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Article ; Online: Hyperbaric oxygen alleviates selective domains of cognitive and motor deficits in female 5xFAD mice.

Mensah-Kane, Paapa / Davis, Delaney L / Shi, Helen S / Trinh, Oanh T / Vann, Philip H / Dory, Ladislav / Sumien, Nathalie

GeroScience

2023 Volume 46, Issue 1, Page(s) 517–530

Abstract: Treatment of Alzheimer's disease (AD) has been limited to managing of symptoms or anti-amyloid therapy with limited results and uncertainty. Seeking out new therapies that can reverse the effects of this devastating disease is important. Hyperbaric ... ...

Abstract	Treatment of Alzheimer's disease (AD) has been limited to managing of symptoms or anti-amyloid therapy with limited results and uncertainty. Seeking out new therapies that can reverse the effects of this devastating disease is important. Hyperbaric oxygen (HBO) therapy could be such a candidate as it has been shown to improve brain function in certain neurological conditions. Furthermore, the role sex plays in the vulnerability/resilience to AD remains equivocal. An understanding of what makes one sex more vulnerable to AD could unveil new pathways for therapy development. In this study, we investigated the effects of HBO on cognitive, motor, and affective function in a mouse model of AD (5xFAD) and assessed protein oxidation in peripheral tissues as a safety indicator. The motor and cognitive abilities of 5xFAD mice were significantly impaired. HBO therapy improved cognitive flexibility and associative learning of 5xFAD females but not males, but HBO had no effect other aspects of cognition. HBO also reversed AD-related declines in balance but had no impact on gait and anxiety-like behavior. HBO did not affect body weights or oxidative stress in peripheral tissues. Our study provides further support for HBO therapy as a potential treatment for AD and emphasizes the importance of considering sex as a biological variable in therapeutic development. Further investigations into the underlying mechanisms of HBO's sex-specific responses are warranted, as well as optimizing treatment protocols for maximum benefits.
MeSH term(s)	Male ; Mice ; Animals ; Female ; Hyperbaric Oxygenation ; Alzheimer Disease/drug therapy ; Cognition ; Oxygen ; Oxidative Stress/physiology
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2023-12-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2886586-8
ISSN	2509-2723 ; 2509-2715
ISSN (online)	2509-2723
ISSN	2509-2715
DOI	10.1007/s11357-023-01047-2
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Zs.A 1502: Show issues

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Article ; Online: Extracellular Superoxide Dismutase Enhances Recruitment of Immature Neutrophils to the Liver.

Break, Timothy J / Witter, Alexandra R / Indramohan, Mohanalaxmi / Mummert, Mark E / Dory, Ladislav / Berg, Rance E

Infection and immunity

2016 Volume 84, Issue 12, Page(s) 3302–3312

Abstract: Listeria monocytogenes is a Gram-positive intracellular pathogen that causes spontaneous abortion in pregnant women, as well as septicemia, meningitis, and gastroenteritis, primarily in immunocompromised individuals. Although L. monocytogenes can usually ...

Abstract	Listeria monocytogenes is a Gram-positive intracellular pathogen that causes spontaneous abortion in pregnant women, as well as septicemia, meningitis, and gastroenteritis, primarily in immunocompromised individuals. Although L. monocytogenes can usually be effectively treated with antibiotics, there is still around a 25% mortality rate with individuals who develop clinical listeriosis. Neutrophils are innate immune cells required for the clearance of pathogenic organisms, including L. monocytogenes The diverse roles of neutrophils during both infectious and noninfectious inflammation have recently gained much attention. However, the impact of reactive oxygen species, and the enzymes that control their production, on neutrophil recruitment and function is not well understood. Using congenic mice with varying levels of extracellular superoxide dismutase (ecSOD) activity, we have recently shown that the presence of ecSOD decreases clearance of L. monocytogenes while increasing the recruitment of neutrophils that are not protective in the liver. The data presented here show that ecSOD activity does not lead to a cell-intrinsic increase in neutrophil-homing potential or a decrease in protection against L. monocytogenes Instead, ecSOD activity enhances the production of neutrophil-attracting factors and protects hyaluronic acid (HA) from damage. Furthermore, neutrophils from the livers of ecSOD-expressing mice have decreased intracellular and surface-bound myeloperoxidase, are less capable of killing phagocytosed L. monocytogenes, and have decreased oxidative burst. Collectively, our data reveal that ecSOD activity modulates neutrophil recruitment and function in a cell-extrinsic fashion, highlighting the importance of the enzyme in protecting tissues from oxidative damage.
MeSH term(s)	Animals ; Chemokines/genetics ; Chemokines/metabolism ; Gene Expression Regulation, Enzymologic ; Listeria monocytogenes ; Liver/enzymology ; Mice ; Neutrophils/physiology ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism
Chemical Substances	Chemokines ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2016-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.00603-16
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Zs.A 684: Show issues

