Apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) contributes to osteoblast differentiation and osteogenesis
The role of apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) in bone healing remains to be understood. To address this issue, we investigated the requirement of inflammasome‐related genes in response to bone morphogenetic protein 7 (BMP7)‐induced osteoblast dif...
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creator | Sartoretto, Suelen Gemini‐Piperni, Sara da Silva, Rodrigo A. Calasans, Monica D. Rucci, Nadia Pires dos Santos, Thais M. Lima, Inayá B. C. Rossi, Alexandre M. Alves, Gutemberg Granjeiro, José M. Teti, Anna Zambuzzi, Willian F. |
description | The role of apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) in bone healing remains to be understood. To address this issue, we investigated the requirement of inflammasome‐related genes in response to bone morphogenetic protein 7 (BMP7)‐induced osteoblast differentiation in vitro. To validate the importance of ASC on osteogenesis, we subjected wild‐type (WT) and ASC knockout C57BL/6 mice (ASC KO) to tibia defect to evaluate the bone healing process (up to 28 days). Our in vitro data showed that there is an involvement of ASC during BMP7‐induced osteoblast differentiation, concomitant to osteogenic biomarker expression. Indeed, primary osteogenic cells from ASC KO presented a lower osteogenic profile than those obtained from WT mice. To validate this hypothesis, we evaluated the bone healing process of tibia defects on both WT and ASC KO mice genotypes and the ASC KO mice were not able to fully heal tibia defects up to 28 days, whereas WT tibia defects presented a higher bone de novo volume at this stage, evidencing ASC as an important molecule during osteogenic phenotype. In addition, we have shown a higher involvement of runt‐related transcription factor 2 in WT sections during bone repair, as well as circulating bone alkaline phosphatase isoform when both were compared with ASC KO mice behavior. Altogether, our results showed for the first time the involvement of inflammasome during osteoblast differentiation and osteogenesis, which opens new avenues to understand the pathways involved in bone healing.
ASC contributes to osteoblast differentiation and bone de novo deposition, opening new avenues to understand the complex mechanism coupling inflammation landscape and osteoblastogenesis during bone healing. |
doi_str_mv | 10.1002/jcp.27226 |
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ASC contributes to osteoblast differentiation and bone de novo deposition, opening new avenues to understand the complex mechanism coupling inflammation landscape and osteoblastogenesis during bone healing.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.27226</identifier><identifier>PMID: 30171612</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>3T3 Cells ; Alkaline phosphatase ; Animals ; Apoptosis ; ASC ; Biocompatibility ; Biomarkers ; Biomedical materials ; bone formation ; Bone healing ; Bone morphogenetic protein 7 ; Bone Morphogenetic Protein 7 - pharmacology ; CARD Signaling Adaptor Proteins - deficiency ; CARD Signaling Adaptor Proteins - genetics ; CARD Signaling Adaptor Proteins - metabolism ; Caspase ; Cell Differentiation - drug effects ; Defects ; Differentiation ; Disease Models, Animal ; Female ; Fracture Healing ; Genotypes ; Healing ; inflammasome ; Inflammasomes ; Inflammasomes - drug effects ; Inflammasomes - metabolism ; Inflammation Mediators - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; osteoblast ; Osteoblastogenesis ; Osteoblasts - drug effects ; Osteoblasts - metabolism ; Osteoblasts - pathology ; Osteogenesis ; Osteogenesis - drug effects ; Phenotypes ; Proteins ; Recruitment ; regenerative medicine ; Rodents ; Signal Transduction ; Tibia ; Tibia - metabolism ; Tibia - pathology ; Tibia - physiopathology ; Tibial Fractures - genetics ; Tibial Fractures - metabolism ; Tibial Fractures - pathology ; Tibial Fractures - physiopathology ; Time Factors</subject><ispartof>Journal of cellular physiology, 2019-04, Vol.234 (4), p.4140-4153</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4196-eee949e9ad217bc1383b433465d11d88313035de2911078bf861900488f8a473</citedby><cites>FETCH-LOGICAL-c4196-eee949e9ad217bc1383b433465d11d88313035de2911078bf861900488f8a473</cites><orcidid>0000-0002-4149-5965</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.27226$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.27226$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30171612$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sartoretto, Suelen</creatorcontrib><creatorcontrib>Gemini‐Piperni, Sara</creatorcontrib><creatorcontrib>da Silva, Rodrigo A.