Inhibitory effects of Formononetin on CoCrMo particle-induced osteoclast activation and bone loss through downregulating NF-κB and MAPK signaling
Wear particle-induced osteoclast over-activation is a major contributor to periprosthetic osteolysis and aseptic loosening, which can cause pathological bone loss and destruction. Hence, inhibiting excessive osteoclast-resorbing activity is an important strategy for preventing periprosthetic osteoly...
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| Veröffentlicht in: | Cellular signalling 2023-06, Vol.106, p.110651-110651, Article 110651 |
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| container_title | Cellular signalling |
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| creator | Yu, Xin Yang, Binkui Chen, Bin Wu, Qi Ren, Zhengrong Wang, Dongsheng Yuan, Tao Ding, Hao Ding, Chao Liu, Yang Zhang, Lei Sun, Zhongyang Zhao, Jianning |
| description | Wear particle-induced osteoclast over-activation is a major contributor to periprosthetic osteolysis and aseptic loosening, which can cause pathological bone loss and destruction. Hence, inhibiting excessive osteoclast-resorbing activity is an important strategy for preventing periprosthetic osteolysis. Formononetin (FMN) has been shown to have protective effects against osteoporosis, but no previous study has evaluated the effects of FMN on wear particle-induced osteolysis. In this study, we found that FMN alleviated CoCrMo alloy particles (CoPs)-induced bone loss in vivo and inhibited the formation and bone-resorptive function of osteoclasts in vitro. Moreover, we revealed that FMN exerted inhibitory effects on the expression of osteoclast-specific genes via the classical NF-κB and MAPK signaling pathways in vitro. Collectively, FMN is a potential therapeutic agent for the prevention and treatment of periprosthetic osteolysis and other osteolytic bone diseases.
•Inhibition of osteoclastogenesis is a key therapeutic strategy for treatment of periprosthetic osteolysis.•FMN could alleviate CoCrMo metal particle-induced osteoclast activation and bone loss.•FMN could inhibit osteoclast differentiation and bone-resorbing activity.•FMN could downregulate the classical NF-κB and MAPK signaling pathways during osteoclastogenesis.•FMN might be a potential therapeutic agent for treating osteolytic bone diseases. |
| doi_str_mv | 10.1016/j.cellsig.2023.110651 |
| format | Article |
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•Inhibition of osteoclastogenesis is a key therapeutic strategy for treatment of periprosthetic osteolysis.•FMN could alleviate CoCrMo metal particle-induced osteoclast activation and bone loss.•FMN could inhibit osteoclast differentiation and bone-resorbing activity.•FMN could downregulate the classical NF-κB and MAPK signaling pathways during osteoclastogenesis.•FMN might be a potential therapeutic agent for treating osteolytic bone diseases.</description><identifier>ISSN: 0898-6568</identifier><identifier>EISSN: 1873-3913</identifier><identifier>DOI: 10.1016/j.cellsig.2023.110651</identifier><identifier>PMID: 36894124</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Animals ; Aseptic loosening ; Bone Resorption - drug therapy ; Bone Resorption - pathology ; Formononetin ; Humans ; MAP Kinase Signaling System ; MAPK ; Mice ; Mice, Inbred C57BL ; NF-kappa B - metabolism ; NF-κB ; Osteoclast ; Osteoclasts - metabolism ; Osteogenesis ; Osteolysis - drug therapy ; Periprosthetic osteolysis ; RANK Ligand - metabolism ; RANK Ligand - pharmacology</subject><ispartof>Cellular signalling, 2023-06, Vol.106, p.110651-110651, Article 110651</ispartof><rights>2023 The Authors</rights><rights>Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-1010ed28e527896ed2da5c8aace71b52fb78fb3a47372e141c764dd07fac612c3</citedby><cites>FETCH-LOGICAL-c412t-1010ed28e527896ed2da5c8aace71b52fb78fb3a47372e141c764dd07fac612c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cellsig.2023.110651$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36894124$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Xin</creatorcontrib><creatorcontrib>Yang, Binkui</creatorcontrib><creatorcontrib>Chen, Bin</creatorcontrib><creatorcontrib>Wu, Qi</creatorcontrib><creatorcontrib>Ren, Zhengrong</creatorcontrib><creatorcontrib>Wang, Dongsheng</creatorcontrib><creatorcontrib>Yuan, Tao</creatorcontrib><creatorcontrib>Ding, Hao</creatorcontrib><creatorcontrib>Ding, Chao</creatorcontrib><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Sun, Zhongyang</creatorcontrib><creatorcontrib>Zhao, Jianning</creatorcontrib><title>Inhibitory effects of Formononetin on CoCrMo particle-induced osteoclast activation and bone loss through downregulating NF-κB and MAPK signaling</title><title>Cellular signalling</title><addtitle>Cell Signal</addtitle><description>Wear particle-induced osteoclast over-activation is a major contributor to periprosthetic osteolysis and aseptic loosening, which can cause pathological bone loss and destruction. Hence, inhibiting excessive osteoclast-resorbing activity is an important strategy for preventing periprosthetic osteolysis. Formononetin (FMN) has been shown to have protective effects against osteoporosis, but no previous study has evaluated the effects of FMN on wear particle-induced osteolysis. In this study, we found that FMN alleviated CoCrMo alloy particles (CoPs)-induced bone loss in vivo and inhibited the formation and bone-resorptive function of osteoclasts in vitro. Moreover, we revealed that FMN exerted inhibitory effects on the expression of osteoclast-specific genes via the classical NF-κB and MAPK signaling pathways in vitro. Collectively, FMN is a potential therapeutic agent for the prevention and treatment of periprosthetic osteolysis and other osteolytic bone diseases.
