Enhanced oxidative stress and impaired thioredoxin expression in spontaneously hypertensive rats
As oxidative stress plays a crucial role in the development and pathogenesis of hypertension, we analyzed the redox (reduction/oxidation) status in tissues from Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP). Expressions of 8-hydroxy-2'-deoxyguanosi...
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| Veröffentlicht in: | Antioxidants & redox signaling 2004-02, Vol.6 (1), p.89-97 |
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| creator | Tanito, Masaki Nakamura, Hajime Kwon, Yong-Won Teratani, Akie Masutani, Hiroshi Shioji, Keisuke Kishimoto, Chiharu Ohira, Akihiro Horie, Ryoichi Yodoi, Junji |
| description | As oxidative stress plays a crucial role in the development and pathogenesis of hypertension, we analyzed the redox (reduction/oxidation) status in tissues from Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP). Expressions of 8-hydroxy-2'-deoxyguanosine, a marker for oxidative stress-induced DNA damage, and protein carbonylation, a marker for oxidation status of proteins, were enhanced in aorta, heart, and kidney from SHR and SHRSP compared with WKY. The expression of redox regulating protein, thioredoxin (TRX), estimated by immunohistochemistry and western blot, and expression of TRX gene estimated by real-time RT-PCR were markedly suppressed in those tissues from SHR and SHRSP compared with WKY. Induction of TRX was impaired after angiotension II treatment in peripheral blood mononuclear cells isolated from SHR and SHRSP compared with those isolated from WKY. Although previous reports have shown that TRX is induced by a variety of oxidative stress in tissues, the present study shows the impaired induction of TRX in tissues from genetically hypertensive rats despite the relative increment of oxidative stress. Redox imbalance in essential organs may play a crucial role in the development and pathogenesis of hypertension. |
| doi_str_mv | 10.1089/152308604771978381 |
| format | Article |
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Expressions of 8-hydroxy-2'-deoxyguanosine, a marker for oxidative stress-induced DNA damage, and protein carbonylation, a marker for oxidation status of proteins, were enhanced in aorta, heart, and kidney from SHR and SHRSP compared with WKY. The expression of redox regulating protein, thioredoxin (TRX), estimated by immunohistochemistry and western blot, and expression of TRX gene estimated by real-time RT-PCR were markedly suppressed in those tissues from SHR and SHRSP compared with WKY. Induction of TRX was impaired after angiotension II treatment in peripheral blood mononuclear cells isolated from SHR and SHRSP compared with those isolated from WKY. Although previous reports have shown that TRX is induced by a variety of oxidative stress in tissues, the present study shows the impaired induction of TRX in tissues from genetically hypertensive rats despite the relative increment of oxidative stress. 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Expressions of 8-hydroxy-2'-deoxyguanosine, a marker for oxidative stress-induced DNA damage, and protein carbonylation, a marker for oxidation status of proteins, were enhanced in aorta, heart, and kidney from SHR and SHRSP compared with WKY. The expression of redox regulating protein, thioredoxin (TRX), estimated by immunohistochemistry and western blot, and expression of TRX gene estimated by real-time RT-PCR were markedly suppressed in those tissues from SHR and SHRSP compared with WKY. Induction of TRX was impaired after angiotension II treatment in peripheral blood mononuclear cells isolated from SHR and SHRSP compared with those isolated from WKY. Although previous reports have shown that TRX is induced by a variety of oxidative stress in tissues, the present study shows the impaired induction of TRX in tissues from genetically hypertensive rats despite the relative increment of oxidative stress. Redox imbalance in essential organs may play a crucial role in the development and pathogenesis of hypertension.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Blotting, Western</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - analysis</subject><subject>Deoxyguanosine - metabolism</subject><subject>Disease Models, Animal</subject><subject>Gene Expression Regulation</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>Immunohistochemistry</subject><subject>Monocytes - drug effects</subject><subject>Monocytes - metabolism</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Thioredoxins - analysis</subject><subject>Thioredoxins - genetics</subject><subject>Thioredoxins - metabolism</subject><issn>1523-0864</issn><issn>1557-7716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNplkL1OwzAUhS0EoqXwAgwoE1vAjhNfZ0RVC0iVWGAOjmOrRokdbBe1b4-jVmJgun_fObo6CN0S_EAwrx9JVVDMGS4BSA2ccnKG5qSqIE8Ldj71Bc0TUc7QVQhfGOOCEHyJZqQEQimt5-hzZbfCStVlbm86Ec2PykL0KoRM2C4zwyiMT9e4NS7VBNlM7ccJMM5maQqjs1FY5XahP2Tbw6h8VDZMRl7EcI0utOiDujnVBfpYr96XL_nm7fl1-bTJJWVVzBkHWdSKt2UFsmu54Fq2khWlZppjwhhAW9UgOIBkRDAuNADrGGilWYk1XaD7o-_o3fdOhdgMJkjV98fXGo4xB1xDAosjKL0LwSvdjN4Mwh8agpsp1-Z_rkl0d3LftYPq_iSnIOkvIfZ1YA</recordid><startdate>20040201</startdate><enddate>20040201</enddate><creator>Tanito, Masaki</creator><creator>Nakamura, Hajime</creator><creator>Kwon, Yong-Won</creator><creator>Teratani, Akie</creator><creator>Masutani, Hiroshi</creator><creator>Shioji, Keisuke</creator><creator>Kishimoto, Chiharu</creator><creator>Ohira, Akihiro</creator><creator>Horie, Ryoichi</creator><creator>Yodoi, Junji</creator><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>Enhanced oxidative stress and impaired thioredoxin expression in spontaneously hypertensive rats</title><author>Tanito, Masaki ; Nakamura, Hajime ; Kwon, Yong-Won ; Teratani, Akie ; Masutani, Hiroshi ; Shioji, Keisuke ; Kishimoto, Chiharu ; Ohira, Akihiro ; Horie, Ryoichi ; Yodoi, Junji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-687c29e8b457cdb8a8fcbc624f6f8016677b597a877c61a68af776d67fef640f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Blotting, Western</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - analysis</topic><topic>Deoxyguanosine - metabolism</topic><topic>Disease Models, Animal</topic><topic>Gene Expression Regulation</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>Immunohistochemistry</topic><topic>Monocytes - drug effects</topic><topic>Monocytes - metabolism</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Thioredoxins - analysis</topic><topic>Thioredoxins - genetics</topic><topic>Thioredoxins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tanito, Masaki</creatorcontrib><creatorcontrib>Nakamura, Hajime</creatorcontrib><creatorcontrib>Kwon, Yong-Won</creatorcontrib><creatorcontrib>Teratani, Akie</creatorcontrib><creatorcontrib>Masutani, Hiroshi</creatorcontrib><creatorcontrib>Shioji, Keisuke</creatorcontrib><creatorcontrib>Kishimoto, Chiharu</creatorcontrib><creatorcontrib>Ohira, Akihiro</creatorcontrib><creatorcontrib>Horie, Ryoichi</creatorcontrib><creatorcontrib>Yodoi, Junji</creatorcontrib><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>Antioxidants & redox signaling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tanito, Masaki</au><au>Nakamura, Hajime</au><au>Kwon, Yong-Won</au><au>Teratani, Akie</au><au>Masutani, Hiroshi</au><au>Shioji, Keisuke</au><au>Kishimoto, Chiharu</au><au>Ohira, Akihiro</au><au>Horie, Ryoichi</au><au>Yodoi, Junji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced oxidative stress and impaired thioredoxin expression in spontaneously hypertensive rats</atitle><jtitle>Antioxidants & redox signaling</jtitle><addtitle>Antioxid Redox Signal</addtitle><date>2004-02-01</date><risdate>2004</risdate><volume>6</volume><issue>1</issue><spage>89</spage><epage>97</epage><pages>89-97</pages><issn>1523-0864</issn><eissn>1557-7716</eissn><abstract>As oxidative stress plays a crucial role in the development and pathogenesis of hypertension, we analyzed the redox (reduction/oxidation) status in tissues from Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP). Expressions of 8-hydroxy-2'-deoxyguanosine, a marker for oxidative stress-induced DNA damage, and protein carbonylation, a marker for oxidation status of proteins, were enhanced in aorta, heart, and kidney from SHR and SHRSP compared with WKY. The expression of redox regulating protein, thioredoxin (TRX), estimated by immunohistochemistry and western blot, and expression of TRX gene estimated by real-time RT-PCR were markedly suppressed in those tissues from SHR and SHRSP compared with WKY. Induction of TRX was impaired after angiotension II treatment in peripheral blood mononuclear cells isolated from SHR and SHRSP compared with those isolated from WKY. Although previous reports have shown that TRX is induced by a variety of oxidative stress in tissues, the present study shows the impaired induction of TRX in tissues from genetically hypertensive rats despite the relative increment of oxidative stress. Redox imbalance in essential organs may play a crucial role in the development and pathogenesis of hypertension.</abstract><cop>United States</cop><pmid>14713339</pmid><doi>10.1089/152308604771978381</doi><tpages>9</tpages></addata></record> |
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| subjects | Angiotensin II - pharmacology Animals Blotting, Western Deoxyguanosine - analogs & derivatives Deoxyguanosine - analysis Deoxyguanosine - metabolism Disease Models, Animal Gene Expression Regulation Hypertension - metabolism Hypertension - physiopathology Immunohistochemistry Monocytes - drug effects Monocytes - metabolism Oxidation-Reduction Oxidative Stress - physiology Rats Rats, Inbred SHR Rats, Inbred WKY Thioredoxins - analysis Thioredoxins - genetics Thioredoxins - metabolism |
| title | Enhanced oxidative stress and impaired thioredoxin expression in spontaneously hypertensive rats |
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