</creatorcontrib><creatorcontrib>Calasans, Monica D.</creatorcontrib><creatorcontrib>Rucci, Nadia</creatorcontrib><creatorcontrib>Pires dos Santos, Thais M.</creatorcontrib><creatorcontrib>Lima, Inayá B. C.</creatorcontrib><creatorcontrib>Rossi, Alexandre M.</creatorcontrib><creatorcontrib>Alves, Gutemberg</creatorcontrib><creatorcontrib>Granjeiro, José M.</creatorcontrib><creatorcontrib>Teti, Anna</creatorcontrib><creatorcontrib>Zambuzzi, Willian F.</creatorcontrib><title>Apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) contributes to osteoblast differentiation and osteogenesis</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>The role of apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) in bone healing remains to be understood. To address this issue, we investigated the requirement of inflammasome‐related genes in response to bone morphogenetic protein 7 (BMP7)‐induced osteoblast differentiation in vitro. To validate the importance of ASC on osteogenesis, we subjected wild‐type (WT) and ASC knockout C57BL/6 mice (ASC KO) to tibia defect to evaluate the bone healing process (up to 28 days). Our in vitro data showed that there is an involvement of ASC during BMP7‐induced osteoblast differentiation, concomitant to osteogenic biomarker expression. Indeed, primary osteogenic cells from ASC KO presented a lower osteogenic profile than those obtained from WT mice. To validate this hypothesis, we evaluated the bone healing process of tibia defects on both WT and ASC KO mice genotypes and the ASC KO mice were not able to fully heal tibia defects up to 28 days, whereas WT tibia defects presented a higher bone de novo volume at this stage, evidencing ASC as an important molecule during osteogenic phenotype. In addition, we have shown a higher involvement of runt‐related transcription factor 2 in WT sections during bone repair, as well as circulating bone alkaline phosphatase isoform when both were compared with ASC KO mice behavior. Altogether, our results showed for the first time the involvement of inflammasome during osteoblast differentiation and osteogenesis, which opens new avenues to understand the pathways involved in bone healing.
ASC contributes to osteoblast differentiation and bone de novo deposition, opening new avenues to understand the complex mechanism coupling inflammation landscape and osteoblastogenesis during bone healing.</description><subject>3T3 Cells</subject><subject>Alkaline phosphatase</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>ASC</subject><subject>Biocompatibility</subject><subject>Biomarkers</subject><subject>Biomedical materials</subject><subject>bone formation</subject><subject>Bone healing</subject><subject>Bone morphogenetic protein 7</subject><subject>Bone Morphogenetic Protein 7 - pharmacology</subject><subject>CARD Signaling Adaptor Proteins - deficiency</subject><subject>CARD Signaling Adaptor Proteins - genetics</subject><subject>CARD Signaling Adaptor Proteins - metabolism</subject><subject>Caspase</subject><subject>Cell Differentiation - drug effects</subject><subject>Defects</subject><subject>Differentiation</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Fracture Healing</subject><subject>Genotypes</subject><subject>Healing</subject><subject>inflammasome</subject><subject>Inflammasomes</subject><subject>Inflammasomes - drug effects</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation Mediators - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>osteoblast</subject><subject>Osteoblastogenesis</subject><subject>Osteoblasts - drug effects</subject><subject>Osteoblasts - metabolism</subject><subject>Osteoblasts - pathology</subject><subject>Osteogenesis</subject><subject>Osteogenesis - drug