Altered osteogenic commitment of human mesenchymal stem cells by ERM protein-dependent modulation of cellular biomechanics
Abstract Cellular mechanics is known to play an important role in many cellular functions including adhesion, migration, proliferation, and differentiation. Human mesenchymal stem cells (hMSCs) demonstrate unique mechanical properties distinct from fully differentiated cells. This observation sugges...
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| Veröffentlicht in: | Journal of biomechanics 2011-10, Vol.44 (15), p.2692-2698 |
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| creator | Titushkin, Igor Cho, Michael |
| description | Abstract Cellular mechanics is known to play an important role in many cellular functions including adhesion, migration, proliferation, and differentiation. Human mesenchymal stem cells (hMSCs) demonstrate unique mechanical properties distinct from fully differentiated cells. This observation suggests that the stem cell mechanics may be modulated to regulate the hMSCs' lineage commitment. Specifically, ERM (ezrin, radixin, moesin) proteins are known to mediate the membrane–cytoskeleton adhesion, cell elasticity, actin cytoskeleton organization, and therefore could serve as potential targets for modulation of the cellular mechanics. Combining silencing RNA, atomic force microscopy, and laser optical tweezers, the role of the ERM proteins involved in the regulation of stem cell biomechanics and osteogenic differentiation was quantitatively determined. Transient ERM knockdown by RNAi causes disassembly of actin stress fibers and focal adhesions, a decrease in the cell stiffness, and membrane separation from the cytoskeleton. The silencing RNA treatment not only induced mechanical changes in stem cells but impaired biochemically-directed osteogenic differentiation. The intact actin cytoskeleton and focal adhesions of hMSCs appear critical for the osteogenic induction. Thus, ERM knockdown modulates the dynamics of cell mechanical changes during hMSC differentiation and regulates the expression of tissue specific molecular markers. These findings are of particular interest for modulation of the cellular biomechanics to control hMSCs' activities and fate in tissue engineering, regenerative medicine, and other stem cell-based therapeutic applications. |
| doi_str_mv | 10.1016/j.jbiomech.2011.07.024 |
| format | Article |
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Human mesenchymal stem cells (hMSCs) demonstrate unique mechanical properties distinct from fully differentiated cells. This observation suggests that the stem cell mechanics may be modulated to regulate the hMSCs' lineage commitment. Specifically, ERM (ezrin, radixin, moesin) proteins are known to mediate the membrane–cytoskeleton adhesion, cell elasticity, actin cytoskeleton organization, and therefore could serve as potential targets for modulation of the cellular mechanics. Combining silencing RNA, atomic force microscopy, and laser optical tweezers, the role of the ERM proteins involved in the regulation of stem cell biomechanics and osteogenic differentiation was quantitatively determined. Transient ERM knockdown by RNAi causes disassembly of actin stress fibers and focal adhesions, a decrease in the cell stiffness, and membrane separation from the cytoskeleton. The silencing RNA treatment not only induced mechanical changes in stem cells but impaired biochemically-directed osteogenic differentiation. The intact actin cytoskeleton and focal adhesions of hMSCs appear critical for the osteogenic induction. Thus, ERM knockdown modulates the dynamics of cell mechanical changes during hMSC differentiation and regulates the expression of tissue specific molecular markers. These findings are of particular interest for modulation of the cellular biomechanics to control hMSCs' activities and fate in tissue engineering, regenerative medicine, and other stem cell-based therapeutic applications.</description><identifier>ISSN: 0021-9290</identifier><identifier>EISSN: 1873-2380</identifier><identifier>DOI: 10.1016/j.jbiomech.2011.07.024</identifier><identifier>PMID: 21864840</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>Actin ; AFM ; Antigens, Differentiation - metabolism ; Biological and medical sciences ; Biotechnology ; Cell Differentiation - physiology ; Cell Membrane - genetics ; Cell Membrane - metabolism ; Cell Membrane - ultrastructure ; Cell physiology ; Cells, Cultured ; Cytoskeletal Proteins - genetics ; Cytoskeletal Proteins - metabolism ; Cytoskeleton ; ERM proteins ; Fundamental and applied biological sciences. Psychology ; Gene Silencing ; Humans ; LOT ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mesenchymal Stromal Cells - metabolism ; Mesenchymal Stromal Cells - ultrastructure ; Microfilament Proteins - genetics ; Microfilament Proteins - metabolism ; Microscopy, Atomic Force ; Molecular and cellular biology ; Osteogenesis - physiology ; Physical Medicine and Rehabilitation ; Proteins ; SiRNA ; Stem cell biomechanics ; Stem cells ; Stress Fibers - genetics ; Stress Fibers - metabolism ; Stress Fibers - ultrastructure</subject><ispartof>Journal of biomechanics, 2011-10, Vol.44 (15), p.2692-2698</ispartof><rights>Elsevier Ltd</rights><rights>2011 Elsevier Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-a53762cb9a438ea94f8bbf3d53cf37a37dada79ef969c5831ec55e03868e340a3</citedby><cites>FETCH-LOGICAL-c513t-a53762cb9a438ea94f8bbf3d53cf37a37dada79ef969c5831ec55e03868e340a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1034965996?