Sam68 Promotes NF-[kappa]B Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis
Objectives To investigate the expression of Sam68 in articular cartilage of knee osteoarthritis (OA) and the relationship between Sam68 and NF-[kappa]B activation and apoptosis signaling in OA articular chondrocytes. Methods Sam68 expression in normal and osteoarthritic cartilage was assessed by imm...
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| Veröffentlicht in: | Inflammation research 2015-11, Vol.64 (11), p.895 |
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| creator | Xu, Libin Sun, Chi Zhang, Sihui Xu, Xinbao Zhai, Leilei Wang, Youhua Wang, Shitao Liu, Zhongbing Cheng, Hongbing Xiao, Min Tao, Ran Zhang, Dongmei |
| description | Objectives To investigate the expression of Sam68 in articular cartilage of knee osteoarthritis (OA) and the relationship between Sam68 and NF-[kappa]B activation and apoptosis signaling in OA articular chondrocytes. Methods Sam68 expression in normal and osteoarthritic cartilage was assessed by immunohistochemistry and RT-PCR on both meniscal/ligamentous injury (MLI)-induced OA rat model and the clinical human OA cartilage tissues. Sam68 expression in chondrocytes under tumor necrosis factor-alpha (TNF-[alpha]) stimuli was also assessed by immunoblot. Inhibiting Sam68 in chondrocytes under TNF-[alpha] stimuli was conducted using small interfering RNA (siRNA) and its influence on the expression of apoptotic marker and catabolic genes was examined by immunoblot. The mechanism of how Sam68 stimulates NF-[kappa]B activity was determined by co-immunoprecipitation and immunoblot analysis of nuclear and cytoplasmic fractions of TNF-[alpha]-treated chondrocytes for p65 and Sam68. Results Sam68 expression was increased in OA cartilage tissues and chondrocytes under TNF-[alpha] stimuli. Inhibition of Sam68 by siRNA significantly decreased the expression of apoptotic markers (cleaved caspase-3 and cleaved PARP) in chondrocytes following TNF-[alpha]-stimulation. Sam68 knockdown suppressed I[kappa]-B degradation and p65 nuclear transportation in TNF-[alpha]-treated chondrocytes, indicating a suppressed NF-[kappa]B activation. Upon TNF-[alpha] exposure, the nuclear transportation of Sam68 and its interaction with p65 was detected in chondrocytes. Furthermore, Sam68 knockdown also alleviated the TNF-[alpha]-induced catabolic marker (MMP13, ADAMTS5, iNOS and IL-6) expression. Conclusions The highly expressed Sam68 promotes NF-[kappa]B signaling activation, catabolic gene expression and cellular apoptosis in TNF-[alpha]-treated chondrocytes, which may provide better insights into the pathophysiology of OA and a potential target for its treatment. |
| doi_str_mv | 10.1007/s00011-015-0872-3 |
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| fullrecord | <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_journals_1721877885</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3835160021</sourcerecordid><originalsourceid>FETCH-proquest_journals_17218778853</originalsourceid><addsrcrecordid>eNqNzMFKAzEUheEgCtbqA7gLuI7eJNbE5VgsXanQLgSRcpkZ29SZ3JibEXx7p-ADuDpn8fELcanhWgO4GwYArRXomQLvjLJHYqJvDah78K_H4wdjlfUWTsUZ837U3ngzEf0K-zsvXzL1VFqWTwv19okp4fuDrOoSvrEEihJjI6tEqRAHlquwjdiFuJUhyiqXUA8dZjnfUWwy1T-HUDPkA3jm0hLmssuhBD4XJx_YcXvxt1NxtXhcz5cqZfoaWi6bPQ15bPNGO6O9c97P7P_ULw1sUG4</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1721877885</pqid></control><display><type>article</type><title>Sam68 Promotes NF-[kappa]B Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis</title><source>SpringerLink Journals - AutoHoldings</source><creator>Xu, Libin ; Sun, Chi ; Zhang, Sihui ; Xu, Xinbao ; Zhai, Leilei ; Wang, Youhua ; Wang, Shitao ; Liu, Zhongbing ; Cheng, Hongbing ; Xiao, Min ; Tao, Ran ; Zhang, Dongmei</creator><creatorcontrib>Xu, Libin ; Sun, Chi ; Zhang, Sihui ; Xu, Xinbao ; Zhai, Leilei ; Wang, Youhua ; Wang, Shitao ; Liu, Zhongbing ; Cheng, Hongbing ; Xiao, Min ; Tao, Ran ; Zhang, Dongmei</creatorcontrib><description>Objectives To investigate the expression of Sam68 in articular cartilage of knee osteoarthritis (OA) and the relationship between Sam68 and NF-[kappa]B activation and apoptosis signaling in OA articular chondrocytes. Methods Sam68 expression in normal and osteoarthritic cartilage was assessed by immunohistochemistry and RT-PCR on both meniscal/ligamentous injury (MLI)-induced OA rat model and the clinical human OA cartilage tissues. Sam68 expression in chondrocytes under tumor necrosis factor-alpha (TNF-[alpha]) stimuli was also assessed by immunoblot. Inhibiting Sam68 in chondrocytes under TNF-[alpha] stimuli was conducted using