effects</subject><subject>Phenotypes</subject><subject>Proteins</subject><subject>Recruitment</subject><subject>regenerative medicine</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Tibia</subject><subject>Tibia - metabolism</subject><subject>Tibia - pathology</subject><subject>Tibia - physiopathology</subject><subject>Tibial Fractures - genetics</subject><subject>Tibial Fractures - metabolism</subject><subject>Tibial Fractures - pathology</subject><subject>Tibial Fractures - physiopathology</subject><subject>Time Factors</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10c1uFSEUB3BiNPZaXfgChsRNu5iWA3NnYHlzY_1IE03snjDMmYbbGRiBSdOdj-DS5-uTiJ3qwsQVCfzO4cCfkNfAzoAxfn6w8xlvOW-ekA0w1VZ1s-VPyaacQaW2NRyRFykdGGNKCfGcHAkGLTTAN-Tnbg5zDsml--8_TErBOpOxp2lGe1O2RneDdI4ho_PUBp-N885fU0OtSbNJWAzQiDYuLk_oM-3DVAw92X3dnz5URNctGRPNgYaUMXSjSYW5YcBYCsp9LnhqfL8eX6PHMs5L8mwwY8JXj-sxubp4d7X_UF1-fv9xv7usbA2qqRBR1QqV6Tm0nQUhRVcLUT6gB-ilFCCY2PbIFQBrZTfIBhRjtZSDNHUrjsnJ2ra88duCKevJJYvjaDyGJWnOlGwbqVpe6Nt_6CEs0ZfhNIeGi-IAijpdlY0hpYiDnqObTLzTwPTvtHRJSz-kVeybx45LN2H_V_6Jp4DzFdy6Ee_-30l_2n9ZW_4CuI-iyQ</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Sartoretto, Suelen</creator><creator>Gemini‐Piperni, Sara</creator><creator>da Silva, Rodrigo A.</creator><creator>Calasans, Monica D.</creator><creator>Rucci, Nadia</creator><creator>Pires dos Santos, Thais M.</creator><creator>Lima, Inayá B. C.</creator><creator>Rossi, Alexandre M.</creator><creator>Alves, Gutemberg</creator><creator>Granjeiro, José M.</creator><creator>Teti, Anna</creator><creator>Zambuzzi, Willian F.</creator><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4149-5965</orcidid></search><sort><creationdate>201904</creationdate><title>Apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) contributes to osteoblast differentiation and osteogenesis</title><author>Sartoretto, Suelen ; Gemini‐Piperni, Sara ; da Silva, Rodrigo A. ; Calasans, Monica D. ; Rucci, Nadia ; Pires dos Santos, Thais M. ; Lima, Inayá B. C. ; Rossi, Alexandre M. ; Alves, Gutemberg ; Granjeiro, José M. ; Teti, Anna ; Zambuzzi, Willian F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4196-eee949e9ad217bc1383b433465d11d88313035de2911078bf861900488f8a473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>3T3 Cells</topic><topic>Alkaline phosphatase</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>ASC</topic><topic>Biocompatibility</topic><topic>Biomarkers</topic><topic>Biomedical materials</topic><topic>bone formation</topic><topic>Bone healing</topic><topic>Bone morphogenetic protein 7</topic><topic>Bone Morphogenetic Protein 7 - pharmacology</topic><topic>CARD Signaling Adaptor Proteins - deficiency</topic><topic>CARD Signaling Adaptor Proteins - genetics</topic><topic>CARD Signaling Adaptor Proteins - metabolism</topic><topic>Caspase</topic><topic>Cell Differentiation - drug effects</topic><topic>Defects</topic><topic>Differentiation</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Fracture Healing</topic><topic>Genotypes</topic><topic>Healing</topic><topic>inflammasome</topic><topic>Inflammasomes</topic><topic>Inflammasomes - drug effects</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation Mediators - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>osteoblast</topic><topic>Osteoblastogenesis</topic><topic>Osteoblasts - drug effects</topic><topic>Osteoblasts - metabolism</topic><topic>Osteoblasts - pathology</topic><topic>Osteogenesis</topic><topic>Osteogenesis - drug effects</topic><topic>Phenotypes</topic><topic>Proteins</topic><topic>Recruitment</topic><topic>regenerative medicine</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Tibia</topic><topic>Tibia - metabolism</topic><topic>Tibia - pathology</topic><topic>Tibia - physiopathology</topic><topic>Tibial Fractures - genetics</topic><topic>Tibial Fractures - metabolism</topic><topic>Tibial Fractures - pathology</topic><topic>Tibial Fractures - physiopathology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sartoretto, Suelen</creatorcontrib><creatorcontrib>Gemini‐Piperni, Sara</creatorcontrib><creatorcontrib>da Silva, Rodrigo A.</creatorcontrib><creatorcontrib>Calasans, Monica D.</creatorcontrib><creatorcontrib>Rucci, Nadia</creatorcontrib><creatorcontrib>Pires dos Santos, Thais M.