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Angiotensin II triggers knee joint lesions in experimental osteoarthritis
This study aimed to evaluate the involvement of Angiotensin II (Ang II) in joint lesions associated with osteoarthritis (OA) in vitro and in vivo. Chondrocyte cultures were obtained from knee joints of neonatal rats and stimulated with Ang II/MIA/ACE inhibitors. In vivo, rats treated or not with the...
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Published in: | Bone (New York, N.Y.) N.Y.), 2021-04, Vol.145, p.115842-115842, Article 115842 |
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creator | de Sá, Grazielle A. dos Santos, Anna Clara P.M. Nogueira, Júlia M. dos Santos, Diogo M. Amaral, Flávio A. Jorge, Erika C. Caliari, Marcelo V. Queiroz-Junior, Celso M. Ferreira, Anderson J. |
description | This study aimed to evaluate the involvement of Angiotensin II (Ang II) in joint lesions associated with osteoarthritis (OA) in vitro and in vivo.
Chondrocyte cultures were obtained from knee joints of neonatal rats and stimulated with Ang II/MIA/ACE inhibitors. In vivo, rats treated or not with the ACE inhibitor captopril, received daily injections of Ang II or sodium monoiodoacetate (MIA) in knee joints for evaluation of cartilage, bone, and synovial lesions.
Cultured chondrocytes expressed the mRNA for Ace, Agtr1, Agtr2, and Mas1. Stimulating cells with Ang II reduced chondrocyte viability and metabolism. Accordingly, in vivo Ang II injection into the knees of rats triggered hyperalgesia, joint edema, increased the number of leukocytes in the joint cavity, and induced cartilage lesions associated with OA alterations. In further experiments, Ang II synthesis was prevented with the ACE inhibitor Captopril in the context of MIA-induced OA. Ang II inhibition with captopril improved the OARSI score, induced chondroprotection, and reduced the leukocyte recruitment from synovium after MIA. Additionally, captopril prevented MIA-induced bone resorption, by decreasing the number of osteoclasts and increasing the expression of IL-10 in the bone. In vitro, inhibiting Ang II synthesis decreased MIA-induced chondrocyte death and increased Col2a1 transcription.
Ang II induces chondrocyte death and joint tissue damages associated with OA and its modulation can be a therapeutic strategy in osteoarthritis.
•Angiotensin II inhibits chondrocyte metabolism and triggers signs of osteoarthritis.•Inhibition of ACE with captopril preserves chondrocytes after Angiotensin II or MIA stimulation.•Inhibition of ACE with captopril in the MIA model attenuates cartilage, bone and synovial lesions. |
doi_str_mv | 10.1016/j.bone.2021.115842 |
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Chondrocyte cultures were obtained from knee joints of neonatal rats and stimulated with Ang II/MIA/ACE inhibitors. In vivo, rats treated or not with the ACE inhibitor captopril, received daily injections of Ang II or sodium monoiodoacetate (MIA) in knee joints for evaluation of cartilage, bone, and synovial lesions.
Cultured chondrocytes expressed the mRNA for Ace, Agtr1, Agtr2, and Mas1. Stimulating cells with Ang II reduced chondrocyte viability and metabolism. Accordingly, in vivo Ang II injection into the knees of rats triggered hyperalgesia, joint edema, increased the number of leukocytes in the joint cavity, and induced cartilage lesions associated with OA alterations. In further experiments, Ang II synthesis was prevented with the ACE inhibitor Captopril in the context of MIA-induced OA. Ang II inhibition with captopril improved the OARSI score, induced chondroprotection, and reduced the leukocyte recruitment from synovium after MIA. Additionally, captopril prevented MIA-induced bone resorption, by decreasing the number of osteoclasts and increasing the expression of IL-10 in the bone. In vitro, inhibiting Ang II synthesis decreased MIA-induced chondrocyte death and increased Col2a1 transcription.
Ang II induces chondrocyte death and joint tissue damages associated with OA and its modulation can be a therapeutic strategy in osteoarthritis.
