Activation of Focal Adhesion Kinase Restores Simulated Microgravity-Induced Inhibition of Osteoblast Differentiation via Wnt/Β-Catenin Pathway
Simulated microgravity (SMG) inhibits osteoblast differentiation (OBD) and induces bone loss via the inhibition of the Wnt/β-catenin pathway. However, the mechanism by which SMG alters the Wnt/β-catenin pathway is unknown. We previously demonstrated that SMG altered the focal adhesion kinase (FAK)-r...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2022-05, Vol.23 (10), p.5593 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 10 |
| container_start_page | 5593 |
| container_title | International journal of molecular sciences |
| container_volume | 23 |
| creator | Fan, Cuihong Wu, Zhaojia Cooper, David M L Magnus, Adam Harrison, Kim Eames, B Frank Chibbar, Rajni Groot, Gary Huang, Junqiong Genth, Harald Zhang, Jun Tan, Xing Deng, Yulin Xiang, Jim |
| description | Simulated microgravity (SMG) inhibits osteoblast differentiation (OBD) and induces bone loss via the inhibition of the Wnt/β-catenin pathway. However, the mechanism by which SMG alters the Wnt/β-catenin pathway is unknown. We previously demonstrated that SMG altered the focal adhesion kinase (FAK)-regulated mTORC1, AMPK and ERK1/2 pathways, leading to the inhibition of tumor cell proliferation/metastasis and promoting cell apoptosis. To examine whether FAK similarly mediates SMG-dependent changes to Wnt/β-catenin in osteoblasts, we characterized mouse MC3T3-E1 cells cultured under clinostat-modeled SMG (µg) conditions. Compared to cells cultured under ground (1 g) conditions, SMG reduces focal adhesions, alters cytoskeleton structures, and down-regulates FAK, Wnt/β-catenin and Wnt/β-catenin-regulated molecules. Consequently, protein-2 (BMP2), type-1 collagen (COL1), alkaline-phosphatase activity and matrix mineralization are all inhibited. In the mouse hindlimb unloading (HU) model, SMG-affected tibial trabecular bone loss is significantly reduced, according to histological and micro-computed tomography analyses. Interestingly, the FAK activator, cytotoxic necrotizing factor-1 (CNF1), significantly suppresses all of the SMG-induced alterations in MC3T3-E1 cells and the HU model. Therefore, our data demonstrate the critical role of FAK in the SMG-induced inhibition of OBD and bone loss via the Wnt/β-catenin pathway, offering FAK signaling as a new therapeutic target not only for astronauts at risk of OBD inhibition and bone loss, but also osteoporotic patients. |
| doi_str_mv | 10.3390/ijms23105593 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9146119</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2671278826</sourcerecordid><originalsourceid>FETCH-LOGICAL-c342t-89805b45a6d44f0c45f10c37c42b72b6b15d5288d4a95620a9d85831288a37fa3</originalsourceid><addsrcrecordid>eNpdkUtv1DAUhSNERR-wY40ssWHRUD8TZ4M0mrYwalERD7G0bhyn41FiF9sZNL8CiR_Gb8KjaauBla3jT8f33FMULwl-y1iDz-xqjJQRLETDnhRHhFNaYlzVT_fuh8VxjCuMKaOieVYcMlFRyTE7Kn7NdLJrSNY75Ht06TUMaNYtTdwqV9ZBNOizickHE9EXO04DJNOhj1YHfxtgbdOmXLhu0llcuKVt7YPXTUzGtwPEhM5t35tgXLK7n9YW0HeXzv78LufZzlmHPkFa_oTN8-KghyGaF_fnSfHt8uLr_EN5ffN-MZ9dl5pxmkrZSCxaLqDqOO-x5qInWLNac9rWtK1aIjpBpew4NDkrhqaTQjKSJWB1D-ykeLfzvZva0XQ6zxZgUHfBjhA2yoNV_744u1S3fq0awitCmmzw5t4g-B9TXpAabdRmGMAZP0VFq5rQWkpaZfT1f-jKT8HleFsKU4xrKTJ1uqPyYmMMpn8chmC1bVrtN53xV_sBHuGHatlfYW2nQg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2670200785</pqid></control><display><type>article</type><title>Activation of Focal Adhesion Kinase Restores Simulated Microgravity-Induced Inhibition of Osteoblast Differentiation via Wnt/Β-Catenin