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Article ; Online: Extracellular superoxide dismutase polymorphism in mice: Allele-specific effects on phenotype.

Jun, Sujung / Pierce, Anson / Dory, Ladislav

Free radical biology & medicine

2009 Volume 48, Issue 4, Page(s) 590–596

Abstract: Extracellular superoxide dismutase (ecSOD) protects the extracellular matrix from oxidative stress. We previously reported a new allele for ecSOD, expressed in 129P3/J mice (129), which differs from the wild type (wt), expressed in C57BL/6J and other ... ...

Abstract	Extracellular superoxide dismutase (ecSOD) protects the extracellular matrix from oxidative stress. We previously reported a new allele for ecSOD, expressed in 129P3/J mice (129), which differs from the wild type (wt), expressed in C57BL/6J and other strains, by two amino acid substitutions and a 10-bp deletion in the 3' UTR of the mRNA (A. Pierce et al., 2003, Arterioscler. Thromb. Vasc. Biol.23:1820-1825). The newly discovered allele is associated with a phenotype of significantly increased circulating and heparin-releasable enzyme activities and levels. To examine the properties of the two forms of ecSOD in an identical environment we generated, by extensive backcrossing of ecSOD heterozygous progeny to C57BL/6J females, a congenic C57 strain with the 129 (or wt) allele of ecSOD. These mice are homozygous for nearly 5000 SNPs across all chromosomes, as determined by the Affymetrix Parallele Mouse 5K SNP panel. This study describes the generation of the congenic mice (genetically >99.8% identical) and their ecSOD phenotype. The congenic mouse plasma ecSOD activity before and after heparin administration recapitulates the differences reported in the founder mice. Tissue enzyme distribution is similar in both congenic groups, although the 129 allele is associated with higher levels of enzyme expression despite lower levels of enzyme mRNA. In these characteristics the phenotype is allele driven, with little impact from the rest of the genome. The congenic mice carrying the 129 allele have mRNA levels that are in between those in the founder 129P3/J and C57BL/6J strains. We conclude that the ecSOD phenotype in most aspects of enzyme expression is allele driven, with the exception of tissue mRNA levels, for which a significant contribution by the surrounding (host) genome is observed. These results also suggest potential allele-specific differences in the regulation of ecSOD synthesis and intracellular processing/secretion of ecSOD, independent of the genotype context. Most importantly, the congenic mice offer an excellent model to examine the regulatory mechanisms of ecSOD expression and the role of ecSOD in various diseases involving oxidative stress.
MeSH term(s)	3' Untranslated Regions ; Alleles ; Animals ; Chromosome Mapping ; Crosses, Genetic ; Female ; Heparin/chemistry ; Male ; Mice ; Mice, Inbred C57BL ; Microsatellite Repeats/genetics ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Polymorphism, Genetic ; Superoxide Dismutase/genetics
Chemical Substances	3' Untranslated Regions ; Heparin (9005-49-6) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2009-12-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2009.12.003
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Zs.A 2109: Show issues

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Article: Caveolins and macrophage lipid metabolism.

Gargalovic, Peter / Dory, Ladislav

Journal of lipid research

2003 Volume 44, Issue 1, Page(s) 11–21

Abstract: The identification of caveolin-1 more than a decade ago initiated active research into its role in the formation of caveolae, membrane trafficking, signal transduction pathways, and lipid homeostasis. Although caveolins are ubiquitously expressed, the ... ...