•Angiotensin II inhibits chondrocyte metabolism and triggers signs of osteoarthritis.•Inhibition of ACE with captopril preserves chondrocytes after Angiotensin II or MIA stimulation.•Inhibition of ACE with captopril in the MIA model attenuates cartilage, bone and synovial lesions.</description><identifier>ISSN: 8756-3282</identifier><identifier>EISSN: 1873-2763</identifier><identifier>DOI: 10.1016/j.bone.2021.115842</identifier><identifier>PMID: 33422700</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Angiotensin II ; Bone fibrous tissue ; Captopril ; Chondroprotection ; Knee ; Sodium monoiodoacetate</subject><ispartof>Bone (New York, N.Y.), 2021-04, Vol.145, p.115842-115842, Article 115842</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-cd5ee593f459fd73eb346a872dad2ab5713b19d991d239d30ed7fb5854d8672c3</citedby><cites>FETCH-LOGICAL-c356t-cd5ee593f459fd73eb346a872dad2ab5713b19d991d239d30ed7fb5854d8672c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33422700$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Sá, Grazielle A.</creatorcontrib><creatorcontrib>dos Santos, Anna Clara P.M.</creatorcontrib><creatorcontrib>Nogueira, Júlia M.</creatorcontrib><creatorcontrib>dos Santos, Diogo M.</creatorcontrib><creatorcontrib>Amaral, Flávio A.</creatorcontrib><creatorcontrib>Jorge, Erika C.</creatorcontrib><creatorcontrib>Caliari, Marcelo V.</creatorcontrib><creatorcontrib>Queiroz-Junior, Celso M.</creatorcontrib><creatorcontrib>Ferreira, Anderson J.</creatorcontrib><title>Angiotensin II triggers knee joint lesions in experimental osteoarthritis</title><title>Bone (New York, N.Y.)</title><addtitle>Bone</addtitle><description>This study aimed to evaluate the involvement of Angiotensin II (Ang II) in joint lesions associated with osteoarthritis (OA) in vitro and in vivo.
Chondrocyte cultures were obtained from knee joints of neonatal rats and stimulated with Ang II/MIA/ACE inhibitors. In vivo, rats treated or not with the ACE inhibitor captopril, received daily injections of Ang II or sodium monoiodoacetate (MIA) in knee joints for evaluation of cartilage, bone, and synovial lesions.
Cultured chondrocytes expressed the mRNA for Ace, Agtr1, Agtr2, and Mas1. Stimulating cells with Ang II reduced chondrocyte viability and metabolism. Accordingly, in vivo Ang II injection into the knees of rats triggered hyperalgesia, joint edema, increased the number of leukocytes in the joint cavity, and induced cartilage lesions associated with OA alterations. In further experiments, Ang II synthesis was prevented with the ACE inhibitor Captopril in the context of MIA-induced OA. Ang II inhibition with captopril improved the OARSI score, induced chondroprotection, and reduced the leukocyte recruitment from synovium after MIA. Additionally, captopril prevented MIA-induced bone resorption, by decreasing the number of osteoclasts and increasing the expression of IL-10 in the bone. In vitro, inhibiting Ang II synthesis decreased MIA-induced chondrocyte death and increased Col2a1 transcription.
Ang II induces chondrocyte death and joint tissue damages associated with OA and its modulation can be a therapeutic strategy in osteoarthritis.
•Angiotensin II inhibits chondrocyte metabolism and triggers signs of osteoarthritis.•Inhibition of ACE with captopril preserves chondrocytes after Angiotensin II or MIA stimulation.•Inhibition of ACE with captopril in the MIA model attenuates cartilage, bone and synovial lesions.</description><subject>Angiotensin II</subject><subject>Bone fibrous tissue</subject><subject>Captopril</subject><subject>Chondroprotection</subject><subject>Knee</subject><subject>Sodium monoiodoacetate</subject><issn>8756-3282</issn><issn>1873-2763</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kDtPwzAUhS0EoqXwBxhQRpYEP2I7kVgqxCNSJRaYrSS-KQ6pXWwXwb8nVQoj012-c3Tuh9AlwRnBRNz0WeMsZBRTkhHCi5weoTkpJEupFOwYzQvJRcpoQWfoLIQeY8xKSU7RjLGcUonxHFVLuzYugg3GJlWVRG_Wa_AhebcASe-MjckAwTgbkpGAry14swEb6yFxIYKrfXzzJppwjk66eghwcbgL9Ppw_3L3lK6eH6u75SptGRcxbTUH4CXrcl52WjJoWC7qQlJda1o3XBLWkFKXJdGUlZph0LJreMFzXQhJW7ZA11Pv1ruPHYSoNia0MAy1BbcLiuZSFJwwIUaUTmjrXQgeOrUdx9f-WxGs9gpVr_YK1V6hmhSOoatD_67ZgP6L_DobgdsJgPHLTwNehdaAbUEbD21U2pn_-n8AenmCvw</recordid><startdate>202104</startdate><enddate>202104</enddate><creator>de Sá, Grazielle A.</creator><creator>dos Santos, Anna Clara P.M.</creator><creator>Nogueira, Júlia M.</creator><creator>dos Santos, Diogo M.