Pathway</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Fan, Cuihong ; Wu, Zhaojia ; Cooper, David M L ; Magnus, Adam ; Harrison, Kim ; Eames, B Frank ; Chibbar, Rajni ; Groot, Gary ; Huang, Junqiong ; Genth, Harald ; Zhang, Jun ; Tan, Xing ; Deng, Yulin ; Xiang, Jim</creator><creatorcontrib>Fan, Cuihong ; Wu, Zhaojia ; Cooper, David M L ; Magnus, Adam ; Harrison, Kim ; Eames, B Frank ; Chibbar, Rajni ; Groot, Gary ; Huang, Junqiong ; Genth, Harald ; Zhang, Jun ; Tan, Xing ; Deng, Yulin ; Xiang, Jim</creatorcontrib><description>Simulated microgravity (SMG) inhibits osteoblast differentiation (OBD) and induces bone loss via the inhibition of the Wnt/β-catenin pathway. However, the mechanism by which SMG alters the Wnt/β-catenin pathway is unknown. We previously demonstrated that SMG altered the focal adhesion kinase (FAK)-regulated mTORC1, AMPK and ERK1/2 pathways, leading to the inhibition of tumor cell proliferation/metastasis and promoting cell apoptosis. To examine whether FAK similarly mediates SMG-dependent changes to Wnt/β-catenin in osteoblasts, we characterized mouse MC3T3-E1 cells cultured under clinostat-modeled SMG (µg) conditions. Compared to cells cultured under ground (1 g) conditions, SMG reduces focal adhesions, alters cytoskeleton structures, and down-regulates FAK, Wnt/β-catenin and Wnt/β-catenin-regulated molecules. Consequently, protein-2 (BMP2), type-1 collagen (COL1), alkaline-phosphatase activity and matrix mineralization are all inhibited. In the mouse hindlimb unloading (HU) model, SMG-affected tibial trabecular bone loss is significantly reduced, according to histological and micro-computed tomography analyses. Interestingly, the FAK activator, cytotoxic necrotizing factor-1 (CNF1), significantly suppresses all of the SMG-induced alterations in MC3T3-E1 cells and the HU model. Therefore, our data demonstrate the critical role of FAK in the SMG-induced inhibition of OBD and bone loss via the Wnt/β-catenin pathway, offering FAK signaling as a new therapeutic target not only for astronauts at risk of OBD inhibition and bone loss, but also osteoporotic patients.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23105593</identifier><identifier>PMID: 35628403</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adhesion ; Apoptosis ; Astronauts ; Biomedical materials ; Bone density ; Bone loss ; Bone morphogenetic protein 2 ; Cancellous bone ; Cell division ; Cell proliferation ; Collagen ; Computed tomography ; Cytoskeleton ; Cytotoxic necrotizing factor 1 ; Cytotoxicity ; Differentiation ; Extracellular signal-regulated kinase ; Focal adhesion kinase ; Gene expression ; Kinases ; Localization ; Metastases ; Microscopy ; Mineralization ; Osteoblastogenesis ; Osteoblasts ; Osteoporosis ; Physiology ; Proteins ; Therapeutic targets ; Transcription factors ; Tumors ; Wnt protein ; β-Catenin</subject><ispartof>International journal of molecular sciences, 2022-05, Vol.23 (10), p.5593</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342t-89805b45a6d44f0c45f10c37c42b72b6b15d5288d4a95620a9d85831288a37fa3</citedby><cites>FETCH-LOGICAL-c342t-89805b45a6d44f0c45f10c37c42b72b6b15d5288d4a95620a9d85831288a37fa3</cites><orcidid>0000-0002-0720-4052 ; 0000-0002-8307-5125</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9146119/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9146119/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35628403$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fan, Cuihong</creatorcontrib><creatorcontrib>Wu, Zhaojia</creatorcontrib><creatorcontrib>Cooper, David M L</creatorcontrib><creatorcontrib>Magnus, Adam</creatorcontrib><creatorcontrib>Harrison, Kim</creatorcontrib><creatorcontrib>Eames, B