MnSOD activity protects mitochondrial morphology of quiescent fibroblasts from age associated abnormalities

Ehab H Sarsour; Monali Goswami; Amanda L Kalen; Prabhat C Goswami

doi:10.1016/j.mito.2010.02.004

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MnSOD activity protects mitochondrial morphology of quiescent fibroblasts from age associated abnormalities

Journal article

Peer reviewed

MnSOD activity protects mitochondrial morphology of quiescent fibroblasts from age associated abnormalities

Ehab H Sarsour, Monali Goswami, Amanda L Kalen and Prabhat C Goswami

Mitochondrion, Vol.10(4), pp.342-349

06/2010

DOI: 10.1016/j.mito.2010.02.004

PMCID: PMC2874624

PMID: 20206302

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Abstract

Previously, we have shown manganese superoxide dismutase (MnSOD) activity protects quiescent human normal skin fibroblasts (NHFs) from age associated loss in proliferative capacity. The loss in proliferative capacity of aged vs. young quiescent cells is often characterized as the chronological life span, which is clearly distinct from replicative senescence. We investigate the hypothesis that MnSOD activity protects the mitochondrial morphology from age associated damage and preserves the chronological life span of quiescent fibroblasts. Aged quiescent NHFs exhibited abnormalities in mitochondrial morphology including abnormal cristae formation and increased number of vacuoles. These results correlate with the levels of cellular reactive oxygen species (ROS) and mitochondrial morphology in MnSOD homozygous and heterozygous knockout mouse embryonic fibroblasts. The abnormalities in mitochondrial morphology in aged quiescent NHFs cultured in presence of 21% oxygen concentration were more severe than NHFs cultured in 4% oxygen environment. The alteration in mitochondrial morphology was associated with a significant increase in cell population doubling: 54h in 21% compared to 44h in 4% oxygen environment. Overexpression of MnSOD decreased ROS levels, and preserved mitochondrial morphology in aged quiescent NHFs. These results demonstrate that MnSOD activity protects mitochondrial morphology and preserves the proliferative capacities of quiescent NHFs from age associated loss.

Microscopy, Electron, Transmission

Fibroblasts - physiology

Humans

Mice, Inbred C57BL

Cells, Cultured

Mitochondria - ultrastructure

Reactive Oxygen Species - analysis

Mice, Knockout

Animals

Cell Division

Mice, Inbred DBA

Mice

Mitochondria - physiology

Superoxide Dismutase - metabolism

Fibroblasts - chemistry

Details

Title: Subtitle: MnSOD activity protects mitochondrial morphology of quiescent fibroblasts from age associated abnormalities
Creators: Ehab H Sarsour - Free Radical and Radiation Biology Program, Department of Radiation Oncology, University of Iowa, Iowa City, IA 52242, USA. ehab-sarsour@uiowa.edu
Monali Goswami
Amanda L Kalen
Prabhat C Goswami
Resource Type: Journal article
Publication Details: Mitochondrion, Vol.10(4), pp.342-349
DOI: 10.1016/j.mito.2010.02.004
PMID: 20206302
PMCID: PMC2874624
NLM abbreviation: Mitochondrion
ISSN: 1567-7249
eISSN: 1872-8278
Publisher: Netherlands
Grant note: R01 GM089866 / NIGMS NIH HHS CA 111365 / NCI NIH HHS R01 CA111365 / NCI NIH HHS R01 CA111365-05 / NCI NIH HHS
Language: English
Date published: 06/2010
Academic Unit: Radiation Oncology
Record Identifier: 9984046827302771

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