Abstract	The identification of caveolin-1 more than a decade ago initiated active research into its role in the formation of caveolae, membrane trafficking, signal transduction pathways, and lipid homeostasis. Although caveolins are ubiquitously expressed, the majority of the available information comes from differentiated cells rich in caveolins, such as fibroblasts, adipocytes, and endothelial cells. During the development of atherosclerosis, macrophages play a pivotal role in the formation of the fatty streak lesions. They take up large amounts of lipids and accumulate in the subendothelial space, forming foam cells that fill up the lesion area. Since caveolins have been implicated in the regulation of cellular cholesterol metabolism in several cell types, it is of interest to examine their potential function in macrophages. In this review, we attempt to summarize current knowledge and views on the role of caveolins in cholesterol metabolism with emphasis on macrophages.
MeSH term(s)	Animals ; Caveolae/metabolism ; Caveolins/genetics ; Caveolins/metabolism ; Cholesterol/metabolism ; Gene Expression Regulation ; Humans ; Lipid Metabolism ; Macrophages/cytology ; Macrophages/metabolism
Chemical Substances	Caveolins ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2003-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.r200005-jlr200
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Zs.A 175: Show issues

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Article: Cellular apoptosis is associated with increased caveolin-1 expression in macrophages.

Gargalovic, Peter / Dory, Ladislav

Journal of lipid research

2003 Volume 44, Issue 9, Page(s) 1622–1632

Abstract: Macrophage apoptosis is an important factor in determining the efficiency of the immune response, atherosclerotic lesion stability, and clearance of aged cells by phagocytosis. The involvement of caveolin-1 in the regulation of apoptosis has been ... ...

Abstract	Macrophage apoptosis is an important factor in determining the efficiency of the immune response, atherosclerotic lesion stability, and clearance of aged cells by phagocytosis. The involvement of caveolin-1 in the regulation of apoptosis has been previously suggested in fibroblasts and epithelial cells. Here we show that treatment of thioglycollate-elicited mouse peritoneal macrophages with various unrelated apoptotic agents, including simvastatin, camptothecin, or glucose deprivation, is associated with a specific and large increase in caveolin-1 expression. In contrast, caveolin-2 levels remain unaffected. Induction of apoptosis was measured by changes in cell morphology, annexin V-labeling, and DNA fragmentation. We demonstrate that caveolin-1 in macrophages is present in lipid rafts and colocalizes with phosphatidylserine (PS) at the cell surface of apoptotic macrophages. Our data suggest that caveolin-1 increase is an early event, closely accompanied by PS externalization and independent of caspase activation and nuclear DNA fragmentation. The increase in caveolin-1 levels does not require new protein synthesis, as cycloheximide does not prevent the apoptosis-mediated increase in caveolin-1 levels. We propose that increased levels of caveolin-1 characterize the apoptotic phenotype of macrophages. Caveolin-1 may be involved in the efficient externalization of PS at the surface of the apoptotic cells.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Caspases/metabolism ; Caveolin 1 ; Caveolin 2 ; Caveolins/genetics ; Caveolins/metabolism ; Cells, Cultured ; Enzyme Activation ; Gene Expression Regulation/drug effects ; Macrophages/cytology ; Macrophages/drug effects ; Macrophages/enzymology ; Macrophages/metabolism ; Membrane Microdomains/metabolism ; Mice ; Protein Biosynthesis ; Simvastatin/pharmacology ; Up-Regulation
Chemical Substances	Cav1 protein, mouse ; Caveolin 1 ; Caveolin 2 ; Caveolins ; Simvastatin (AGG2FN16EV) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2003-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.M300140-JLR200
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Zs.A 175: Show issues

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Article ; Online: Hyperbaric oxygen treatment attenuates the pro-inflammatory and immune responses in apolipoprotein E knockout mice.

Kudchodkar, Bhalchandra / Jones, Harlan / Simecka, Jerry / Dory, Ladislav

Clinical immunology (Orlando, Fla.)

