Uncoupling protein 2 deficiency results in higher neutrophil counts and lower B-cell counts during aging in mice.

Abstract:

:Progress of age-related hematopoietic diseases such as myelodysplastic syndrome has previously been linked to enhanced levels of reactive oxygen species (ROS). Uncoupling protein 2 (UCP2) was found to reduce mitochondrial ROS production through uncoupling of the respiratory chain. The impact of UCP2 loss and elevated ROS on hematopoiesis during aging has not yet been investigated. In this study, UCP2 knockout mice were analyzed at aging stages of 3, 12, and 24 months with respect to oxidative and energy status of bone marrow cells. Further, the cellular bone marrow subpopulation composition was characterized, as were the differential blood counts at all time points. UCP2 knockout mice revealed enhanced levels of mitochondrial superoxide in elderly animals. Following oxidative stress, adenosine triphosphate (ATP) levels decreased more in the knockout mice than in the wild type. Investigation of bone marrow and blood counts of the knockout mice revealed an enhanced amount of monocytes and neutrophils, as well as a decreased amount of B cells and impaired erythropoiesis throughout aging. In summary, UCP2 induces protective effects on ROS and ATP levels during aging. Additionally, the results suggest an imbalance in hematopoiesis because of the lack of UCP2.

journal_name

Exp Hematol

journal_title

Experimental hematology

authors

Kretzschmar C,Roolf C,Timmer K,Sekora A,Knübel G,Murua Escobar H,Jaster R,Müller S,Fuellen G,Köhling R,Junghanss C

doi

10.1016/j.exphem.2016.08.003

subject

Has Abstract

pub_date

2016-11-01 00:00:00

pages

1085-1091.e2

issue

11

eissn

0301-472X

issn

1873-2399

pii

S0301-472X(16)30562-8

journal_volume

44

pub_type

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