Frank</creatorcontrib><creatorcontrib>Chibbar, Rajni</creatorcontrib><creatorcontrib>Groot, Gary</creatorcontrib><creatorcontrib>Huang, Junqiong</creatorcontrib><creatorcontrib>Genth, Harald</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Tan, Xing</creatorcontrib><creatorcontrib>Deng, Yulin</creatorcontrib><creatorcontrib>Xiang, Jim</creatorcontrib><title>Activation of Focal Adhesion Kinase Restores Simulated Microgravity-Induced Inhibition of Osteoblast Differentiation via Wnt/Β-Catenin Pathway</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Simulated microgravity (SMG) inhibits osteoblast differentiation (OBD) and induces bone loss via the inhibition of the Wnt/β-catenin pathway. However, the mechanism by which SMG alters the Wnt/β-catenin pathway is unknown. We previously demonstrated that SMG altered the focal adhesion kinase (FAK)-regulated mTORC1, AMPK and ERK1/2 pathways, leading to the inhibition of tumor cell proliferation/metastasis and promoting cell apoptosis. To examine whether FAK similarly mediates SMG-dependent changes to Wnt/β-catenin in osteoblasts, we characterized mouse MC3T3-E1 cells cultured under clinostat-modeled SMG (µg) conditions. Compared to cells cultured under ground (1 g) conditions, SMG reduces focal adhesions, alters cytoskeleton structures, and down-regulates FAK, Wnt/β-catenin and Wnt/β-catenin-regulated molecules. Consequently, protein-2 (BMP2), type-1 collagen (COL1), alkaline-phosphatase activity and matrix mineralization are all inhibited. In the mouse hindlimb unloading (HU) model, SMG-affected tibial trabecular bone loss is significantly reduced, according to histological and micro-computed tomography analyses. Interestingly, the FAK activator, cytotoxic necrotizing factor-1 (CNF1), significantly suppresses all of the SMG-induced alterations in MC3T3-E1 cells and the HU model. Therefore, our data demonstrate the critical role of FAK in the SMG-induced inhibition of OBD and bone loss via the Wnt/β-catenin pathway, offering FAK signaling as a new therapeutic target not only for astronauts at risk of OBD inhibition and bone loss, but also osteoporotic patients.</description><subject>Adhesion</subject><subject>Apoptosis</subject><subject>Astronauts</subject><subject>Biomedical materials</subject><subject>Bone density</subject><subject>Bone loss</subject><subject>Bone morphogenetic protein 2</subject><subject>Cancellous bone</subject><subject>Cell division</subject><subject>Cell proliferation</subject><subject>Collagen</subject><subject>Computed tomography</subject><subject>Cytoskeleton</subject><subject>Cytotoxic necrotizing factor 1</subject><subject>Cytotoxicity</subject><subject>Differentiation</subject><subject>Extracellular signal-regulated kinase</subject><subject>Focal adhesion kinase</subject><subject>Gene expression</subject><subject>Kinases</subject><subject>Localization</subject><subject>Metastases</subject><subject>Microscopy</subject><subject>Mineralization</subject><subject>Osteoblastogenesis</subject><subject>Osteoblasts</subject><subject>Osteoporosis</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Therapeutic targets</subject><subject>Transcription factors</subject><subject>Tumors</subject><subject>Wnt