Aquaporin 1 contributes to chondrocyte apoptosis in a rat model of osteoarthritis
Aquaporins (AQPs) have been found to be associated with a number of diseases. However, the role of AQP-1 in the pathogenesis of osteoarthritis remains unclear. We previously found that AQP-1 expression was upregulated in osteoarthritic cartilage and strongly correlated with caspase-3 expression and...
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| Veröffentlicht in: | International journal of molecular medicine 2016-12, Vol.38 (6), p.1752-1758 |
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| container_title | International journal of molecular medicine |
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| creator | Gao, Hangfei Gui, Jiancao Wang, Liming Xu, Yan Jiang, Yiqiu Xiong, Mingyue Cui, Yongguang |
| description | Aquaporins (AQPs) have been found to be associated with a number of diseases. However, the role of AQP-1 in the pathogenesis of osteoarthritis remains unclear. We previously found that AQP-1 expression was upregulated in osteoarthritic cartilage and strongly correlated with caspase-3 expression and activity. The aim of this study was to further investigate the association of AQP-1 expression with chondrocyte apoptosis in a rat model of osteoarthritis, using RNA interference to knock down AQP-1. For this purspose, 72 male Sprague-Dawley rats were randomly assigned to 3 groups as follows: the control group not treated surgically (n=24), the sham-operated group (n=24), and the osteoarthritis group (n=24). Osteoarthritis was induced by amputating the anterior cruciate ligament and medial collateral ligament and partially excising the medial meniscus. Chondrocytes from the rats with osteoarthritis were isolated and cultured. shRNAs were used to knock down AQP-1 expression in the cultured chondrocytes. The expression of AQP-1 and caspase-3 was determined by reverse transcription-quantitative polymerase chain reaction. Caspase-3 activity was measured using a caspase-3 colorimetric assay. The rats in our model of osteoarthritis exhibited severe cartilage damage. The knockdown of AQP-1 decreased caspase-3 expression and activity in the cultured chondrocytes. In addition, the expression of AQP-1 positively correlated with caspase-3 expression and activity. Thus, the findings of our study, suggest that AQP-1 promotes caspase-3 activation and thereby contributes to chondrocyte apoptosis and to the development of osteoarthritis. |
| doi_str_mv | 10.3892/ijmm.2016.2785 |
| format | Article |
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However, the role of AQP-1 in the pathogenesis of osteoarthritis remains unclear. We previously found that AQP-1 expression was upregulated in osteoarthritic cartilage and strongly correlated with caspase-3 expression and activity. The aim of this study was to further investigate the association of AQP-1 expression with chondrocyte apoptosis in a rat model of osteoarthritis, using RNA interference to knock down AQP-1. For this purspose, 72 male Sprague-Dawley rats were randomly assigned to 3 groups as follows: the control group not treated surgically (n=24), the sham-operated group (n=24), and the osteoarthritis group (n=24). Osteoarthritis was induced by amputating the anterior cruciate ligament and medial collateral ligament and partially excising the medial meniscus. Chondrocytes from the rats with osteoarthritis were isolated and cultured. shRNAs were used to knock down AQP-1 expression in the cultured chondrocytes. The expression of AQP-1 and caspase-3 was determined by reverse transcription-quantitative polymerase chain reaction. Caspase-3 activity was measured using a caspase-3 colorimetric assay. The rats in our model of osteoarthritis exhibited severe cartilage damage. The knockdown of AQP-1 decreased caspase-3 expression and activity in the cultured chondrocytes. In addition, the expression of AQP-1 positively correlated with caspase-3 expression and activity. Thus, the findings of our study, suggest that AQP-1 promotes caspase-3 activation and thereby contributes to chondrocyte apoptosis and to the development of osteoarthritis.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2016.2785</identifier><identifier>PMID: 27779640</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Animals ; Apoptosis ; Apoptosis - genetics ; aquaporin 1 ; Aquaporin 1 - genetics ; Aquaporin 1 - metabolism ; Aquaporins ; Arthritis ; Cartilage, Articular - metabolism ; Cartilage, Articular - pathology ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Cells, Cultured ; chondrocyte ; Chondrocytes - metabolism ; Development and progression ; Disease Models, Animal ; Enzyme Activation ; Enzymes ; Gene Expression ; Gene Knockdown Techniques ; Knee ; Ligaments ; Male ; Osteoarthritis ; Osteoarthritis - genetics ; Osteoarthritis - metabolism ; Osteoarthritis - pathology ; Pathogenesis ; Penicillin ; Rats ; Rodents</subject><ispartof>International journal of molecular medicine, 2016-12, Vol.38 (6), p.1752-1758</ispartof><rights>Copyright: © Gao et al.