small interfering RNA (siRNA) and its influence on the expression of apoptotic marker and catabolic genes was examined by immunoblot. The mechanism of how Sam68 stimulates NF-[kappa]B activity was determined by co-immunoprecipitation and immunoblot analysis of nuclear and cytoplasmic fractions of TNF-[alpha]-treated chondrocytes for p65 and Sam68. Results Sam68 expression was increased in OA cartilage tissues and chondrocytes under TNF-[alpha] stimuli. Inhibition of Sam68 by siRNA significantly decreased the expression of apoptotic markers (cleaved caspase-3 and cleaved PARP) in chondrocytes following TNF-[alpha]-stimulation. Sam68 knockdown suppressed I[kappa]-B degradation and p65 nuclear transportation in TNF-[alpha]-treated chondrocytes, indicating a suppressed NF-[kappa]B activation. Upon TNF-[alpha] exposure, the nuclear transportation of Sam68 and its interaction with p65 was detected in chondrocytes. Furthermore, Sam68 knockdown also alleviated the TNF-[alpha]-induced catabolic marker (MMP13, ADAMTS5, iNOS and IL-6) expression. Conclusions The highly expressed Sam68 promotes NF-[kappa]B signaling activation, catabolic gene expression and cellular apoptosis in TNF-[alpha]-treated chondrocytes, which may provide better insights into the pathophysiology of OA and a potential target for its treatment.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-015-0872-3</identifier><language>eng</language><publisher>New York: Springer Nature B.V</publisher><ispartof>Inflammation research, 2015-11, Vol.64 (11), p.895</ispartof><rights>Springer Basel 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids></links><search><creatorcontrib>Xu, Libin</creatorcontrib><creatorcontrib>Sun, Chi</creatorcontrib><creatorcontrib>Zhang, Sihui</creatorcontrib><creatorcontrib>Xu, Xinbao</creatorcontrib><creatorcontrib>Zhai, Leilei</creatorcontrib><creatorcontrib>Wang, Youhua</creatorcontrib><creatorcontrib>Wang, Shitao</creatorcontrib><creatorcontrib>Liu, Zhongbing</creatorcontrib><creatorcontrib>Cheng, Hongbing</creatorcontrib><creatorcontrib>Xiao, Min</creatorcontrib><creatorcontrib>Tao, Ran</creatorcontrib><creatorcontrib>Zhang, Dongmei</creatorcontrib><title>Sam68 Promotes NF-[kappa]B Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis</title><title>Inflammation research</title><description>Objectives To investigate the expression of Sam68 in articular cartilage of knee osteoarthritis (OA) and the relationship between Sam68 and NF-[kappa]B activation and apoptosis signaling in OA articular chondrocytes. Methods Sam68 expression in normal and osteoarthritic cartilage was assessed by immunohistochemistry and RT-PCR on both meniscal/ligamentous injury (MLI)-induced OA rat model and the clinical human OA cartilage tissues. Sam68 expression in chondrocytes under tumor necrosis factor-alpha (TNF-[alpha]) stimuli was also assessed by immunoblot. Inhibiting Sam68 in chondrocytes under TNF-[alpha] stimuli was conducted using small interfering RNA (siRNA) and its influence on the expression of apoptotic marker and catabolic genes was examined by immunoblot. The mechanism of how Sam68 stimulates NF-[kappa]B activity was determined by co-immunoprecipitation and immunoblot analysis of nuclear and cytoplasmic fractions of TNF-[alpha]-treated chondrocytes for p65 and Sam68. Results Sam68 expression was increased in OA cartilage tissues and chondrocytes under TNF-[alpha] stimuli. Inhibition of Sam68 by siRNA significantly decreased the expression of apoptotic markers (cleaved caspase-3 and cleaved PARP) in chondrocytes following TNF-[alpha]-stimulation. Sam68 knockdown suppressed I[kappa]-B degradation and p65 nuclear transportation in TNF-[alpha]-treated chondrocytes, indicating a suppressed NF-[kappa]B activation. Upon TNF-[alpha] exposure, the nuclear transportation of Sam68 and its interaction with p65 was detected in chondrocytes. Furthermore, Sam68 knockdown also alleviated the TNF-[alpha]-induced catabolic marker (MMP13, ADAMTS5, iNOS and IL-6) expression. Conclusions The highly expressed Sam68 promotes NF-[kappa]B signaling activation, catabolic gene expression and cellular apoptosis in TNF-[alpha]-treated chondrocytes, which may provide better insights into the pathophysiology of OA and a potential target for its treatment.