Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts
Identifieur interne : 001663 ( Istex/Checkpoint ); précédent : 001662; suivant : 001664Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts
Auteurs : Toshiaki Nakamura [Japon] ; Kozue Hasegawa-Nakamura [Japon] ; Kenji Sakoda [Japon] ; Takashi Matsuyama [Japon] ; Kazuyuki Noguchi [Japon]Source :
- European Journal of Oral Sciences [ 0909-8836 ] ; 2011-10.
English descriptors
- KwdEn :
- Angiotensin, Assay, At1r, At1r hgfs, At1r mrna, At1r protein, Broblastic cells, Broblasts, Cathepsin, Cell types, Control hgfs, Control sirna, Culture supernatants, Cultured hgfs, Dental sciences, Gapdh, Gingival, Gingival tissues, Hgfs, Human gingival, Human gingival tissue, Kagoshima university graduate school, Mrna, Muscle cells, Periodontal, Physiol, Present study, Protein levels, Receptor, Receptor expression, Santa cruz biotechnology, Separate experiments, Sirna.
- Teeft :
- Angiotensin, Assay, At1r, At1r hgfs, At1r mrna, At1r protein, Broblastic cells, Broblasts, Cathepsin, Cell types, Control hgfs, Control sirna, Culture supernatants, Cultured hgfs, Dental sciences, Gapdh, Gingival, Gingival tissues, Hgfs, Human gingival, Human gingival tissue, Kagoshima university graduate school, Mrna, Muscle cells, Periodontal, Physiol, Present study, Protein levels, Receptor, Receptor expression, Santa cruz biotechnology, Separate experiments, Sirna.
Abstract
Nakamura T, Hasegawa‐Nakamura K, Sakoda K, Matsuyama T, Noguchi K. Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts.
Eur J Oral Sci 2011; 119: 345–351. © 2011 Eur J Oral Sci The renin‐angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin‐1β (IL‐1β)‐induced interleukin‐6 (IL‐6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast‐like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of AT1R mRNA and AT1R protein increased in HGFs after stimulation with IL‐1β. The levels of IL‐1β‐induced IL6 mRNA and IL‐6 protein were significantly reduced in AT1R gene‐silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL‐1β‐induced IL‐6 production in HGFs.
Url:
DOI: 10.1111/j.1600-0722.2011.00850.x
Affiliations:
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xml:lang="en"><term>Angiotensin</term><term>Assay</term><term>At1r</term><term>At1r hgfs</term><term>At1r mrna</term><term>At1r protein</term><term>Broblastic cells</term><term>Broblasts</term><term>Cathepsin</term><term>Cell types</term><term>Control hgfs</term><term>Control sirna</term><term>Culture supernatants</term><term>Cultured hgfs</term><term>Dental sciences</term><term>Gapdh</term><term>Gingival</term><term>Gingival tissues</term><term>Hgfs</term><term>Human gingival</term><term>Human gingival tissue</term><term>Kagoshima university graduate school</term><term>Mrna</term><term>Muscle cells</term><term>Periodontal</term><term>Physiol</term><term>Present study</term><term>Protein levels</term><term>Receptor</term><term>Receptor expression</term><term>Santa cruz biotechnology</term><term>Separate experiments</term><term>Sirna</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Angiotensin</term><term>Assay</term><term>At1r</term><term>At1r hgfs</term><term>At1r mrna</term><term>At1r protein</term><term>Broblastic cells</term><term>Broblasts</term><term>Cathepsin</term><term>Cell types</term><term>Control hgfs</term><term>Control sirna</term><term>Culture supernatants</term><term>Cultured hgfs</term><term>Dental sciences</term><term>Gapdh</term><term>Gingival</term><term>Gingival tissues</term><term>Hgfs</term><term>Human gingival</term><term>Human gingival tissue</term><term>Kagoshima university graduate school</term><term>Mrna</term><term>Muscle cells</term><term>Periodontal</term><term>Physiol</term><term>Present study</term><term>Protein levels</term><term>Receptor</term><term>Receptor expression</term><term>Santa cruz biotechnology</term><term>Separate experiments</term><term>Sirna</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Nakamura T, Hasegawa‐Nakamura K, Sakoda K, Matsuyama T, Noguchi K. Involvement of angiotensin II type 1 receptors in interleukin‐1β‐induced interleukin‐6 production in human gingival fibroblasts.
Eur J Oral Sci 2011; 119: 345–351. © 2011 Eur J Oral Sci The renin‐angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin‐1β (IL‐1β)‐induced interleukin‐6 (IL‐6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast‐like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of AT1R mRNA and AT1R protein increased in HGFs after stimulation with IL‐1β. The levels of IL‐1β‐induced IL6 mRNA and IL‐6 protein were significantly reduced in AT1R gene‐silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL‐1β‐induced IL‐6 production in HGFs.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Nakamura, Toshiaki" sort="Nakamura, Toshiaki" uniqKey="Nakamura T" first="Toshiaki" last="Nakamura">Toshiaki Nakamura</name></noRegion><name sortKey="Hasegawa Akamura, Kozue" sort="Hasegawa Akamura, Kozue" uniqKey="Hasegawa Akamura K" first="Kozue" last="Hasegawa-Nakamura">Kozue Hasegawa-Nakamura</name><name sortKey="Matsuyama, Takashi" sort="Matsuyama, Takashi" uniqKey="Matsuyama T" first="Takashi" last="Matsuyama">Takashi Matsuyama</name><name sortKey="Noguchi, Kazuyuki" sort="Noguchi, Kazuyuki" uniqKey="Noguchi K" first="Kazuyuki" last="Noguchi">Kazuyuki Noguchi</name><name sortKey="Sakoda, Kenji" sort="Sakoda, Kenji" uniqKey="Sakoda K" first="Kenji" last="Sakoda">Kenji Sakoda</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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