protein</subject><subject>β-Catenin</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUtv1DAUhSNERR-wY40ssWHRUD8TZ4M0mrYwalERD7G0bhyn41FiF9sZNL8CiR_Gb8KjaauBla3jT8f33FMULwl-y1iDz-xqjJQRLETDnhRHhFNaYlzVT_fuh8VxjCuMKaOieVYcMlFRyTE7Kn7NdLJrSNY75Ht06TUMaNYtTdwqV9ZBNOizickHE9EXO04DJNOhj1YHfxtgbdOmXLhu0llcuKVt7YPXTUzGtwPEhM5t35tgXLK7n9YW0HeXzv78LufZzlmHPkFa_oTN8-KghyGaF_fnSfHt8uLr_EN5ffN-MZ9dl5pxmkrZSCxaLqDqOO-x5qInWLNac9rWtK1aIjpBpew4NDkrhqaTQjKSJWB1D-ykeLfzvZva0XQ6zxZgUHfBjhA2yoNV_744u1S3fq0awitCmmzw5t4g-B9TXpAabdRmGMAZP0VFq5rQWkpaZfT1f-jKT8HleFsKU4xrKTJ1uqPyYmMMpn8chmC1bVrtN53xV_sBHuGHatlfYW2nQg</recordid><startdate>20220517</startdate><enddate>20220517</enddate><creator>Fan, Cuihong</creator><creator>Wu, Zhaojia</creator><creator>Cooper, David M L</creator><creator>Magnus, Adam</creator><creator>Harrison, Kim</creator><creator>Eames, B Frank</creator><creator>Chibbar, Rajni</creator><creator>Groot, Gary</creator><creator>Huang, Junqiong</creator><creator>Genth, Harald</creator><creator>Zhang, Jun</creator><creator>Tan, Xing</creator><creator>Deng, Yulin</creator><creator>Xiang, Jim</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0720-4052</orcidid><orcidid>https://orcid.org/0000-0002-8307-5125</orcidid></search><sort><creationdate>20220517</creationdate><title>Activation of Focal Adhesion Kinase Restores Simulated Microgravity-Induced Inhibition of Osteoblast Differentiation via Wnt/Β-Catenin Pathway</title><author>Fan, Cuihong ; Wu, Zhaojia ; Cooper, David M L ; Magnus, Adam ; Harrison, Kim ; Eames, B Frank ; Chibbar, Rajni ; Groot, Gary ; Huang, Junqiong ; Genth, Harald ; Zhang, Jun ; Tan, Xing ; Deng, Yulin ; Xiang, Jim</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342t-89805b45a6d44f0c45f10c37c42b72b6b15d5288d4a95620a9d85831288a37fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adhesion</topic><topic>Apoptosis</topic><topic>Astronauts</topic><topic>Biomedical materials</topic><topic>Bone density</topic><topic>Bone loss</topic><topic>Bone morphogenetic protein 2</topic><topic>Cancellous bone</topic><topic>Cell division</topic><topic>Cell proliferation</topic><topic>Collagen</topic><topic>Computed tomography</topic><topic>Cytoskeleton</topic><topic>Cytotoxic necrotizing factor 1</topic><topic>Cytotoxicity</topic><topic>Differentiation</topic><topic>Extracellular signal-regulated kinase</topic><topic>Focal adhesion kinase</topic><topic>Gene expression</topic><topic>Kinases</topic><topic>Localization</topic><topic>Metastases</topic><topic>Microscopy</topic><topic>Mineralization</topic><topic>Osteoblastogenesis</topic><topic>Osteoblasts</topic><topic>Osteoporosis</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Therapeutic targets</topic><topic>Transcription factors</topic><topic>Tumors</topic><topic>Wnt protein</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fan, Cuihong</creatorcontrib><creatorcontrib>Wu, Zhaojia</creatorcontrib><creatorcontrib>Cooper, David M L</creatorcontrib><creatorcontrib>Magnus, Adam</creatorcontrib><creatorcontrib>Harrison, Kim</creatorcontrib><creatorcontrib>Eames, B Frank</creatorcontrib><creatorcontrib>Chibbar, Rajni</creatorcontrib><creatorcontrib>Groot, Gary</creatorcontrib><creatorcontrib>Huang, Junqiong</creatorcontrib><creatorcontrib>Genth, Harald</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Tan, Xing</creatorcontrib><creatorcontrib>Deng, Yulin</creatorcontrib><creatorcontrib>Xiang, Jim</creatorcontrib><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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fan, Cuihong</au><au>Wu, Zhaojia</au><au>Cooper, David M L</au><au>Magnus, Adam</au><au>Harrison, Kim</au><au>Eames, B Frank</au><au>Chibbar, Rajni</au><au>Groot, Gary</au><au>Huang, Junqiong</au><au>Genth, Harald</au><au>Zhang, Jun</au><au>Tan, Xing</au><au>Deng, Yulin</au><au>Xiang, Jim</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of Focal Adhesion Kinase Restores Simulated Microgravity-Induced Inhibition of