gms | German Medical Science

Introduction: Atrophy of the olfactory epithelium (OE) associated with impaired olfaction and dry nose represent 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. 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.

Methods: we analyzed the influence of telomere shortening (a basic mechanism of cellular aging) on homeostasis and regeneration reserve in response to chemical induced injury of the OE in late generation telomere knockout mice (G3 mTERC-/-) with short telomeres compared to wild type mice (mTERC+/+) with long telomeres by using Histology and Immunohistochemical staining (OMP, GAP43, PCNA, BrdU).

Results: The study revealed no influence of telomere shortening on homeostatic maintenance of the OE during mouse aging. In contrast, the regenerative response to chemical induced injury of the OE was significantly impaire in G3 mTERC-/- mice compared to mTERC+/+ mice. 7 days after chemical (Triton) induced damage, G3 mTERC-/- mice exhibited significantly enlarged areas of persisting atrophy compared to mTERC+/+ mice (p=0.03). During the regenerative response (7 days after damage induction), the OE of G3mTERC-/- mice exhibited zonal impairments in cell proliferation in areas of persisting atrophy.

Conclusion: These data indicate that telomere shortening leads to zonal impairments in regeneration of the OE. These findings could be relevant for the impairment in OE function in elderly people.