</creatorcontrib><creatorcontrib>Lima, Inayá B. C.</creatorcontrib><creatorcontrib>Rossi, Alexandre M.</creatorcontrib><creatorcontrib>Alves, Gutemberg</creatorcontrib><creatorcontrib>Granjeiro, José M.</creatorcontrib><creatorcontrib>Teti, Anna</creatorcontrib><creatorcontrib>Zambuzzi, Willian F.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sartoretto, Suelen</au><au>Gemini‐Piperni, Sara</au><au>da Silva, Rodrigo A.</au><au>Calasans, Monica D.</au><au>Rucci, Nadia</au><au>Pires dos Santos, Thais M.</au><au>Lima, Inayá B. C.</au><au>Rossi, Alexandre M.</au><au>Alves, Gutemberg</au><au>Granjeiro, José M.</au><au>Teti, Anna</au><au>Zambuzzi, Willian F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) contributes to osteoblast differentiation and osteogenesis</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2019-04</date><risdate>2019</risdate><volume>234</volume><issue>4</issue><spage>4140</spage><epage>4153</epage><pages>4140-4153</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>The role of apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) in bone healing remains to be understood. To address this issue, we investigated the requirement of inflammasome‐related genes in response to bone morphogenetic protein 7 (BMP7)‐induced osteoblast differentiation in vitro. To validate the importance of ASC on osteogenesis, we subjected wild‐type (WT) and ASC knockout C57BL/6 mice (ASC KO) to tibia defect to evaluate the bone healing process (up to 28 days). Our in vitro data showed that there is an involvement of ASC during BMP7‐induced osteoblast differentiation, concomitant to osteogenic biomarker expression. Indeed, primary osteogenic cells from ASC KO presented a lower osteogenic profile than those obtained from WT mice. To validate this hypothesis, we evaluated the bone healing process of tibia defects on both WT and ASC KO mice genotypes and the ASC KO mice were not able to fully heal tibia defects up to 28 days, whereas WT tibia defects presented a higher bone de novo volume at this stage, evidencing ASC as an important molecule during osteogenic phenotype. In addition, we have shown a higher involvement of runt‐related transcription factor 2 in WT sections during bone repair, as well as circulating bone alkaline phosphatase isoform when both were compared with ASC KO mice behavior. Altogether, our results showed for the first time the involvement of inflammasome during osteoblast differentiation and osteogenesis, which opens new avenues to understand the pathways involved in bone healing.
ASC contributes to osteoblast differentiation and bone de novo deposition, opening new avenues to understand the complex mechanism coupling inflammation landscape and osteoblastogenesis during bone healing.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30171612</pmid><doi>10.1002/jcp.27226</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-4149-5965</orcidid></addata></record> |
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subjects | 3T3 Cells Alkaline phosphatase Animals Apoptosis ASC Biocompatibility Biomarkers Biomedical materials bone formation Bone healing Bone morphogenetic protein 7 Bone Morphogenetic Protein 7 - pharmacology CARD Signaling Adaptor Proteins - deficiency CARD Signaling Adaptor Proteins - genetics CARD Signaling Adaptor Proteins - metabolism Caspase Cell Differentiation - drug effects Defects Differentiation Disease Models, Animal Female Fracture Healing Genotypes Healing inflammasome Inflammasomes Inflammasomes - drug effects Inflammasomes - metabolism Inflammation Mediators - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout osteoblast Osteoblastogenesis Osteoblasts - drug effects Osteoblasts - metabolism Osteoblasts - pathology Osteogenesis Osteogenesis - drug effects Phenotypes Proteins Recruitment regenerative medicine Rodents Signal Transduction Tibia Tibia - metabolism Tibia - pathology Tibia - physiopathology Tibial Fractures - genetics Tibial Fractures - metabolism Tibial Fractures - pathology Tibial Fractures - physiopathology Time Factors |
title | Apoptosis‐associated speck‐like protein containing a caspase‐1 recruitment domain (ASC) contributes to osteoblast differentiation and osteogenesis |
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