Peroxynitrite production by TNF-alpha and IL-1beta : implication for suppression of osteoblastic differentiation
1 Department of Oral and Maxillofacial Surgery, 2 Second Department of Internal Medicine, Faculty of Medicine, and 3 Health Service Center, University of Tokyo, Bunkyo-ku, Tokyo 113-8865, Japan To determine the roles of nitric oxide (NO) and its metabolite, peroxynitrite (ONOO ), on osteoblastic...
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| Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 2000-06, Vol.278 (6), p.E1031 |
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| container_title | American journal of physiology: endocrinology and metabolism |
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| creator | Hikiji, Hisako Shin, Wee Soo Koizumi, Toshiyuki Takato, Tsuyoshi Susami, Takafumi Koizumi, Yoko Okai-Matsuo, Yoko Toyo-Oka, Teruhiko |
| description | 1 Department of Oral and Maxillofacial
Surgery, 2 Second Department of Internal
Medicine, Faculty of Medicine, and 3 Health
Service Center, University of Tokyo, Bunkyo-ku, Tokyo 113-8865, Japan
To determine the roles of nitric oxide
(NO) and its metabolite, peroxynitrite (ONOO ), on
osteoblastic activation, we investigated the effects of a NO
donor [ethanamine, 2,2'-(hydroxynitrosohydrazono)bis-
(dNO)], an O 2 donor
(pyrogallol), and an ONOO scavenger (urate) on
alkaline phosphatase (ALPase) activity and osteocalcin gene expression,
which are indexes of osteoblastic differentiation. dNO elevated ALPase
activity in the osteogenic MC3T3-E1 cell line. The combination of dNO
and pyrogallol reduced both ALPase activity and osteocalcin gene
expression. Because both indexes were recovered by urate,
ONOO , unlike NO itself, inhibited the osteoblastic
differentiation. Furthermore, treatment with a combination of the
proinflammatory cytokines tumor necrosis factor- (TNF- ) and
interleukin-1 (IL-1 ) was found to yield ONOO
as well as NO and O 2 . The reductions
in ALPase activity and osteocalcin gene expression were also restored
by urate. We conclude that ONOO produced by TNF-
and IL-1 , but not NO per se, would overcome the stimulatory effect
of NO on osteoblastic activity and inhibit osteoblastic differentiation.
nitric oxide; osteoblasts; proinflammatory cytokines |
| format | Article |
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Surgery, 2 Second Department of Internal
Medicine, Faculty of Medicine, and 3 Health
Service Center, University of Tokyo, Bunkyo-ku, Tokyo 113-8865, Japan
To determine the roles of nitric oxide
(NO) and its metabolite, peroxynitrite (ONOO ), on
osteoblastic activation, we investigated the effects of a NO
donor [ethanamine, 2,2'-(hydroxynitrosohydrazono)bis-
(dNO)], an O 2 donor
(pyrogallol), and an ONOO scavenger (urate) on
alkaline phosphatase (ALPase) activity and osteocalcin gene expression,
which are indexes of osteoblastic differentiation. dNO elevated ALPase
activity in the osteogenic MC3T3-E1 cell line. The combination of dNO
and pyrogallol reduced both ALPase activity and osteocalcin gene
expression. Because both indexes were recovered by urate,
ONOO , unlike NO itself, inhibited the osteoblastic
differentiation. Furthermore, treatment with a combination of the
proinflammatory cytokines tumor necrosis factor- (TNF- ) and
interleukin-1 (IL-1 ) was found to yield ONOO
as well as NO and O 2 . The reductions
in ALPase activity and osteocalcin gene expression were also restored
by urate. We conclude that ONOO produced by TNF-
and IL-1 , but not NO per se, would overcome the stimulatory effect
of NO on osteoblastic activity and inhibit osteoblastic differentiation.