2008 Volume 128, Issue 3, Page(s) 435–441

Abstract: Chronic hyperbaric oxygen (HBO) therapy significantly attenuates atherosclerosis in New Zealand white rabbits as well as the apoE knockout (KO) mice, independent of plasma lipid concentrations and lipoprotein profiles. Because atherosclerosis has many ... ...

Abstract	Chronic hyperbaric oxygen (HBO) therapy significantly attenuates atherosclerosis in New Zealand white rabbits as well as the apoE knockout (KO) mice, independent of plasma lipid concentrations and lipoprotein profiles. Because atherosclerosis has many features of a chronic inflammatory disease, in which both cell-mediated and humoral immune responses participate, we examined the effect of HBO treatment on various aspects of the immune response. We now demonstrate that in apoE KO mice, HBO treatment significantly reduces the circulating levels of antibodies to (MDA)LDL, both in the IgG and IgM class, as well as the delayed-type hypersensitivity (DTH) response to oxLDL challenge. Furthermore, HBO treatment results in a profound attenuation in the production of pro-inflammatory cytokines in response to an inflammatory stimulus (LPS), which is accompanied by a marked increase in the constitutive production of the anti-inflammatory cytokine IL-10 by spleen cells, independent of antigen specificity, as indicated by polyclonal activation of T cells. Our results demonstrate that HBO treatment results in the dampening of T and B cell-mediated responses to oxLDL or inflammatory stimuli.
MeSH term(s)	Animals ; Apolipoproteins E ; Autoantibodies/blood ; Autoantibodies/immunology ; Cytokines/immunology ; Cytokines/metabolism ; Female ; Hyperbaric Oxygenation ; Hypersensitivity, Delayed/immunology ; Hypersensitivity, Delayed/metabolism ; Interleukin-10/metabolism ; Lipopolysaccharides/immunology ; Lipoproteins, LDL/immunology ; Lipoproteins, LDL/metabolism ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Spleen/cytology ; Spleen/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Apolipoproteins E ; Autoantibodies ; Cytokines ; Lipopolysaccharides ; Lipoproteins, LDL ; oxidized low density lipoprotein ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2008-07-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2008.05.004
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Zs.A 880: Show issues

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Article: Allele-specific effects of ecSOD on asbestos-induced fibroproliferative lung disease in mice

Jun, Sujung / Fattman, Cheryl L / Kim, Byung-Jin / Jones, Harlan / Dory, Ladislav

Free radical biology & medicine. 2011 May 15, v. 50, no. 10

2011

Abstract: Previous work by others suggests that there is a strain-dependent variation in the susceptibility to inflammatory lung injury in mice. Specifically, the 129/J mice appear to be more resistant to asbestos-induced pulmonary fibrosis than the C57BL/6 strain. ...

Abstract	Previous work by others suggests that there is a strain-dependent variation in the susceptibility to inflammatory lung injury in mice. Specifically, the 129/J mice appear to be more resistant to asbestos-induced pulmonary fibrosis than the C57BL/6 strain. A separate line of evidence suggests that extracellular superoxide dismutase (ecSOD) may play an important role in protecting the lung from such injuries. We have recently reported that the 129/J strain of mice has an ecSOD genotype and phenotype distinctly different from those of the C57BL/6 mice. In order to identify ecSOD as a potential “asbestos-injury resistance” gene, we bred congenic mice, on the C57BL/6 background, carrying the wild type (sod3wt) or the 129/J (sod3129) allele for ecSOD. This allowed us to examine the role of ecSOD polymorphism in susceptibility to lung injury in an otherwise identical genetic background. Interestingly, asbestos treatment induces a significant (~40%) increase in plasma ecSOD activity in the sod3129 mice, but not in the sod3wt mice. Asbestos administration results in a loss of ecSOD activity and protein from lung tissue of both congenic strains, but the lung ecSOD activity remains significantly higher in sod3129 mice. As expected, asbestos treatment results in a significant recovery of ecSOD protein in bronchoalveolar lavage fluid (BALF). The BALF of sod3129 mice also have significantly lower levels of proteins and inflammatory cells, especially neutrophils, accompanied by a significantly lower extent of lung injury, as measured by a pathology index score or hydroxyproline content. Immunohistochemistry reveals a significant loss of ecSOD from the tips of the respiratory epithelial cells in response to asbestos treatment and that the loss of immunodetectable ecSOD is compensated for by enzyme expression by infiltrating cells, especially in the sod3wt mice. Our studies thus identify ecSOD as an important anti-inflammatory gene, responsible for most, if not all of the resistance to asbestos-induced lung injury reported for the 129/J strain of mice. The data further suggest allele-specific differences in the regulation of ecSOD expression. These congenic mice therefore represent a very useful model to study the role of this enzyme in all inflammatory diseases. Polymorphisms in human ecSOD have also been reported and it appears logical to assume that such variations may have a profound effect on disease susceptibility.
Keywords	alleles ; asbestos ; disease resistance ; epithelial cells ; fibrosis ; genetic background ; humans ; hydroxyproline ; immunohistochemistry ; mice ; models ; neutrophils ; phenotype ; proteins ; superoxide dismutase
Language	English
Dates of publication	2011-0515
Size	p. 1288-1296.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2011.02.023
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 2109: Show issues

