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Article: Effect of a high salt diet on microvascular antioxidant enzymes.

Lenda, Deborah M / Boegehold, Matthew A

2002 Volume 39, Issue 1, Page(s) 41–50

Abstract: High dietary salt intake decreases the endothelium-dependent dilation of skeletal muscle arterioles by inhibiting local nitric oxide (NO) activity without changing vascular smooth muscle responsiveness to NO. Under these conditions, microvascular walls ... ...

Abstract	High dietary salt intake decreases the endothelium-dependent dilation of skeletal muscle arterioles by inhibiting local nitric oxide (NO) activity without changing vascular smooth muscle responsiveness to NO. Under these conditions, microvascular walls show evidence of oxidative stress, and scavengers of reactive oxygen species (ROS) abolish this oxidative stress and restore normal arteriolar responses to acetylcholine (ACh). We tested the hypothesis that the salt-dependent appearance of microvascular ROS, and accompanying reduction in endothelium-dependent dilation, is due to a decrease in antioxidant enzyme expression or activity. We studied spinotrapezius muscle microvessels in rats fed normal (NS) (0.45%) or high (HS) (7%) salt diets for 4-5 weeks. Western analysis of arteriolar and venular protein showed no difference between groups in the content of superoxide dismutase (Cu/Zn SOD), catalase, or glutathione peroxidase. The catalase inhibitor 3-amino-1,2,4-triazole (3AT) increased arteriolar and venular oxidant activity (assessed by tetranitroblue tetrazolium reduction) by the same amount in both groups, suggesting similar levels of catalase activity. 3AT did not affect arteriolar responses to ACh in either group. The Cu/Zn SOD inhibitor diethyldithiocarbamate increased arteriolar and venular oxidant activity to a lesser extent in HS rats, suggesting reduced Cu/Zn SOD activity in this group. Cu/Zn SOD inhibition decreased arteriolar responses to ACh only in NS rats. These findings suggest that endogenous Cu/Zn SOD preserves the endothelium-dependent control of arteriolar tone in NS rats, and that a reduction in Cu/Zn SOD activity contributes to the loss of arteriolar NO activity in HS rats.
MeSH term(s)	Acetylcholine/pharmacology ; Amitrole/pharmacology ; Animals ; Antioxidants ; Arterioles/drug effects ; Arterioles/physiology ; Catalase/analysis ; Catalase/antagonists & inhibitors ; Ditiocarb/pharmacology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/physiology ; Enzyme Inhibitors/pharmacology ; Glutathione Peroxidase/analysis ; Male ; Microcirculation/drug effects ; Microcirculation/enzymology ; Muscle, Skeletal/blood supply ; Nitric Oxide/pharmacology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride, Dietary/administration & dosage ; Superoxide Dismutase/analysis ; Superoxide Dismutase/antagonists & inhibitors ; Vasodilation ; Vasodilator Agents/pharmacology ; Venules/enzymology
Chemical Substances	Antioxidants ; Enzyme Inhibitors ; Sodium Chloride, Dietary ; Vasodilator Agents ; Nitric Oxide (31C4KY9ESH) ; Ditiocarb (99Z2744345) ; Catalase (EC 1.11.1.6) ; Glutathione Peroxidase (EC 1.11.1.9) ; Superoxide Dismutase (EC 1.15.1.1) ; Acetylcholine (N9YNS0M02X) ; Amitrole (ZF80H5GXUF)
Language	English
Publishing date	2002-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1105259-4
ISSN	1423-0135 ; 1018-1172
ISSN (online)	1423-0135
ISSN	1018-1172
DOI	10.1159/000048992
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Article: Effect of a high-salt diet on oxidant enzyme activity in skeletal muscle microcirculation.

Lenda, Deborah M / Boegehold, Matthew A

American journal of physiology. Heart and circulatory physiology

2001 Volume 282, Issue 2, Page(s) H395–402

Abstract: Increased salt intake attenuates the endothelium-dependent dilation of skeletal muscle arterioles by abolishing local nitric oxide (NO) activity. There is evidence of oxidative stress in arteriolar and venular walls of rats fed a high-salt diet, and ... ...

Abstract	Increased salt intake attenuates the endothelium-dependent dilation of skeletal muscle arterioles by abolishing local nitric oxide (NO) activity. There is evidence of oxidative stress in arteriolar and venular walls of rats fed a high-salt diet, and depressed arteriolar responses to acetylcholine (ACh) in these rats are reversed by scavengers of reactive oxygen species (ROS). In this study, we tested the hypothesis that this salt-dependent increase in microvascular ROS and the resulting attenuation of endothelium-dependent dilation are due to increased expression and/or activity of oxidant enzymes in the microvascular wall. Resting arteriolar and venular wall oxidant activity, as assessed by tetranitroblue tetrazolium reduction, was consistently higher in the spinotrapezius muscle of rats fed a high-salt diet (7% NaCl, HS) for 4-5 wk than in those fed a normal diet (0.45% NaCl, NS) for the same duration. Western analysis of protein from isolated microvessels showed no difference between HS and NS rats in the expression of NAD(P)H oxidase or xanthine oxidase. Inhibition of NAD(P)H oxidase and/or xanthine oxidase with diphenyleneiodonium chloride and oxypurinol, respectively, reduced resting arteriolar wall oxidant activity to normal levels in HS rats but had no effect in NS rats, suggesting that the basal activities of NAD(P)H oxidase and xanthine oxidase are increased in HS microvessels. However, inhibition of these enzymes in HS rats did not restore normal arteriolar responses to ACh, suggesting that this stimulus activates an alternate source of ROS that eliminates the role of NO in the subsequent dilation.
MeSH term(s)	Animals ; Capillaries/enzymology ; Endothelium, Vascular/enzymology ; Enzyme Activation/drug effects ; Enzyme Inhibitors/pharmacology ; Male ; Muscle, Skeletal/blood supply ; NADPH Oxidases/antagonists & inhibitors ; NADPH Oxidases/metabolism ; Nitric Oxide/metabolism ; Onium Compounds/pharmacology ; Oxypurinol/pharmacology ; Phosphoproteins/metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride, Dietary/pharmacology ; Vasodilation/drug effects ; Xanthine Oxidase/antagonists & inhibitors ; Xanthine Oxidase/metabolism
Chemical Substances	Enzyme Inhibitors ; Onium Compounds ; Phosphoproteins ; Sodium Chloride, Dietary ; neutrophil cytosol factor 67K ; Nitric Oxide (31C4KY9ESH) ; diphenyleneiodonium (6HJ411TU98) ; Xanthine Oxidase (EC 1.17.3.2) ; NADPH Oxidases (EC 1.6.3.-) ; Oxypurinol (G97OZE5068)
Language	English
Publishing date	2001-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.0354.2001
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Article: Negative role of colony-stimulating factor-1 in macrophage, T cell, and B cell mediated autoimmune disease in MRL-Fas(lpr) mice.

Lenda, Deborah M / Stanley, E Richard / Kelley, Vicki R

Journal of immunology (Baltimore, Md. : 1950)

2004 Volume 173, Issue 7, Page(s) 4744–4754

Abstract: Inflammation in the kidney and other tissues (lung, and salivary and lacrimal glands) is characteristic of MRL-Fas(lpr) mice with features of lupus. Macrophages (Mphi) are prominent in these tissues. Given that 1) Mphi survival, recruitment, ... ...

Abstract	Inflammation in the kidney and other tissues (lung, and salivary and lacrimal glands) is characteristic of MRL-Fas(lpr) mice with features of lupus. Macrophages (Mphi) are prominent in these tissues. Given that 1) Mphi survival, recruitment, proliferation, and activation during inflammation is dependent on CSF-1, 2) Mphi mediate renal resident cell apoptosis, and 3) CSF-1 is up-regulated in MRL-Fas(lpr) mice before, and during nephritis, we hypothesized that CSF-1-deficient MRL-Fas(lpr) mice would be protected from Mphi-mediated nephritis, and the systemic illness. To test this hypothesis, we compared CSF-1-deficient MRL-Fas(lpr) with wild-type strains. Renal pathology is suppressed and function improved in CSF-1-deficient MRL-Fas(lpr) mice. There are far fewer intrarenal Mphi and T cells in CSF-1-deficient MRL-Fas(lpr) vs wild-type kidneys. This leukocytic reduction results from suppressed infiltration, and intrarenal proliferation, but not enhanced apoptosis. The CSF-1-deficient MRL-Fas(lpr) kidneys remain preserved as indicated by greatly reduced indices of injury (nephritogenic cytokines, tubular apoptosis, and proliferation). The renal protective mechanism in CSF-1-deficient mice is not limited to reduced intrarenal leukocytes; circulating Igs and autoantibodies, and renal Ig deposits are decreased. This may result from enhanced B cell apoptosis and fewer B cells in CSF-1-deficient MRL-Fas(lpr) mice. Furthermore, the systemic illness including, skin, lung, and lacrimal and salivary glands pathology, lymphadenopathy, and splenomegaly are dramatically suppressed in CSF-1-deficient MRL-Fas(lpr) as compared with wild-type mice. These results indicate that CSF-1 is an attractive therapeutic target to combat Mphi-, T cell-, and B cell-mediated autoimmune lupus.
MeSH term(s)	Animals ; Apoptosis/genetics ; Apoptosis/immunology ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Bone Marrow/immunology ; Bone Marrow/pathology ; Cell Migration Inhibition ; Chemokines/antagonists & inhibitors ; Chemokines/physiology ; Complement C3/metabolism ; Cytokines/antagonists & inhibitors ; Cytokines/physiology ; Down-Regulation/genetics ; Down-Regulation/immunology ; Epithelium/immunology ; Epithelium/pathology ; Growth Inhibitors/deficiency ; Growth Inhibitors/genetics ; Growth Inhibitors/physiology ; Immunoglobulin G/metabolism ; Immunoglobulin Isotypes/biosynthesis ; Kidney Glomerulus/immunology ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Kidney Tubules/immunology ; Kidney Tubules/pathology ; Lacrimal Apparatus/immunology ; Lacrimal Apparatus/pathology ; Leukocytes/pathology ; Leukopenia/genetics ; Leukopenia/immunology ; Leukopenia/pathology ; Lung/immunology ; Lung/pathology ; Lupus Nephritis/genetics ; Lupus Nephritis/immunology ; Lupus Nephritis/pathology ; Lupus Nephritis/prevention & control ; Lymphatic Diseases/genetics ; Lymphatic Diseases/immunology ; Lymphatic Diseases/pathology ; Lymphatic Diseases/prevention & control ; Macrophage Activation/genetics ; Macrophage Activation/immunology ; Macrophage Colony-Stimulating Factor/deficiency ; Macrophage Colony-Stimulating Factor/genetics ; Macrophage Colony-Stimulating Factor/physiology ; Macrophages/immunology ; Macrophages/pathology ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Inbred MRL lpr ; Mice, Knockout ; Mice, Transgenic ; Salivary Glands/immunology ; Salivary Glands/pathology ; Severity of Illness Index ; Skin/immunology ; Skin/pathology ; Spleen/immunology ; Spleen/pathology ; Splenomegaly/genetics ; Splenomegaly/immunology ; Splenomegaly/prevention & control ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
Chemical Substances	Chemokines ; Complement C3 ; Cytokines ; Growth Inhibitors ; Immunoglobulin G ; Immunoglobulin Isotypes ; Macrophage Colony-Stimulating Factor (81627-83-0)
Language	English
Publishing date	2004-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.173.7.4744
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Article: IL-12 deficiency in MRL-Fas(lpr) mice delays nephritis and intrarenal IFN-gamma expression, and diminishes systemic pathology.

Kikawada, Eriya / Lenda, Deborah M / Kelley, Vicki R

Journal of immunology (Baltimore, Md. : 1950)

2003 Volume 170, Issue 7, Page(s) 3915–3925

Abstract: Autoimmune disease in MRL-Fas(lpr) mice is characterized by fatal nephritis, systemic pathology, and autoantibodies, mimicking human lupus. We previously reported that 1) intrarenal IL-12 elicits nephritis by fostering the accumulation of intrarenal IFN- ... ...

Abstract	Autoimmune disease in MRL-Fas(lpr) mice is characterized by fatal nephritis, systemic pathology, and autoantibodies, mimicking human lupus. We previously reported that 1) intrarenal IL-12 elicits nephritis by fostering the accumulation of intrarenal IFN-gamma-secreting T cells, and 2) MRL-Fas(lpr) mice deficient in the IFN-gamma receptor were spared from nephritis. Therefore, we hypothesized that eliminating IL-12 in MRL-Fas(lpr) mice reduces IFN-gamma-secreting cells and thereby prevents systemic pathology. For this purpose, we constructed an IL-12p40-deficient MRL-Fas(lpr)(IL-12(-/-)) strain. We determined that glomerular and interstitial, but not perivascular, renal pathology were decreased in IL-12(-/-) mice vs the wild-type (WT) strain (5 mo of age). Similarly, systemic pathology (lung, lacrimal and salivary glands, skin, and lymphadenopathy) was diminished. The intrarenal accumulation of T cells (CD4(+), CD8(+), CD4(-)CD8(-)B220(+)) and macrophages was dramatically reduced in IL-12(-/-) MRL-Fas(lpr) kidneys. We determined that there were fewer IFN-gamma transcripts (>70%) in the IL-12(-/-) protected kidneys compared with the WT kidneys. Similarly, cells propagated from IL-12(-/-) MRL-Fas(lpr) kidneys generated substantially less IFN-gamma when stimulated with IL-12 and IL-18 compared with those from WT kidneys, and we detected fewer CD8 and B220 T cells producing IFN-gamma in these IL-12(-/-) MRL-Fas(lpr) kidneys. Of note, survival was modestly extended in the IL-12(-/-) MRL-Fas(lpr) mice. While lung and lacrimal and salivary gland pathology remained reduced in moribund IL-12(-/-) MRL-Fas(lpr) mice, renal pathology and IFN-gamma expression were equivalent to those in the WT strain. Thus, we suggest that IL-12 is a therapeutic target for multiple tissues in lupus; however blocking IL-12 alone is not sufficient to confer enduring protection from lupus nephritis.
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Complement C3/deficiency ; Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors ; Granulocyte-Macrophage Colony-Stimulating Factor/biosynthesis ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; IgG Deficiency/genetics ; IgG Deficiency/immunology ; IgG Deficiency/pathology ; Immunoglobulin Isotypes/blood ; Interferon-gamma/antagonists & inhibitors ; Interferon-gamma/biosynthesis ; Interferon-gamma/genetics ; Interleukin-12/deficiency ; Interleukin-12/genetics ; Interleukin-18/biosynthesis ; Interleukin-4/antagonists & inhibitors ; Interleukin-4/biosynthesis ; Interleukin-4/genetics ; Kidney/immunology ; Kidney/metabolism ; Kidney/pathology ; Kidney Glomerulus/blood supply ; Kidney Glomerulus/immunology ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Kidney Tubules/blood supply ; Kidney Tubules/immunology ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Lacrimal Apparatus/immunology ; Lacrimal Apparatus/pathology ; Leukocyte Common Antigens/biosynthesis ; Leukopenia/genetics ; Leukopenia/immunology ; Leukopenia/pathology ; Lung/immunology ; Lung/pathology ; Lupus Nephritis/genetics ; Lupus Nephritis/immunology ; Lupus Nephritis/pathology ; Lupus Nephritis/prevention & control ; Lymph Nodes/immunology ; Lymph Nodes/metabolism ; Lymphatic Diseases/genetics ; Lymphatic Diseases/immunology ; Lymphatic Diseases/pathology ; Lymphatic Diseases/prevention & control ; Lymphopenia/genetics ; Lymphopenia/immunology ; Macrophage Colony-Stimulating Factor/antagonists & inhibitors ; Macrophage Colony-Stimulating Factor/biosynthesis ; Macrophage Colony-Stimulating Factor/genetics ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Inbred MRL lpr ; Mice, Knockout ; Salivary Glands/immunology ; Salivary Glands/pathology ; Skin/immunology ; Skin/pathology ; Survival Rate ; fas Receptor/genetics
Chemical Substances	Complement C3 ; Immunoglobulin Isotypes ; Interleukin-18 ; fas Receptor ; Interleukin-12 (187348-17-0) ; Interleukin-4 (207137-56-2) ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Interferon-gamma (82115-62-6) ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1) ; Leukocyte Common Antigens (EC 3.1.3.48)
Language	English
Publishing date	2003-03-17
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.170.7.3915
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Article: Effect of a High Salt Diet on Microvascular Antioxidant Enzymes

Lenda, Deborah M. / Boegehold, Matthew A.

Journal of Vascular Research

2002 Volume 39, Issue 1, Page(s) 41–50

Institution	Department of Physiology, West Virginia University School of Medicine, Morgantown, W.Va., USA
Abstract	High dietary salt intake decreases the endothelium-dependent dilation of skeletal muscle arterioles by inhibiting local nitric oxide (NO) activity without changing vascular smooth muscle responsiveness to NO. Under these conditions, microvascular walls show evidence of oxidative stress, and scavengers of reactive oxygen species (ROS) abolish this oxidative stress and restore normal arteriolar responses to acetylcholine (ACh). We tested the hypothesis that the salt-dependent appearance of microvascular ROS, and accompanying reduction in endothelium-dependent dilation, is due to a decrease in antioxidant enzyme expression or activity. We studied spinotrapezius muscle microvessels in rats fed normal (NS) (0.45%) or high (HS) (7%) salt diets for 4–5 weeks. Western analysis of arteriolar and venular protein showed no difference between groups in the content of superoxide dismutase (Cu/Zn SOD), catalase, or glutathione peroxidase. The catalase inhibitor 3-amino-1,2,4-triazole (3AT) increased arteriolar and venular oxidant activity (assessed by tetranitroblue tetrazolium reduction) by the same amount in both groups, suggesting similar levels of catalase activity. 3AT did not affect arteriolar responses to ACh in either group. The Cu/Zn SOD inhibitor diethyldithiocarbamate increased arteriolar and venular oxidant activity to a lesser extent in HS rats, suggesting reduced Cu/Zn SOD activity in this group. Cu/Zn SOD inhibition decreased arteriolar responses to ACh only in NS rats. These findings suggest that endogenous Cu/Zn SOD preserves the endothelium-dependent control of arteriolar tone in NS rats, and that a reduction in Cu/Zn SOD activity contributes to the loss of arteriolar NO activity in HS rats.
Keywords	Nitric oxide ; Free radicals ; Microcirculation ; Endothelium ; Dietary salt
Language	English
Publishing date	2002-02-13
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Research Paper
ZDB-ID	1105259-4
ISSN	1423-0135 ; 1018-1172
ISSN (online)	1423-0135
ISSN	1018-1172
DOI	10.1159/000048992
Database	Karger publisher's database

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Article: Reduced macrophage recruitment, proliferation, and activation in colony-stimulating factor-1-deficient mice results in decreased tubular apoptosis during renal inflammation.

Lenda, Deborah M / Kikawada, Eriya / Stanley, E Richard / Kelley, Vicki R

Journal of immunology (Baltimore, Md. : 1950)

2003 Volume 170, Issue 6, Page(s) 3254–3262

Abstract: ... of macrophages (M phi) during inflammation. Our prior studies indicate that activated M phi release soluble ... mediators that incite TEC death, and reducing intrarenal M phi during kidney disease diminishes TEC ... apoptosis. CSF-1 is required for M phi proliferation and survival. We hypothesized that in the absence ...

Abstract	Kidney tubular epithelial cell (TEC) death may be dependent on the number and activation state of macrophages (M phi) during inflammation. Our prior studies indicate that activated M phi release soluble mediators that incite TEC death, and reducing intrarenal M phi during kidney disease diminishes TEC apoptosis. CSF-1 is required for M phi proliferation and survival. We hypothesized that in the absence of CSF-1, M phi-mediated TEC apoptosis would be prevented during renal inflammation. To test this hypothesis, we evaluated renal inflammation during unilateral ureter obstruction in CSF-1-deficient (Csf1(op)/Csf1(op)) mice. We detected fewer M phi and T cells and less apoptotic TEC in the obstructed kidneys of Csf1(op)/Csf1(op) mice compared with wild-type (WT) mice. The decrease in intrarenal M phi resulted from diminished recruitment and proliferation, not enhanced apoptosis. CSF-1 enhanced M phi activation. There were far fewer activated (CD69, CD23, Ia, surface expression) M phi in obstructed CSF-1-deficient compared with WT obstructed kidneys. Similarly, bone marrow M phi preincubated with anti-CSF-1 receptor Ab or anti-CSF-1 neutralizing Ab were resistant to LPS- and IFN-gamma-induced activation. We detected fewer apoptotic-inducing molecules (reactive oxygen species, TNF-alpha, inducible NO synthase) in 1) M phi propagated from obstructed Csf1(op)/Csf1(op) compared with WT kidneys, and 2) WT bone marrow M phi blocked with anti-CSF-1 receptor or anti-CSF-1 Ab compared with the isotype control. Furthermore, blocking CSF-1 or the CSF-1 receptor induced less TEC apoptosis than the isotype control. We suggest that during renal inflammation, CSF-1 mediates M phi recruitment, proliferation, activation, and, in turn, TEC apoptosis.
MeSH term(s)	Animals ; Apoptosis/genetics ; Apoptosis/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/pathology ; Cell Count ; Cell Division/genetics ; Cell Division/immunology ; Cell Movement/genetics ; Cell Movement/immunology ; Cells, Cultured ; Chemokine CCL2/antagonists & inhibitors ; Chemokine CCL2/biosynthesis ; Down-Regulation/genetics ; Down-Regulation/immunology ; Epithelial Cells/immunology ; Epithelial Cells/pathology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Kidney Pelvis/immunology ; Kidney Pelvis/pathology ; Kidney Tubules/immunology ; Kidney Tubules/pathology ; Macrophage Activation/genetics ; Macrophage Colony-Stimulating Factor/deficiency ; Macrophage Colony-Stimulating Factor/genetics ; Macrophages/immunology ; Macrophages/pathology ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Knockout ; Ureteral Obstruction/genetics ; Ureteral Obstruction/immunology ; Ureteral Obstruction/metabolism ; Ureteral Obstruction/pathology
Chemical Substances	Chemokine CCL2 ; Macrophage Colony-Stimulating Factor (81627-83-0)
Language	English
Publishing date	2003-03-03
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.170.6.3254
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Article: Effect of a high salt diet on microvascular antioxidant enzymes.

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Article: Effect of a high-salt diet on oxidant enzyme activity in skeletal muscle microcirculation.

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Article: Negative role of colony-stimulating factor-1 in macrophage, T cell, and B cell mediated autoimmune disease in MRL-Fas(lpr) mice.

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Article: IL-12 deficiency in MRL-Fas(lpr) mice delays nephritis and intrarenal IFN-gamma expression, and diminishes systemic pathology.

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Article: Effect of a High Salt Diet on Microvascular Antioxidant Enzymes

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Article: Reduced macrophage recruitment, proliferation, and activation in colony-stimulating factor-1-deficient mice results in decreased tubular apoptosis during renal inflammation.

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