Rettinger , Dietmar Rudolf Thal , Karl Lenhard Rudolph * 1 Department of Otorhinolaryngology, University of Ulm, Ulm, Germany, 2 Max-Planck-Research Department of Stem Cell Aging and Institute of Molecular Medicine, University of Ulm, Ulm, Germany, 3 Department of Pathology, University of Ulm, Ulm, Germany Abstract Atrophy of the olfactory epithelium (OE) associated with impaired olfaction and dry nose represents one of the most common phenotypes of human aging. Impairment in regeneration of a functional olfactory epithelium can also occur in response to injury due to infection or nasal surgery. These complications occur more frequently in aged patients. Although age is the most unifying risk factor for atrophic changes and functional decline of the olfactory epithelium, little is known about molecular mechanisms that could influence maintenance and repair of the olfactory epithelium. Here, we analyzed the influence of telomere shortening (a basic mechanism of cellular aging) on homeostasis and regenerative reserve in response to chemical induced injury of the OE in late generation telomere knockout mice (G3 mTerc2/ 2) with short telomeres compared to wild type mice (mTerc+/+) with long telomeres. The study revealed no significant influence of telomere shortening on homeostatic maintenance of th