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Article: Chronic hyperbaric oxygen treatment elicits an anti-oxidant response and attenuates atherosclerosis in apoE knockout mice.

Kudchodkar, Bhalchandra J / Pierce, Anson / Dory, Ladislav

Atherosclerosis

2007 Volume 193, Issue 1, Page(s) 28–35

Abstract: We previously demonstrated that hyperbaric oxygen (HBO) treatment inhibits diet-induced atherosclerosis in New Zealand White rabbits. In the present study we investigate the mechanisms that might be involved in the athero-protective effect of HBO ... ...

Abstract	We previously demonstrated that hyperbaric oxygen (HBO) treatment inhibits diet-induced atherosclerosis in New Zealand White rabbits. In the present study we investigate the mechanisms that might be involved in the athero-protective effect of HBO treatment in a well-accepted model of atherosclerosis, the apoE knockout (KO) mouse. We examine the effects of daily HBO treatment (for 5 and 10 weeks) on the components of the anti-oxidant defense mechanism and the redox state in blood, liver and aortic tissues and compare them to those of untreated apoE KO mice. HBO treatment results in a significant reduction of aortic cholesterol content and decreased fatty streak formation. These changes are accompanied by a significant reduction of autoantibodies against oxidatively modified LDL and profound changes in the redox state of the liver and aortic tissues. A 10-week treatment significantly reduces hepatic levels of TBARS and oxidized glutathione, while significantly increases the levels of reduced glutathione, glutathione reductase (GR), transferase, Se-dependent glutathione peroxidase and catalase (CAT). The effects of HBO treatment are similar in the aortic tissues. These observations provide evidence that HBO treatment has a powerful effect on the redox state of relevant tissues and produces an environment that inhibits oxidation. The anti-oxidant response may be the key to the anti-atherogenic effect of HBO treatment.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Aorta, Thoracic/pathology ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Aryldialkylphosphatase/blood ; Atherosclerosis/etiology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Autoantibodies/blood ; Cholesterol/blood ; Female ; Glutathione/metabolism ; Glutathione Disulfide/metabolism ; Hyperbaric Oxygenation ; Lipid Peroxidation ; Lipoproteins, LDL/immunology ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oxidation-Reduction ; Oxidative Stress ; Rabbits ; Thiobarbituric Acid Reactive Substances/metabolism
Chemical Substances	Antioxidants ; Apolipoproteins E ; Autoantibodies ; Lipoproteins, LDL ; Thiobarbituric Acid Reactive Substances ; oxidized low density lipoprotein ; Cholesterol (97C5T2UQ7J) ; Aryldialkylphosphatase (EC 3.1.8.1) ; Glutathione (GAN16C9B8O) ; Glutathione Disulfide (ULW86O013H)
Language	English
Publishing date	2007-07
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2006.08.018
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Zs.A 226: Show issues

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Article: Cloning and characterization of two alleles of the murine extracellular superoxide dismutase gene.

Mirossay, Andrej / Jun, Sujung / Dory, Ladislav

Biochemical and biophysical research communications

2007 Volume 352, Issue 3, Page(s) 739–743

Abstract: We have recently documented the existence of a second allele of ecSOD in mice. Thus far, this allele was only found in the 129P3/J strain. It is characterized by two point mutations leading to amino acid changes as well as a 10 bp deletion from the 3' ... ...