</description><issn>1023-3830</issn><issn>1420-908X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNzMFKAzEUheEgCtbqA7gLuI7eJNbE5VgsXanQLgSRcpkZ29SZ3JibEXx7p-ADuDpn8fELcanhWgO4GwYArRXomQLvjLJHYqJvDah78K_H4wdjlfUWTsUZ837U3ngzEf0K-zsvXzL1VFqWTwv19okp4fuDrOoSvrEEihJjI6tEqRAHlquwjdiFuJUhyiqXUA8dZjnfUWwy1T-HUDPkA3jm0hLmssuhBD4XJx_YcXvxt1NxtXhcz5cqZfoaWi6bPQ15bPNGO6O9c97P7P_ULw1sUG4</recordid><startdate>20151101</startdate><enddate>20151101</enddate><creator>Xu, Libin</creator><creator>Sun, Chi</creator><creator>Zhang, Sihui</creator><creator>Xu, Xinbao</creator><creator>Zhai, Leilei</creator><creator>Wang, Youhua</creator><creator>Wang, Shitao</creator><creator>Liu, Zhongbing</creator><creator>Cheng, Hongbing</creator><creator>Xiao, Min</creator><creator>Tao, Ran</creator><creator>Zhang, Dongmei</creator><general>Springer Nature B.V</general><scope>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20151101</creationdate><title>Sam68 Promotes NF-[kappa]B Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis</title><author>Xu, Libin ; Sun, Chi ; Zhang, Sihui ; Xu, Xinbao ; Zhai, Leilei ; Wang, Youhua ; Wang, Shitao ; Liu, Zhongbing ; Cheng, Hongbing ; Xiao, Min ; Tao, Ran ; Zhang, Dongmei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_17218778853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Libin</creatorcontrib><creatorcontrib>Sun, Chi</creatorcontrib><creatorcontrib>Zhang, Sihui</creatorcontrib><creatorcontrib>Xu, Xinbao</creatorcontrib><creatorcontrib>Zhai, Leilei</creatorcontrib><creatorcontrib>Wang, Youhua</creatorcontrib><creatorcontrib>Wang, Shitao</creatorcontrib><creatorcontrib>Liu, Zhongbing</creatorcontrib><creatorcontrib>Cheng, Hongbing</creatorcontrib><creatorcontrib>Xiao, Min</creatorcontrib><creatorcontrib>Tao, Ran</creatorcontrib><creatorcontrib>Zhang, Dongmei</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</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>Technology Research Database</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</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><jtitle>Inflammation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Libin</au><au>Sun, Chi</au><au>Zhang, Sihui</au><au>Xu, Xinbao</au><au>Zhai, Leilei</au><au>Wang, Youhua</au><au>Wang, Shitao</au><au>Liu, Zhongbing</au><au>Cheng, Hongbing</au><au>Xiao, Min</au><au>Tao, Ran</au><au>Zhang, Dongmei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sam68 Promotes NF-[kappa]B Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis</atitle><jtitle>Inflammation research</jtitle><date>2015-11-01</date><risdate>2015</risdate><volume>64</volume><issue>11</issue><spage>895</spage><pages>895-</pages><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Objectives To investigate the expression of Sam68 in articular cartilage of knee osteoarthritis (OA) and the relationship between Sam68 and NF-[kappa]B activation and apoptosis signaling in OA articular chondrocytes. Methods Sam68 expression in normal and osteoarthritic cartilage was assessed by immunohistochemistry and RT-PCR on both meniscal/ligamentous injury (MLI)-induced OA rat model and the clinical human OA cartilage tissues. Sam68 expression in chondrocytes under tumor necrosis factor-alpha (TNF-[alpha]) stimuli was also assessed by immunoblot. Inhibiting Sam68 in chondrocytes under TNF-[alpha] stimuli was conducted using small interfering RNA (siRNA) and its influence on the expression of apoptotic marker and catabolic genes was examined by immunoblot. The mechanism of how Sam68 stimulates NF-[kappa]B activity was determined by co-immunoprecipitation and immunoblot analysis of nuclear and cytoplasmic fractions of TNF-[alpha]-treated chondrocytes for p65 and Sam68. Results Sam68 expression was increased in OA cartilage tissues and chondrocytes under TNF-[alpha] stimuli. Inhibition of Sam68 by siRNA significantly decreased the expression of apoptotic markers (cleaved caspase-3 and cleaved PARP) in chondrocytes following TNF-[alpha]-stimulation. Sam68 knockdown suppressed I[kappa]-B degradation and p65 nuclear transportation in TNF-[alpha]-treated chondrocytes, indicating a suppressed NF-[kappa]B activation. Upon TNF-[alpha] exposure, the nuclear transportation of Sam68 and its interaction with p65 was detected in chondrocytes. Furthermore, Sam68 knockdown also alleviated the TNF-[alpha]-induced catabolic marker (MMP13, ADAMTS5, iNOS and IL-6) expression. Conclusions The highly expressed Sam68 promotes NF-[kappa]B signaling activation, catabolic gene expression and cellular apoptosis in TNF-[alpha]-treated chondrocytes, which may provide better insights into the pathophysiology of OA and a potential target for its treatment.</abstract><cop>New York</cop><pub>Springer Nature B.V</pub><doi>10.1007/s00011-015-0872-3</doi></addata></record> |
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| title | Sam68 Promotes NF-[kappa]B Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis |
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