Osteoblast Differentiation via Wnt/Β-Catenin Pathway</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-05-17</date><risdate>2022</risdate><volume>23</volume><issue>10</issue><spage>5593</spage><pages>5593-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Simulated microgravity (SMG) inhibits osteoblast differentiation (OBD) and induces bone loss via the inhibition of the Wnt/β-catenin pathway. However, the mechanism by which SMG alters the Wnt/β-catenin pathway is unknown. We previously demonstrated that SMG altered the focal adhesion kinase (FAK)-regulated mTORC1, AMPK and ERK1/2 pathways, leading to the inhibition of tumor cell proliferation/metastasis and promoting cell apoptosis. To examine whether FAK similarly mediates SMG-dependent changes to Wnt/β-catenin in osteoblasts, we characterized mouse MC3T3-E1 cells cultured under clinostat-modeled SMG (µg) conditions. Compared to cells cultured under ground (1 g) conditions, SMG reduces focal adhesions, alters cytoskeleton structures, and down-regulates FAK, Wnt/β-catenin and Wnt/β-catenin-regulated molecules. Consequently, protein-2 (BMP2), type-1 collagen (COL1), alkaline-phosphatase activity and matrix mineralization are all inhibited. In the mouse hindlimb unloading (HU) model, SMG-affected tibial trabecular bone loss is significantly reduced, according to histological and micro-computed tomography analyses. Interestingly, the FAK activator, cytotoxic necrotizing factor-1 (CNF1), significantly suppresses all of the SMG-induced alterations in MC3T3-E1 cells and the HU model. Therefore, our data demonstrate the critical role of FAK in the SMG-induced inhibition of OBD and bone loss via the Wnt/β-catenin pathway, offering FAK signaling as a new therapeutic target not only for astronauts at risk of OBD inhibition and bone loss, but also osteoporotic patients.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35628403</pmid><doi>10.3390/ijms23105593</doi><orcidid>https://orcid.org/0000-0002-0720-4052</orcidid><orcidid>https://orcid.org/0000-0002-8307-5125</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2022-05, Vol.23 (10), p.5593 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9146119 |
| source | MDPI - Multidisciplinary Digital Publishing Institute; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Adhesion Apoptosis Astronauts Biomedical materials Bone density Bone loss Bone morphogenetic protein 2 Cancellous bone Cell division Cell proliferation Collagen Computed tomography Cytoskeleton Cytotoxic necrotizing factor 1 Cytotoxicity Differentiation Extracellular signal-regulated kinase Focal adhesion kinase Gene expression Kinases Localization Metastases Microscopy Mineralization Osteoblastogenesis Osteoblasts Osteoporosis Physiology Proteins Therapeutic targets Transcription factors Tumors Wnt protein β-Catenin |
| title | Activation of Focal Adhesion Kinase Restores Simulated Microgravity-Induced Inhibition of Osteoblast Differentiation via Wnt/Β-Catenin Pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-28T04%3A49%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Activation%20of%20Focal%20Adhesion%20Kinase%20Restores%20Simulated%20Microgravity-Induced%20Inhibition%20of%20Osteoblast%20Differentiation%20via%20Wnt/%CE%92-Catenin%20Pathway&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Fan,%20Cuihong&rft.date=2022-05-17&rft.volume=23&rft.issue=10&rft.spage=5593&rft.pages=5593-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms23105593&rft_dat=%3Cproquest_pubme%3E2671278826%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2670200785&rft_id=info:pmid/35628403&rfr_iscdi=true |