Abstract	We have recently documented the existence of a second allele of ecSOD in mice. Thus far, this allele was only found in the 129P3/J strain. It is characterized by two point mutations leading to amino acid changes as well as a 10 bp deletion from the 3' UTR. We have also shown that the phenotype is profoundly affected by the genotype. In order to obtain a tool to investigate the differences in the properties as well as the posttranscriptional regulation of expression of the two alleles we now describe the creation and characterization of stably transfected CHO-K1 cell lines expressing either of these alleles. CHO-K1 cells were chosen because they do not express endogenous ecSOD and are easy to transfect. We demonstrate that the transfected cells secrete substantial amounts of glycosylated ecSOD, detected by Western blot analyses, ConA-Sepharose affinity chromatography and activity measurements.
MeSH term(s)	Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; CHO Cells ; Cloning, Molecular/methods ; Cricetinae ; Cricetulus ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Superoxide Dismutase/chemistry ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism
Chemical Substances	Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2007-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2006.11.081
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Zs.A 116: Show issues

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Article ; Online: Allele-specific effects of ecSOD on asbestos-induced fibroproliferative lung disease in mice.

Jun, Sujung / Fattman, Cheryl L / Kim, Byung-Jin / Jones, Harlan / Dory, Ladislav

Free radical biology & medicine

2011 Volume 50, Issue 10, Page(s) 1288–1296

Abstract	Previous work by others suggests that there is a strain-dependent variation in the susceptibility to inflammatory lung injury in mice. Specifically, the 129/J mice appear to be more resistant to asbestos-induced pulmonary fibrosis than the C57BL/6 strain. A separate line of evidence suggests that extracellular superoxide dismutase (ecSOD) may play an important role in protecting the lung from such injuries. We have recently reported that the 129/J strain of mice has an ecSOD genotype and phenotype distinctly different from those of the C57BL/6 mice. In order to identify ecSOD as a potential "asbestos-injury resistance" gene, we bred congenic mice, on the C57BL/6 background, carrying the wild type (sod3wt) or the 129/J (sod3129) allele for ecSOD. This allowed us to examine the role of ecSOD polymorphism in susceptibility to lung injury in an otherwise identical genetic background. Interestingly, asbestos treatment induces a significant (~40%) increase in plasma ecSOD activity in the sod3129 mice, but not in the sod3wt mice. Asbestos administration results in a loss of ecSOD activity and protein from lung tissue of both congenic strains, but the lung ecSOD activity remains significantly higher in sod3129 mice. As expected, asbestos treatment results in a significant recovery of ecSOD protein in bronchoalveolar lavage fluid (BALF). The BALF of sod3129 mice also have significantly lower levels of proteins and inflammatory cells, especially neutrophils, accompanied by a significantly lower extent of lung injury, as measured by a pathology index score or hydroxyproline content. Immunohistochemistry reveals a significant loss of ecSOD from the tips of the respiratory epithelial cells in response to asbestos treatment and that the loss of immunodetectable ecSOD is compensated for by enzyme expression by infiltrating cells, especially in the sod3wt mice. Our studies thus identify ecSOD as an important anti-inflammatory gene, responsible for most, if not all of the resistance to asbestos-induced lung injury reported for the 129/J strain of mice. The data further suggest allele-specific differences in the regulation of ecSOD expression. These congenic mice therefore represent a very useful model to study the role of this enzyme in all inflammatory diseases. Polymorphisms in human ecSOD have also been reported and it appears logical to assume that such variations may have a profound effect on disease susceptibility.
MeSH term(s)	Alleles ; Animals ; Asbestos ; Extracellular Space/enzymology ; Female ; Gene Expression Regulation, Enzymologic ; Humans ; Mice ; Mice, Congenic ; Mice, Inbred C57BL ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/metabolism ; Pulmonary Fibrosis/pathology ; Superoxide Dismutase/blood ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism
Chemical Substances	Asbestos (1332-21-4) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2011-03-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2011.02.023
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