</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><rights>Copyright: © Gao et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c518t-347c035c1d2d64107b4f771c080680e66867992e48bf757725d7023a7a61af0e3</citedby><cites>FETCH-LOGICAL-c518t-347c035c1d2d64107b4f771c080680e66867992e48bf757725d7023a7a61af0e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27779640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Hangfei</creatorcontrib><creatorcontrib>Gui, Jiancao</creatorcontrib><creatorcontrib>Wang, Liming</creatorcontrib><creatorcontrib>Xu, Yan</creatorcontrib><creatorcontrib>Jiang, Yiqiu</creatorcontrib><creatorcontrib>Xiong, Mingyue</creatorcontrib><creatorcontrib>Cui, Yongguang</creatorcontrib><title>Aquaporin 1 contributes to chondrocyte apoptosis in a rat model of osteoarthritis</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Aquaporins (AQPs) have been found to be associated with a number of diseases. However, the role of AQP-1 in the pathogenesis of osteoarthritis remains unclear. We previously found that AQP-1 expression was upregulated in osteoarthritic cartilage and strongly correlated with caspase-3 expression and activity. The aim of this study was to further investigate the association of AQP-1 expression with chondrocyte apoptosis in a rat model of osteoarthritis, using RNA interference to knock down AQP-1. For this purspose, 72 male Sprague-Dawley rats were randomly assigned to 3 groups as follows: the control group not treated surgically (n=24), the sham-operated group (n=24), and the osteoarthritis group (n=24). Osteoarthritis was induced by amputating the anterior cruciate ligament and medial collateral ligament and partially excising the medial meniscus. Chondrocytes from the rats with osteoarthritis were isolated and cultured. shRNAs were used to knock down AQP-1 expression in the cultured chondrocytes. The expression of AQP-1 and caspase-3 was determined by reverse transcription-quantitative polymerase chain reaction. Caspase-3 activity was measured using a caspase-3 colorimetric assay. The rats in our model of osteoarthritis exhibited severe cartilage damage. The knockdown of AQP-1 decreased caspase-3 expression and activity in the cultured chondrocytes. In addition, the expression of AQP-1 positively correlated with caspase-3 expression and activity. Thus, the findings of our study, suggest that AQP-1 promotes caspase-3 activation and thereby contributes to chondrocyte apoptosis and to the development of osteoarthritis.</description><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>aquaporin 1</subject><subject>Aquaporin 1 - genetics</subject><subject>Aquaporin 1 - metabolism</subject><subject>Aquaporins</subject><subject>Arthritis</subject><subject>Cartilage, Articular - metabolism</subject><subject>Cartilage, Articular - pathology</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Cells, Cultured</subject><subject>chondrocyte</subject><subject>Chondrocytes - metabolism</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>Enzyme Activation</subject><subject>Enzymes</subject><subject>Gene Expression</subject><subject>Gene Knockdown Techniques</subject><subject>Knee</subject><subject>Ligaments</subject><subject>Male</subject><subject>Osteoarthritis</subject><subject>Osteoarthritis - genetics</subject><subject>Osteoarthritis - metabolism</subject><subject>Osteoarthritis - pathology</subject><subject>Pathogenesis</subject><subject>Penicillin</subject><subject>Rats</subject><subject>Rodents</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkc2LFDEQxRtR3HX16lECXrz0mO9KLsKw-AULIih4C5kkvZNhutObpBf2vzfNrqPCUocUlV89XvK67jXBG6Y0fR8P47ihmMgNBSWedOcENOkp57-etp5g6BkIeda9KOWAMRVcq-fdGQUALTk-775vbxY7pxwnRJBLU81xt9RQUE3I7dPkc3J3NaDGzDWVWFAjLcq2ojH5cERpQKnUkGyu-xxrLC-7Z4M9lvDq4bzofn76-OPyS3_17fPXy-1V7wRRtWccHGbCEU-95M3ojg8AxGGFpcJBSiVBaxq42g0gAKjwgCmzYCWxAw7sovtwrzsvuzF4F5p3ezRzjqPNdybZaP6_meLeXKdbIwgBYNAE3j4I5HSzhFLNIS15ap4N0YwypoGrv9S1PQYTpyE1MTfG4syWgwbCtVipzSNUKx_G2L41DLHNH1twOZWSw3AyTrBZkzVrsmZN1qzJtoU3_z73hP-JsgHv7oEy28lHn8qJWaV6pnosewKCst-FPav0</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Gao, Hangfei</creator><creator>Gui, Jiancao</creator><creator>Wang, Liming</creator><creator>Xu, Yan</creator><creator>Jiang, Yiqiu</creator><creator>Xiong, Mingyue</creator><creator>Cui, Yongguang</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20161201</creationdate><title>Aquaporin 