•Inhibition of osteoclastogenesis is a key therapeutic strategy for treatment of periprosthetic osteolysis.•FMN could alleviate CoCrMo metal particle-induced osteoclast activation and bone loss.•FMN could inhibit osteoclast differentiation and bone-resorbing activity.•FMN could downregulate the classical NF-κB and MAPK signaling pathways during osteoclastogenesis.•FMN might be a potential therapeutic agent for treating osteolytic bone diseases.</description><subject>Animals</subject><subject>Aseptic loosening</subject><subject>Bone Resorption - drug therapy</subject><subject>Bone Resorption - pathology</subject><subject>Formononetin</subject><subject>Humans</subject><subject>MAP Kinase Signaling System</subject><subject>MAPK</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>Osteoclast</subject><subject>Osteoclasts - metabolism</subject><subject>Osteogenesis</subject><subject>Osteolysis - drug therapy</subject><subject>Periprosthetic osteolysis</subject><subject>RANK Ligand - metabolism</subject><subject>RANK Ligand - pharmacology</subject><issn>0898-6568</issn><issn>1873-3913</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2OEzEUhC0EYsLAEUBesungn27bvUJDRGDEDLCAteW2XyeOOnaw3YPmGhyHQ3AmHBLYsrIlf_Weqwqh55QsKaHi1W5pYZqy3ywZYXxJKREdfYAWVEne8J7yh2hBVK8a0Ql1gZ7kvCOEdkSwx-iCC9W3lLUL9OM6bP3gS0z3GMYRbMk4jngd0z6GGKD4gGPAq7hKtxEfTCreTtD44GYLDsdcINrJ5IKNLf7OFF9pExweqhhPMWdctinOmy128XtIsJmnCoUN_rhufv1884e9vfr8AVcrwUz15Sl6NJopw7PzeYm-rt9-Wb1vbj69u15d3TS2fr00NQUCjinomFS9qFdnOquMsSDp0LFxkGocuGkllwxoS60UrXNEjsYKyiy_RC9Pcw8pfpshF733-RiqCRDnrOtYQXoue17R7oTaVB0lGPUh-b1J95oSfaxD7_S5Dn2sQ5_qqLoX5xXzsAf3T_U3_wq8PgFQjd55SDpbD6FG61PtQrvo_7PiN36eoa0</recordid><startdate>202306</startdate><enddate>202306</enddate><creator>Yu, Xin</creator><creator>Yang, Binkui</creator><creator>Chen, Bin</creator><creator>Wu, Qi</creator><creator>Ren, Zhengrong</creator><creator>Wang, Dongsheng</creator><creator>Yuan, Tao</creator><creator>Ding, Hao</creator><creator>Ding, Chao</creator><creator>Liu, Yang</creator><creator>Zhang, Lei</creator><creator>Sun, Zhongyang</creator><creator>Zhao, Jianning</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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>7X8</scope></search><sort><creationdate>202306</creationdate><title>Inhibitory effects of Formononetin on CoCrMo particle-induced osteoclast activation and bone loss through downregulating NF-κB and MAPK signaling</title><author>Yu, Xin ; Yang, Binkui ; Chen, Bin ; Wu, Qi ; Ren, Zhengrong ; Wang, Dongsheng ; Yuan, Tao ; Ding, Hao ; Ding, Chao ; Liu, Yang ; Zhang, Lei ; Sun, Zhongyang ; Zhao, Jianning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-1010ed28e527896ed2da5c8aace71b52fb78fb3a47372e141c764dd07fac612c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Aseptic loosening</topic><topic>Bone Resorption - drug therapy</topic><topic>Bone Resorption - pathology</topic><topic>Formononetin</topic><topic>Humans</topic><topic>MAP Kinase Signaling System</topic><topic>MAPK</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>Osteoclast</topic><topic>Osteoclasts - metabolism</topic><topic>Osteogenesis</topic><topic>Osteolysis - drug therapy</topic><topic>Periprosthetic osteolysis</topic><topic>RANK Ligand - metabolism</topic><topic>RANK Ligand - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Xin</creatorcontrib><creatorcontrib>Yang, Binkui</creatorcontrib><creatorcontrib>Chen, Bin</creatorcontrib><creatorcontrib>Wu, Qi</creatorcontrib><creatorcontrib>Ren, Zhengrong</creatorcontrib><creatorcontrib>Wang, Dongsheng</creatorcontrib><creatorcontrib>Yuan, Tao</creatorcontrib><creatorcontrib>Ding, Hao</creatorcontrib><creatorcontrib>Ding, Chao</creatorcontrib><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Sun, Zhongyang</creatorcontrib><creatorcontrib>Zhao, Jianning</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cellular signalling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Xin</au><au>Yang, Binkui</au><au>Chen, Bin</au><au>Wu, Qi</au><au>Ren, Zhengrong</au><au>Wang, Dongsheng</au><au>Yuan, Tao</au><au>Ding, Hao</au><au>Ding, Chao</au><au>Liu, Yang</au><au>Zhang, Lei</au><au>Sun, Zhongyang</au><au>Zhao, Jianning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibitory effects of Formononetin on CoCrMo particle-induced osteoclast activation and bone loss through downregulating NF-κB and MAPK signaling</atitle><jtitle>Cellular signalling</jtitle><addtitle>Cell Signal</addtitle><date>2023-06</date><risdate>2023</risdate><volume>106</volume><spage>110651</spage><epage>110651</epage><pages>110651-110651</pages><artnum>110651</artnum><issn>0898-6568</issn><eissn>1873-3913</eissn><abstract>Wear particle-induced osteoclast over-activation is a major contributor to periprosthetic osteolysis and aseptic loosening, which can cause pathological bone loss and destruction. Hence, inhibiting excessive osteoclast-resorbing activity is an important strategy for preventing periprosthetic osteolysis. Formononetin (FMN) has been shown to have protective effects against osteoporosis, but no previous study has evaluated the effects of FMN on wear particle-induced osteolysis. In this study, we found that FMN alleviated CoCrMo alloy particles (CoPs)-induced bone loss in vivo and inhibited the formation and bone-resorptive function of osteoclasts in vitro. Moreover, we revealed that FMN exerted inhibitory effects on the expression of osteoclast-specific genes via the classical NF-κB and MAPK signaling pathways in vitro. Collectively, FMN is a potential therapeutic agent for the prevention and treatment of periprosthetic osteolysis and other osteolytic bone diseases.
•Inhibition of osteoclastogenesis is a key therapeutic strategy for treatment of periprosthetic osteolysis.•FMN could alleviate CoCrMo metal particle-induced osteoclast activation and bone loss.•FMN could inhibit osteoclast differentiation and bone-resorbing activity.•FMN could downregulate the classical NF-κB and MAPK signaling pathways during osteoclastogenesis.•FMN might be a potential therapeutic agent for treating osteolytic bone diseases.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>36894124</pmid><doi>10.1016/j.cellsig.2023.110651</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cellular signalling, 2023-06, Vol.106, p.110651-110651, Article 110651 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Animals Aseptic loosening Bone Resorption - drug therapy Bone Resorption - pathology Formononetin Humans MAP Kinase Signaling System MAPK Mice Mice, Inbred C57BL NF-kappa B - metabolism NF-κB Osteoclast Osteoclasts - metabolism Osteogenesis Osteolysis - drug therapy Periprosthetic osteolysis RANK Ligand - metabolism RANK Ligand - pharmacology |
| title | Inhibitory effects of Formononetin on CoCrMo particle-induced osteoclast activation and bone loss through downregulating NF-κB and MAPK signaling |
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