PMID- 22834911
OWN - NLM
STAT- MEDLINE
DCOM- 20130521
LR  - 20211021
IS  - 1029-2470 (Electronic)
IS  - 1071-5762 (Print)
IS  - 1029-2470 (Linking)
VI  - 46
IP  - 11
DP  - 2012 Nov
TI  - Manganese superoxide dismutase is dispensable for post-natal development and 
      lactation in the murine mammary gland.
PG  - 1361-8
LID - 10.3109/10715762.2012.715370 [doi]
AB  - Mammary gland development is a multistage process requiring tightly regulated 
      spatial and temporal signalling pathways. Many of these pathways have been shown 
      to be sensitive to oxidative stress. Understanding that the loss of manganese 
      superoxide dismutase (Sod2) leads to increased cellular oxidative stress, and 
      that the loss or silencing of this enzyme has been implicated in numerous 
      pathologies including those of the mammary gland, we sought to examine the role 
      of Sod2 in mammary gland development and function in situ in the mouse mammary 
      gland. Using Cre-recombination driven by the mouse mammary tumor virus (MMTV) 
      promoter, we created a mammary-specific post-natal conditional Sod2 knock-out 
      mouse model. Surprisingly, while substantial decreases in Sod2 were noted 
      throughout both virgin and lactating adult mammary glands, no significant changes 
      in developmental structures either pre- or post-pregnancy were observed 
      histologically. Moreover, mothers lacking mammary gland expression of Sod2 were 
      able to sustain equal numbers of litters, equal pups per litter, and equal pup 
      weights as were control animals. Overall, our results demonstrate that loss of 
      Sod2 expression is not universally toxic to all cell types and that excess 
      mitochondrial superoxide can apparently be tolerated during the development and 
      function of post-natal mammary glands.
FAU - Case, Adam J
AU  - Case AJ
AD  - Free Radical and Radiation Biology Program, Department of Radiation Oncology, 
      Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, IA 52240, 
      USA.
FAU - Domann, Frederick E
AU  - Domann FE
LA  - eng
GR  - R01 CA073612/CA/NCI NIH HHS/United States
GR  - R01 CA115438/CA/NCI NIH HHS/United States
GR  - T32 CA078586/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20120905
PL  - England
TA  - Free Radic Res
JT  - Free radical research
JID - 9423872
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Animals
MH  - Female
MH  - Immunohistochemistry
MH  - Lactation/*metabolism
MH  - Mammary Glands, Animal/*enzymology/*growth & development/metabolism/pathology
MH  - Mammary Tumor Virus, Mouse/genetics
MH  - Mice
MH  - Mice, Knockout
MH  - Oxidative Stress/physiology
MH  - Superoxide Dismutase/deficiency/genetics/*metabolism
PMC - PMC3569059
MID - NIHMS438929
COIS- Declaration of interest The authors have no financial, consulting, or personal 
      conflicts of interest pertaining to this work. This work was supported by the 
      following grants: NIH RO1 CA073612, NIH RO1 CA115438, DOD PC073831, and T32 
      CA078586.
EDAT- 2012/07/28 06:00
MHDA- 2013/05/23 06:00
PMCR- 2013/02/11
CRDT- 2012/07/28 06:00
PHST- 2012/07/28 06:00 [entrez]
PHST- 2012/07/28 06:00 [pubmed]
PHST- 2013/05/23 06:00 [medline]
PHST- 2013/02/11 00:00 [pmc-release]
AID - 10.3109/10715762.2012.715370 [doi]
PST - ppublish
SO  - Free Radic Res. 2012 Nov;46(11):1361-8. doi: 10.3109/10715762.2012.715370. Epub 
      2012 Sep 5.