NEIL3-deficient bone marrow displays decreased hematopoietic capacity and reduced telomere length.

ABSTRACT: Deficiency of NEIL3, a DNA repair enzyme, has significant impact on mouse physiology, including vascular biology and gut health, processes related to aging. Leukocyte telomere length (LTL) is suggested as a marker of biological aging, and shortened LTL is associated with increased risk of cardiovascular disease. NEIL3 has been shown to repair DNA damage in telomere regions in vitro. Herein, we explored the role of NEIL3 in telomere maintenance in vivo by studying bone marrow cells from atherosclerosis-prone NEIL3-deficient mice. We found shortened telomeres and decreased activity of the telomerase enzyme in bone marrow cells derived from Apoe ^-/- Neil3 ^-/- as compared to Apoe ^-/- mice. Furthermore,

SUBMITTER: Karlsen TR 

PROVIDER: S-EPMC8777121 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature