The SOD mimetic tempol ameliorates glomerular injury and reduces mitogen-activated protein kinase activity in dahl salt-sensitive rats
It was shown recently that renal injury in Dahl salt-sensitive (DS) hypertensive rats is accompanied by mitogen-activated protein kinase (MAPK) activation. The present study was conducted to elucidate the contribution of reactive oxygen species to MAPK activities and renal injury in DS rats. DS rats...
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| creator | NISHIYAMA, Akira YOSHIZUMI, Masanori SHOKOJI, Takatomi KIMURA, Shoji ABE, Youichi HITOMI, Hirofumi KAGAMI, Shoji KONDO, Shuji MIYATAKE, Akira FUKUNAGA, Megumu TAMAKI, Toshiaki KIYOMOTO, Hideyasu KOHNO, Masakazu |
| description | It was shown recently that renal injury in Dahl salt-sensitive (DS) hypertensive rats is accompanied by mitogen-activated protein kinase (MAPK) activation. The present study was conducted to elucidate the contribution of reactive oxygen species to MAPK activities and renal injury in DS rats. DS rats were maintained on high salt (H; 8.0% NaCl; n = 7) or low salt (L; 0.3% NaCl; n = 6) diets; H + a superoxide dismutase mimetic, tempol (3 mmol/L in drinking water; n = 8); or H + hydralazine (0.5 mmol/L in drinking water; n = 8) for 4 wk. Mean BP (MBP) in DS/H and DS/L rats was 185 +/- 7 and 113 +/- 3 mmHg, respectively. DS/H rats showed a higher ratio of urinary protein excretion and creatinine (U(protein)V/U(cr)V; 20.3 +/- 1.1) and a higher cortical collagen content (22 +/- 1 micro g/mg) than in DS/L rats (2.4 +/- 0.1 and 13 +/- 1 micro g/mg, respectively). The expression of p22-phox and Nox-1, essential components of NAD(P)H oxidase, in renal cortical tissue was approximately threefold higher in DS/H rats than in DS/L rats. Increased activities of renal cortical MAPK, including extracellular signal-regulated kinases (ERK) 1/ERK2 and c-Jun NH(2)-terminal kinases (JNK) were also observed in DS/H rats by 7.0 +/- 0.7- and 4.3 +/- 0.2-fold, respectively. Tempol treatment significantly decreased MBP (128 +/- 3 mmHg), U(protein)V/U(cr)V (4.8 +/- 0.4), and cortical collagen content (14 +/- 1 micro g/mg) and normalized ERK1/ERK2 and JNK activities in DS/H rats. Histologically, tempol markedly ameliorated progressive sclerotic and proliferative glomerular changes in DS/H rats. Hydralazine-treated DS/H rats showed similar MBP (127 +/- 5 mmHg) to tempol-treated DS/H rats. Hydralazine also decreased U(protein)V/U(cr)V (16.2 +/- 1.5) and cortical collagen content (19 +/- 1 micro g/mg) in DS/H rats. However, these values were significantly higher than those of tempol-treated rats. Furthermore, although hydralazine significantly reduced JNK activity (-56 +/- 3%), ERK1/ERK2 activities were unaffected. These data suggest that reactive oxygen species, generated by NAD(P)H oxidase, contribute to the progression of renal injury through ERK1/ERK2 activation in DS/H hypertensive rats. |
| doi_str_mv | 10.1097/01.asn.0000108523.02100.e0 |
| format | Article |
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The present study was conducted to elucidate the contribution of reactive oxygen species to MAPK activities and renal injury in DS rats. DS rats were maintained on high salt (H; 8.0% NaCl; n = 7) or low salt (L; 0.3% NaCl; n = 6) diets; H + a superoxide dismutase mimetic, tempol (3 mmol/L in drinking water; n = 8); or H + hydralazine (0.5 mmol/L in drinking water; n = 8) for 4 wk. Mean BP (MBP) in DS/H and DS/L rats was 185 +/- 7 and 113 +/- 3 mmHg, respectively. DS/H rats showed a higher ratio of urinary protein excretion and creatinine (U(protein)V/U(cr)V; 20.3 +/- 1.1) and a higher cortical collagen content (22 +/- 1 micro g/mg) than in DS/L rats (2.4 +/- 0.1 and 13 +/- 1 micro g/mg, respectively). The expression of p22-phox and Nox-1, essential components of NAD(P)H oxidase, in renal cortical tissue was approximately threefold higher in DS/H rats than in DS/L rats. Increased activities of renal cortical MAPK, including extracellular signal-regulated kinases (ERK) 1/ERK2 and c-Jun NH(2)-terminal kinases (JNK) were also observed in DS/H rats by 7.0 +/- 0.7- and 4.3 +/- 0.2-fold, respectively. Tempol treatment significantly decreased MBP (128 +/- 3 mmHg), U(protein)V/U(cr)V (4.8 +/- 0.4), and cortical collagen content (14 +/- 1 micro g/mg) and normalized ERK1/ERK2 and JNK activities in DS/H rats. Histologically, tempol markedly ameliorated progressive sclerotic and proliferative glomerular changes in DS/H rats. Hydralazine-treated DS/H rats showed similar MBP (127 +/- 5 mmHg) to tempol-treated DS/H rats. Hydralazine also decreased U(protein)V/U(cr)V (16.2 +/- 1.5) and cortical collagen content (19 +/- 1 micro g/mg) in DS/H rats. However, these values were significantly higher than those of tempol-treated rats. Furthermore, although hydralazine significantly reduced JNK activity (-56 +/- 3%), ERK1/ERK2 activities were unaffected. These data suggest that reactive oxygen species, generated by NAD(P)H oxidase, contribute to the progression of renal injury through ERK1/ERK2 activation in DS/H hypertensive rats.</description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1097/01.asn.0000108523.02100.e0</identifier><identifier>PMID: 14747377</identifier><identifier>CODEN: JASNEU</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Collagen - urine ; Cyclic N-Oxides - pharmacology ; Glomerulonephritis ; JNK Mitogen-Activated Protein Kinases ; Kidney Glomerulus - drug effects ; Kidney Glomerulus - enzymology ; Kidney Glomerulus - pathology ; Medical sciences ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases - drug effects ; Mitogen-Activated Protein Kinases - metabolism ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; p38 Mitogen-Activated Protein Kinases ; Proteinuria - metabolism ; Rats ; Rats, Inbred Dahl ; Spin Labels</subject><ispartof>Journal of the American Society of Nephrology, 2004-02, Vol.15 (2), p.306-315</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-9c29720022dd8d52411f85ee63c489044616890456d99430b46d1b44d796520f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15437109$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14747377$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NISHIYAMA, Akira</creatorcontrib><creatorcontrib>YOSHIZUMI, Masanori</creatorcontrib><creatorcontrib>SHOKOJI, Takatomi</creatorcontrib><creatorcontrib>KIMURA, Shoji</creatorcontrib><creatorcontrib>ABE, Youichi</creatorcontrib><creatorcontrib>HITOMI, Hirofumi</creatorcontrib><creatorcontrib>KAGAMI, Shoji</creatorcontrib><creatorcontrib>KONDO, Shuji</creatorcontrib><creatorcontrib>MIYATAKE, Akira</creatorcontrib><creatorcontrib>FUKUNAGA, Megumu</creatorcontrib><creatorcontrib>TAMAKI, Toshiaki</creatorcontrib><creatorcontrib>KIYOMOTO, Hideyasu</creatorcontrib><creatorcontrib>KOHNO, Masakazu</creatorcontrib><title>The SOD mimetic tempol ameliorates glomerular injury and reduces mitogen-activated protein kinase activity in dahl salt-sensitive rats</title><title>Journal of the American Society of Nephrology</title><addtitle>J Am Soc Nephrol</addtitle><description>It was shown recently that renal injury in Dahl salt-sensitive (DS) hypertensive rats is accompanied by mitogen-activated protein kinase (MAPK) activation. The present study was conducted to elucidate the contribution of reactive oxygen species to MAPK activities and renal injury in DS rats. DS rats were maintained on high salt (H; 8.0% NaCl; n = 7) or low salt (L; 0.3% NaCl; n = 6) diets; H + a superoxide dismutase mimetic, tempol (3 mmol/L in drinking water; n = 8); or H + hydralazine (0.5 mmol/L in drinking water; n = 8) for 4 wk. Mean BP (MBP) in DS/H and DS/L rats was 185 +/- 7 and 113 +/- 3 mmHg, respectively. DS/H rats showed a higher ratio of urinary protein excretion and creatinine (U(protein)V/U(cr)V; 20.3 +/- 1.1) and a higher cortical collagen content (22 +/- 1 micro g/mg) than in DS/L rats (2.4 +/- 0.1 and 13 +/- 1 micro g/mg, respectively). The expression of p22-phox and Nox-1, essential components of NAD(P)H oxidase, in renal cortical tissue was approximately threefold higher in DS/H rats than in DS/L rats. Increased activities of renal cortical MAPK, including extracellular signal-regulated kinases (ERK) 1/ERK2 and c-Jun NH(2)-terminal kinases (JNK) were also observed in DS/H rats by 7.0 +/- 0.7- and 4.3 +/- 0.2-fold, respectively. Tempol treatment significantly decreased MBP (128 +/- 3 mmHg), U(protein)V/U(cr)V (4.8 +/- 0.4), and cortical collagen content (14 +/- 1 micro g/mg) and normalized ERK1/ERK2 and JNK activities in DS/H rats. Histologically, tempol markedly ameliorated progressive sclerotic and proliferative glomerular changes in DS/H rats. Hydralazine-treated DS/H rats showed similar MBP (127 +/- 5 mmHg) to tempol-treated DS/H rats. Hydralazine also decreased U(protein)V/U(cr)V (16.2 +/- 1.5) and cortical collagen content (19 +/- 1 micro g/mg) in DS/H rats. However, these values were significantly higher than those of tempol-treated rats. Furthermore, although hydralazine significantly reduced JNK activity (-56 +/- 3%), ERK1/ERK2 activities were unaffected. These data suggest that reactive oxygen species, generated by NAD(P)H oxidase, contribute to the progression of renal injury through ERK1/ERK2 activation in DS/H hypertensive rats.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Collagen - urine</subject><subject>Cyclic N-Oxides - pharmacology</subject><subject>Glomerulonephritis</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>Kidney Glomerulus - drug effects</subject><subject>Kidney Glomerulus - enzymology</subject><subject>Kidney Glomerulus - pathology</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3</subject><subject>Mitogen-Activated Protein Kinases - drug effects</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Proteinuria - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred Dahl</subject><subject>Spin Labels</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkUtr3DAUhUVpaR7tXyii0O7sXj0s2d2FJH1AaBZJ10IjXSdKZXsqyYH5A_3dVZKB0eYKznd0xD2EfGTQMhj0F2CtzXML9TDoOy5a4AygRXhFjlknRCNkB6_rHaRqlNLiiJzk_FDxjmv9lhwxqaUWWh-Tf7f3SG-uL-gUJizB0YLTdonUThjDkmzBTO_iMmFao000zA9r2lE7e5rQr66qUyjLHc6NdSU8Vt7TbVoKhpn-CbPNSJ-FUHbVTL29jzTbWJqMcw5VQFpD8jvyZrQx4_v9PCW_v13env9orq6__zw_u2qcVKI0g-OD5gCce9_7jkvGxr5DVMLJfgApFVNPs1N-GKSAjVSebaT0elAdh1Gcks8v79Y__l0xFzOF7DBGO-OyZtMDq6tkuoJfX0CXlpwTjmabwmTTzjAwTy0YYObs5pc5tGCeWzCXUM0f9inrZkJ_sO7XXoFPe8BmZ-OY7OxCPnCdFLqGiP_9DJHq</recordid><startdate>20040201</startdate><enddate>20040201</enddate><creator>NISHIYAMA, Akira</creator><creator>YOSHIZUMI, Masanori</creator><creator>SHOKOJI, Takatomi</creator><creator>KIMURA, Shoji</creator><creator>ABE, Youichi</creator><creator>HITOMI, Hirofumi</creator><creator>KAGAMI, Shoji</creator><creator>KONDO, Shuji</creator><creator>MIYATAKE, Akira</creator><creator>FUKUNAGA, Megumu</creator><creator>TAMAKI, Toshiaki</creator><creator>KIYOMOTO, Hideyasu</creator><creator>KOHNO, Masakazu</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20040201</creationdate><title>The SOD mimetic tempol ameliorates glomerular injury and reduces mitogen-activated protein kinase activity in dahl salt-sensitive rats</title><author>NISHIYAMA, Akira ; YOSHIZUMI, Masanori ; SHOKOJI, Takatomi ; KIMURA, Shoji ; ABE, Youichi ; HITOMI, Hirofumi ; KAGAMI, Shoji ; KONDO, Shuji ; MIYATAKE, Akira ; FUKUNAGA, Megumu ; TAMAKI, Toshiaki ; KIYOMOTO, Hideyasu ; KOHNO, Masakazu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-9c29720022dd8d52411f85ee63c489044616890456d99430b46d1b44d796520f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Collagen - urine</topic><topic>Cyclic N-Oxides - pharmacology</topic><topic>Glomerulonephritis</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>Kidney Glomerulus - drug effects</topic><topic>Kidney Glomerulus - enzymology</topic><topic>Kidney Glomerulus - pathology</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3</topic><topic>Mitogen-Activated Protein Kinases - drug effects</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>Proteinuria - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred Dahl</topic><topic>Spin Labels</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NISHIYAMA, Akira</creatorcontrib><creatorcontrib>YOSHIZUMI, Masanori</creatorcontrib><creatorcontrib>SHOKOJI, Takatomi</creatorcontrib><creatorcontrib>KIMURA, Shoji</creatorcontrib><creatorcontrib>ABE, Youichi</creatorcontrib><creatorcontrib>HITOMI, Hirofumi</creatorcontrib><creatorcontrib>KAGAMI, Shoji</creatorcontrib><creatorcontrib>KONDO, Shuji</creatorcontrib><creatorcontrib>MIYATAKE, Akira</creatorcontrib><creatorcontrib>FUKUNAGA, Megumu</creatorcontrib><creatorcontrib>TAMAKI, Toshiaki</creatorcontrib><creatorcontrib>KIYOMOTO, Hideyasu</creatorcontrib><creatorcontrib>KOHNO, Masakazu</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of the American Society of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NISHIYAMA, Akira</au><au>YOSHIZUMI, Masanori</au><au>SHOKOJI, Takatomi</au><au>KIMURA, Shoji</au><au>ABE, Youichi</au><au>HITOMI, Hirofumi</au><au>KAGAMI, Shoji</au><au>KONDO, Shuji</au><au>MIYATAKE, Akira</au><au>FUKUNAGA, Megumu</au><au>TAMAKI, Toshiaki</au><au>KIYOMOTO, Hideyasu</au><au>KOHNO, Masakazu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The SOD mimetic tempol ameliorates glomerular injury and reduces mitogen-activated protein kinase activity in dahl salt-sensitive rats</atitle><jtitle>Journal of the American Society of Nephrology</jtitle><addtitle>J Am Soc Nephrol</addtitle><date>2004-02-01</date><risdate>2004</risdate><volume>15</volume><issue>2</issue><spage>306</spage><epage>315</epage><pages>306-315</pages><issn>1046-6673</issn><eissn>1533-3450</eissn><coden>JASNEU</coden><abstract>It was shown recently that renal injury in Dahl salt-sensitive (DS) hypertensive rats is accompanied by mitogen-activated protein kinase (MAPK) activation. The present study was conducted to elucidate the contribution of reactive oxygen species to MAPK activities and renal injury in DS rats. DS rats were maintained on high salt (H; 8.0% NaCl; n = 7) or low salt (L; 0.3% NaCl; n = 6) diets; H + a superoxide dismutase mimetic, tempol (3 mmol/L in drinking water; n = 8); or H + hydralazine (0.5 mmol/L in drinking water; n = 8) for 4 wk. Mean BP (MBP) in DS/H and DS/L rats was 185 +/- 7 and 113 +/- 3 mmHg, respectively. DS/H rats showed a higher ratio of urinary protein excretion and creatinine (U(protein)V/U(cr)V; 20.3 +/- 1.1) and a higher cortical collagen content (22 +/- 1 micro g/mg) than in DS/L rats (2.4 +/- 0.1 and 13 +/- 1 micro g/mg, respectively). The expression of p22-phox and Nox-1, essential components of NAD(P)H oxidase, in renal cortical tissue was approximately threefold higher in DS/H rats than in DS/L rats. Increased activities of renal cortical MAPK, including extracellular signal-regulated kinases (ERK) 1/ERK2 and c-Jun NH(2)-terminal kinases (JNK) were also observed in DS/H rats by 7.0 +/- 0.7- and 4.3 +/- 0.2-fold, respectively. Tempol treatment significantly decreased MBP (128 +/- 3 mmHg), U(protein)V/U(cr)V (4.8 +/- 0.4), and cortical collagen content (14 +/- 1 micro g/mg) and normalized ERK1/ERK2 and JNK activities in DS/H rats. Histologically, tempol markedly ameliorated progressive sclerotic and proliferative glomerular changes in DS/H rats. Hydralazine-treated DS/H rats showed similar MBP (127 +/- 5 mmHg) to tempol-treated DS/H rats. Hydralazine also decreased U(protein)V/U(cr)V (16.2 +/- 1.5) and cortical collagen content (19 +/- 1 micro g/mg) in DS/H rats. However, these values were significantly higher than those of tempol-treated rats. Furthermore, although hydralazine significantly reduced JNK activity (-56 +/- 3%), ERK1/ERK2 activities were unaffected. These data suggest that reactive oxygen species, generated by NAD(P)H oxidase, contribute to the progression of renal injury through ERK1/ERK2 activation in DS/H hypertensive rats.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>14747377</pmid><doi>10.1097/01.asn.0000108523.02100.e0</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Collagen - urine Cyclic N-Oxides - pharmacology Glomerulonephritis JNK Mitogen-Activated Protein Kinases Kidney Glomerulus - drug effects Kidney Glomerulus - enzymology Kidney Glomerulus - pathology Medical sciences Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases - drug effects Mitogen-Activated Protein Kinases - metabolism Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure p38 Mitogen-Activated Protein Kinases Proteinuria - metabolism Rats Rats, Inbred Dahl Spin Labels |
| title | The SOD mimetic tempol ameliorates glomerular injury and reduces mitogen-activated protein kinase activity in dahl salt-sensitive rats |
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