1 contributes to chondrocyte apoptosis in a rat model of osteoarthritis</title><author>Gao, Hangfei ; Gui, Jiancao ; Wang, Liming ; Xu, Yan ; Jiang, Yiqiu ; Xiong, Mingyue ; Cui, Yongguang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c518t-347c035c1d2d64107b4f771c080680e66867992e48bf757725d7023a7a61af0e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>aquaporin 1</topic><topic>Aquaporin 1 - genetics</topic><topic>Aquaporin 1 - metabolism</topic><topic>Aquaporins</topic><topic>Arthritis</topic><topic>Cartilage, Articular - metabolism</topic><topic>Cartilage, Articular - pathology</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Cells, Cultured</topic><topic>chondrocyte</topic><topic>Chondrocytes - metabolism</topic><topic>Development and progression</topic><topic>Disease Models, Animal</topic><topic>Enzyme Activation</topic><topic>Enzymes</topic><topic>Gene Expression</topic><topic>Gene Knockdown Techniques</topic><topic>Knee</topic><topic>Ligaments</topic><topic>Male</topic><topic>Osteoarthritis</topic><topic>Osteoarthritis - genetics</topic><topic>Osteoarthritis - metabolism</topic><topic>Osteoarthritis - pathology</topic><topic>Pathogenesis</topic><topic>Penicillin</topic><topic>Rats</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Hangfei</creatorcontrib><creatorcontrib>Gui, Jiancao</creatorcontrib><creatorcontrib>Wang, Liming</creatorcontrib><creatorcontrib>Xu, Yan</creatorcontrib><creatorcontrib>Jiang, Yiqiu</creatorcontrib><creatorcontrib>Xiong, Mingyue</creatorcontrib><creatorcontrib>Cui, Yongguang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Hangfei</au><au>Gui, Jiancao</au><au>Wang, Liming</au><au>Xu, Yan</au><au>Jiang, Yiqiu</au><au>Xiong, Mingyue</au><au>Cui, Yongguang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aquaporin 1 contributes to chondrocyte apoptosis in a rat model of osteoarthritis</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>38</volume><issue>6</issue><spage>1752</spage><epage>1758</epage><pages>1752-1758</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>Aquaporins (AQPs) have been found to be associated with a number of diseases. However, the role of AQP-1 in the pathogenesis of osteoarthritis remains unclear. We previously found that AQP-1 expression was upregulated in osteoarthritic cartilage and strongly correlated with caspase-3 expression and activity. The aim of this study was to further investigate the association of AQP-1 expression with chondrocyte apoptosis in a rat model of osteoarthritis, using RNA interference to knock down AQP-1. For this purspose, 72 male Sprague-Dawley rats were randomly assigned to 3 groups as follows: the control group not treated surgically (n=24), the sham-operated group (n=24), and the osteoarthritis group (n=24). Osteoarthritis was induced by amputating the anterior cruciate ligament and medial collateral ligament and partially excising the medial meniscus. Chondrocytes from the rats with osteoarthritis were isolated and cultured. shRNAs were used to knock down AQP-1 expression in the cultured chondrocytes. The expression of AQP-1 and caspase-3 was determined by reverse transcription-quantitative polymerase chain reaction. Caspase-3 activity was measured using a caspase-3 colorimetric assay. The rats in our model of osteoarthritis exhibited severe cartilage damage. The knockdown of AQP-1 decreased caspase-3 expression and activity in the cultured chondrocytes. In addition, the expression of AQP-1 positively correlated with caspase-3 expression and activity. Thus, the findings of our study, suggest that AQP-1 promotes caspase-3 activation and thereby contributes to chondrocyte apoptosis and to the development of osteoarthritis.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>27779640</pmid><doi>10.3892/ijmm.2016.2785</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Apoptosis Apoptosis - genetics aquaporin 1 Aquaporin 1 - genetics Aquaporin 1 - metabolism Aquaporins Arthritis Cartilage, Articular - metabolism Cartilage, Articular - pathology Caspase 3 - genetics Caspase 3 - metabolism Cells, Cultured chondrocyte Chondrocytes - metabolism Development and progression Disease Models, Animal Enzyme Activation Enzymes Gene Expression Gene Knockdown Techniques Knee Ligaments Male Osteoarthritis Osteoarthritis - genetics Osteoarthritis - metabolism Osteoarthritis - pathology Pathogenesis Penicillin Rats Rodents |
| title | Aquaporin 1 contributes to chondrocyte apoptosis in a rat model of osteoarthritis |
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