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Surgery, 2 Second Department of Internal
Medicine, Faculty of Medicine, and 3 Health
Service Center, University of Tokyo, Bunkyo-ku, Tokyo 113-8865, Japan
To determine the roles of nitric oxide
(NO) and its metabolite, peroxynitrite (ONOO ), on
osteoblastic activation, we investigated the effects of a NO
donor [ethanamine, 2,2'-(hydroxynitrosohydrazono)bis-
(dNO)], an O 2 donor
(pyrogallol), and an ONOO scavenger (urate) on
alkaline phosphatase (ALPase) activity and osteocalcin gene expression,
which are indexes of osteoblastic differentiation. dNO elevated ALPase
activity in the osteogenic MC3T3-E1 cell line. The combination of dNO
and pyrogallol reduced both ALPase activity and osteocalcin gene
expression. Because both indexes were recovered by urate,
ONOO , unlike NO itself, inhibited the osteoblastic
differentiation. Furthermore, treatment with a combination of the
proinflammatory cytokines tumor necrosis factor- (TNF- ) and
interleukin-1 (IL-1 ) was found to yield ONOO
as well as NO and O 2 . The reductions
in ALPase activity and osteocalcin gene expression were also restored
by urate. We conclude that ONOO produced by TNF-
and IL-1 , but not NO per se, would overcome the stimulatory effect
of NO on osteoblastic activity and inhibit osteoblastic differentiation.
nitric oxide; osteoblasts; proinflammatory cytokines</description><subject>Alkaline Phosphatase - metabolism</subject><subject>Animals</subject><subject>Cell Line</subject><subject>Drug Synergism</subject><subject>Free Radical Scavengers</subject><subject>Gene Expression</subject><subject>Interleukin-1 - pharmacology</subject><subject>Mice</subject><subject>Nitrates - analysis</subject><subject>Nitrates - metabolism</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>Osteoblasts - physiology</subject><subject>Osteocalcin - genetics</subject><subject>Pyrogallol - pharmacology</subject><subject>RNA, Messenger - metabolism</subject><subject>Superoxide Dismutase - pharmacology</subject><subject>Superoxides - metabolism</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1j99KwzAYR4Mobk5fQfIClaRt2nR3MjYdDPViXof8XTO6JiQtrm9v3Rx449XHB-f84FyBKSZpmmBCyDWYIlxlCaZ5NQF3Me4RQiXJ01swwYimJUJkCvyHDu44tLYLttPQB6d62VnXQjHA7dsq4Y2vOeStgutNgoXuOJxDe_CNlfzEGRdg7L0POsaf3xnoYqedaHjsrITKGqODbjt74u_BjeFN1A-_dwY-V8vt4jXZvL-sF8-bpMZ5ThJJhDFjBZWFFIUphaS8QIXiVJWU8jytspLmwihSCpRKWhU5QQprhTgSEqfZDDyed30vDloxH-yBh4Fd0kfg6QzUdld_2aCZr4exoHG7gfG9161yLC0pK9gSowyPwvx_YdU3zVYfu4v5R2RemewbobN9tQ</recordid><startdate>20000601</startdate><enddate>20000601</enddate><creator>Hikiji, Hisako</creator><creator>Shin, Wee Soo</creator><creator>Koizumi, Toshiyuki</creator><creator>Takato, Tsuyoshi</creator><creator>Susami, Takafumi</creator><creator>Koizumi, Yoko</creator><creator>Okai-Matsuo, Yoko</creator><creator>Toyo-Oka, Teruhiko</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20000601</creationdate><title>Peroxynitrite production by TNF-alpha and IL-1beta : implication for suppression of osteoblastic differentiation</title><author>Hikiji, Hisako ; Shin, Wee Soo ; Koizumi, Toshiyuki ; Takato, Tsuyoshi ; Susami, Takafumi ; Koizumi, Yoko ; Okai-Matsuo, Yoko ; Toyo-Oka, Teruhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h1445-c5bff5558c6cb6f7bc8a606da8d788a4293784bfd57b02c896450d1ed0a0bc123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Alkaline Phosphatase - metabolism</topic><topic>Animals</topic><topic>Cell Line</topic><topic>Drug Synergism</topic><topic>Free Radical Scavengers</topic><topic>Gene Expression</topic><topic>Interleukin-1 - pharmacology</topic><topic>Mice</topic><topic>Nitrates - analysis</topic><topic>Nitrates - metabolism</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Osteoblasts - physiology</topic><topic>Osteocalcin - genetics</topic><topic>Pyrogallol - pharmacology</topic><topic>RNA, Messenger - metabolism</topic><topic>Superoxide Dismutase - pharmacology</topic><topic>Superoxides - metabolism</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hikiji, Hisako</creatorcontrib><creatorcontrib>Shin, Wee Soo</creatorcontrib><creatorcontrib>Koizumi, Toshiyuki</creatorcontrib><creatorcontrib>Takato, Tsuyoshi</creatorcontrib><creatorcontrib>Susami, Takafumi</creatorcontrib><creatorcontrib>Koizumi, Yoko</creatorcontrib><creatorcontrib>Okai-Matsuo, Yoko</creatorcontrib><creatorcontrib>Toyo-Oka, Teruhiko</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>American journal of physiology: endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hikiji, Hisako</au><au>Shin, Wee Soo</au><au>Koizumi, Toshiyuki</au><au>Takato, Tsuyoshi</au><au>Susami, Takafumi</au><au>Koizumi, Yoko</au><au>Okai-Matsuo, Yoko</au><au>Toyo-Oka, Teruhiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxynitrite production by TNF-alpha and IL-1beta : implication for suppression of osteoblastic differentiation</atitle><jtitle>American journal of physiology: endocrinology and metabolism</jtitle><addtitle>Am J Physiol Endocrinol Metab</addtitle><date>2000-06-01</date><risdate>2000</risdate><volume>278</volume><issue>6</issue><spage>E1031</spage><pages>E1031-</pages><issn>0193-1849</issn><eissn>1522-1555</eissn><abstract>1 Department of Oral and Maxillofacial
Surgery, 2 Second Department of Internal
Medicine, Faculty of Medicine, and 3 Health
Service Center, University of Tokyo, Bunkyo-ku, Tokyo 113-8865, Japan
To determine the roles of nitric oxide
(NO) and its metabolite, peroxynitrite (ONOO ), on
osteoblastic activation, we investigated the effects of a NO
donor [ethanamine, 2,2'-(hydroxynitrosohydrazono)bis-
(dNO)], an O 2 donor
(pyrogallol), and an ONOO scavenger (urate) on
alkaline phosphatase (ALPase) activity and osteocalcin gene expression,
which are indexes of osteoblastic differentiation. dNO elevated ALPase
activity in the osteogenic MC3T3-E1 cell line. The combination of dNO
and pyrogallol reduced both ALPase activity and osteocalcin gene
expression. Because both indexes were recovered by urate,
ONOO , unlike NO itself, inhibited the osteoblastic
differentiation. Furthermore, treatment with a combination of the
proinflammatory cytokines tumor necrosis factor- (TNF- ) and
interleukin-1 (IL-1 ) was found to yield ONOO
as well as NO and O 2 . The reductions
in ALPase activity and osteocalcin gene expression were also restored
by urate. We conclude that ONOO produced by TNF-
and IL-1 , but not NO per se, would overcome the stimulatory effect
of NO on osteoblastic activity and inhibit osteoblastic differentiation.
nitric oxide; osteoblasts; proinflammatory cytokines</abstract><cop>United States</cop><pmid>10827005</pmid></addata></record> |
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| identifier | ISSN: 0193-1849 |
| ispartof | American journal of physiology: endocrinology and metabolism, 2000-06, Vol.278 (6), p.E1031 |
| issn | 0193-1849 1522-1555 |
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| recordid | cdi_pubmed_primary_10827005 |
| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals |
| subjects | Alkaline Phosphatase - metabolism Animals Cell Line Drug Synergism Free Radical Scavengers Gene Expression Interleukin-1 - pharmacology Mice Nitrates - analysis Nitrates - metabolism Nitric Oxide Donors - pharmacology Osteoblasts - physiology Osteocalcin - genetics Pyrogallol - pharmacology RNA, Messenger - metabolism Superoxide Dismutase - pharmacology Superoxides - metabolism Tumor Necrosis Factor-alpha - pharmacology |
| title | Peroxynitrite production by TNF-alpha and IL-1beta : implication for suppression of osteoblastic differentiation |
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