</creator><creator>Amaral, Flávio A.</creator><creator>Jorge, Erika C.</creator><creator>Caliari, Marcelo V.</creator><creator>Queiroz-Junior, Celso M.</creator><creator>Ferreira, Anderson J.</creator><general>Elsevier Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202104</creationdate><title>Angiotensin II triggers knee joint lesions in experimental osteoarthritis</title><author>de Sá, Grazielle A. ; dos Santos, Anna Clara P.M. ; Nogueira, Júlia M. ; dos Santos, Diogo M. ; Amaral, Flávio A. ; Jorge, Erika C. ; Caliari, Marcelo V. ; Queiroz-Junior, Celso M. ; Ferreira, Anderson J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-cd5ee593f459fd73eb346a872dad2ab5713b19d991d239d30ed7fb5854d8672c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Angiotensin II</topic><topic>Bone fibrous tissue</topic><topic>Captopril</topic><topic>Chondroprotection</topic><topic>Knee</topic><topic>Sodium monoiodoacetate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Sá, Grazielle A.</creatorcontrib><creatorcontrib>dos Santos, Anna Clara P.M.</creatorcontrib><creatorcontrib>Nogueira, Júlia M.</creatorcontrib><creatorcontrib>dos Santos, Diogo M.</creatorcontrib><creatorcontrib>Amaral, Flávio A.</creatorcontrib><creatorcontrib>Jorge, Erika C.</creatorcontrib><creatorcontrib>Caliari, Marcelo V.</creatorcontrib><creatorcontrib>Queiroz-Junior, Celso M.</creatorcontrib><creatorcontrib>Ferreira, Anderson J.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Bone (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Sá, Grazielle A.</au><au>dos Santos, Anna Clara P.M.</au><au>Nogueira, Júlia M.</au><au>dos Santos, Diogo M.</au><au>Amaral, Flávio A.</au><au>Jorge, Erika C.</au><au>Caliari, Marcelo V.</au><au>Queiroz-Junior, Celso M.</au><au>Ferreira, Anderson J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin II triggers knee joint lesions in experimental osteoarthritis</atitle><jtitle>Bone (New York, N.Y.)</jtitle><addtitle>Bone</addtitle><date>2021-04</date><risdate>2021</risdate><volume>145</volume><spage>115842</spage><epage>115842</epage><pages>115842-115842</pages><artnum>115842</artnum><issn>8756-3282</issn><eissn>1873-2763</eissn><abstract>This study aimed to evaluate the involvement of Angiotensin II (Ang II) in joint lesions associated with osteoarthritis (OA) in vitro and in vivo.
Chondrocyte cultures were obtained from knee joints of neonatal rats and stimulated with Ang II/MIA/ACE inhibitors. In vivo, rats treated or not with the ACE inhibitor captopril, received daily injections of Ang II or sodium monoiodoacetate (MIA) in knee joints for evaluation of cartilage, bone, and synovial lesions.
Cultured chondrocytes expressed the mRNA for Ace, Agtr1, Agtr2, and Mas1. Stimulating cells with Ang II reduced chondrocyte viability and metabolism. Accordingly, in vivo Ang II injection into the knees of rats triggered hyperalgesia, joint edema, increased the number of leukocytes in the joint cavity, and induced cartilage lesions associated with OA alterations. In further experiments, Ang II synthesis was prevented with the ACE inhibitor Captopril in the context of MIA-induced OA. Ang II inhibition with captopril improved the OARSI score, induced chondroprotection, and reduced the leukocyte recruitment from synovium after MIA. Additionally, captopril prevented MIA-induced bone resorption, by decreasing the number of osteoclasts and increasing the expression of IL-10 in the bone. In vitro, inhibiting Ang II synthesis decreased MIA-induced chondrocyte death and increased Col2a1 transcription.
Ang II induces chondrocyte death and joint tissue damages associated with OA and its modulation can be a therapeutic strategy in osteoarthritis.
•Angiotensin II inhibits chondrocyte metabolism and triggers signs of osteoarthritis.•Inhibition of ACE with captopril preserves chondrocytes after Angiotensin II or MIA stimulation.•Inhibition of ACE with captopril in the MIA model attenuates cartilage, bone and synovial lesions.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>33422700</pmid><doi>10.1016/j.bone.2021.115842</doi><tpages>1</tpages></addata></record> |
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subjects | Angiotensin II Bone fibrous tissue Captopril Chondroprotection Knee Sodium monoiodoacetate |
title | Angiotensin II triggers knee joint lesions in experimental osteoarthritis |
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