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24628573$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21864840$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Titushkin, Igor</creatorcontrib><creatorcontrib>Cho, Michael</creatorcontrib><title>Altered osteogenic commitment of human mesenchymal stem cells by ERM protein-dependent modulation of cellular biomechanics</title><title>Journal of biomechanics</title><addtitle>J Biomech</addtitle><description>Abstract Cellular mechanics is known to play an important role in many cellular functions including adhesion, migration, proliferation, and differentiation. Human mesenchymal stem cells (hMSCs) demonstrate unique mechanical properties distinct from fully differentiated cells. This observation suggests that the stem cell mechanics may be modulated to regulate the hMSCs' lineage commitment. Specifically, ERM (ezrin, radixin, moesin) proteins are known to mediate the membrane–cytoskeleton adhesion, cell elasticity, actin cytoskeleton organization, and therefore could serve as potential targets for modulation of the cellular mechanics. Combining silencing RNA, atomic force microscopy, and laser optical tweezers, the role of the ERM proteins involved in the regulation of stem cell biomechanics and osteogenic differentiation was quantitatively determined. Transient ERM knockdown by RNAi causes disassembly of actin stress fibers and focal adhesions, a decrease in the cell stiffness, and membrane separation from the cytoskeleton. The silencing RNA treatment not only induced mechanical changes in stem cells but impaired biochemically-directed osteogenic differentiation. The intact actin cytoskeleton and focal adhesions of hMSCs appear critical for the osteogenic induction. Thus, ERM knockdown modulates the dynamics of cell mechanical changes during hMSC differentiation and regulates the expression of tissue specific molecular markers. These findings are of particular interest for modulation of the cellular biomechanics to control hMSCs' activities and fate in tissue engineering, regenerative medicine, and other stem cell-based therapeutic applications.</description><subject>Actin</subject><subject>AFM</subject><subject>Antigens, Differentiation - metabolism</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Cell Differentiation - physiology</subject><subject>Cell Membrane - genetics</subject><subject>Cell Membrane - metabolism</subject><subject>Cell Membrane - ultrastructure</subject><subject>Cell physiology</subject><subject>Cells, Cultured</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Cytoskeleton</subject><subject>ERM proteins</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Silencing</subject><subject>Humans</subject><subject>LOT</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mesenchymal Stromal Cells - metabolism</subject><subject>Mesenchymal Stromal Cells - ultrastructure</subject><subject>Microfilament Proteins - genetics</subject><subject>Microfilament Proteins - metabolism</subject><subject>Microscopy, Atomic Force</subject><subject>Molecular and cellular biology</subject><subject>Osteogenesis - physiology</subject><subject>Physical Medicine and Rehabilitation</subject><subject>Proteins</subject><subject>SiRNA</subject><subject>Stem cell biomechanics</subject><subject>Stem cells</subject><subject>Stress Fibers - genetics</subject><subject>Stress Fibers - metabolism</subject><subject>Stress Fibers - ultrastructure</subject><issn>0021-9290</issn><issn>1873-2380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkt2L1DAUxYso7rj6LywBEX3peJO0-XgRl2VXhRXBD_AtpOmtk7FpxqYVZv96U2bWhX3QpxD43ZNzcm5RnFFYU6Di9Xa9bXwM6DZrBpSuQa6BVQ-KFVWSl4wreFisABgtNdNwUjxJaQsAspL6cXHCqBKVqmBV3Jz3E47YkpgmjD9w8I64GIKfAg4TiR3ZzMEOJGDCwW32wfYkk4E47PtEmj25_PyR7MY4oR_KFnc4tMtgiO3c28nHYdFY4HwdydGzzc-kp8WjzvYJnx3P0-Lb1eXXi_fl9ad3Hy7Or0tXUz6VtuZSMNdoW3GFVledapqOtzV3HZeWy9a2VmrstNCuVpyiq2sEroRCXoHlp8XLg252-WvGNJng0-LIDhjnZJQWinMJPJOv_klSYAqkEppl9Pk9dBvnccg5MsUrLWqtRabEgXJjTGnEzuxGH-y4z5BZejRbc9ujWXo0IE3uMQ-eHeXnJmD7d-y2uAy8OAI2Odt3ox2cT3dcJZiq5RLp7YHD_MO_PY4mOZ-bxNaP6CbTRv9_L2_uSbje5wJt_xP3mO5ym8QMmC_L1i1LRylAXYnv_A-m0tUQ</recordid><startdate>20111013</startdate><enddate>20111013</enddate><creator>Titushkin, Igor</creator><creator>Cho, Michael</creator><general>Elsevier Ltd</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</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>3V.</scope><scope>7QP</scope><scope>7TB</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7QO</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20111013</creationdate><title>Altered osteogenic commitment of human mesenchymal stem cells by ERM protein-dependent modulation of cellular biomechanics</title><author>Titushkin, Igor ; Cho, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c513t-a53762cb9a438ea94f8bbf3d53cf37a37dada79ef969c5831ec55e03868e340a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Actin</topic><topic>AFM</topic><topic>Antigens, Differentiation - metabolism</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Cell Differentiation - physiology</topic><topic>Cell Membrane - genetics</topic><topic>Cell Membrane - metabolism</topic><topic>Cell Membrane - ultrastructure</topic><topic>Cell physiology</topic><topic>Cells, Cultured</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Cytoskeleton</topic><topic>ERM proteins</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Silencing</topic><topic>Humans</topic><topic>LOT</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mesenchymal Stromal Cells - metabolism</topic><topic>Mesenchymal Stromal Cells - ultrastructure</topic><topic>Microfilament Proteins - genetics</topic><topic>Microfilament Proteins - metabolism</topic><topic>Microscopy, Atomic Force</topic><topic>Molecular and cellular biology</topic><topic>Osteogenesis - physiology</topic><topic>Physical Medicine and Rehabilitation</topic><topic>Proteins</topic><topic>SiRNA</topic><topic>Stem cell biomechanics</topic><topic>Stem cells</topic><topic>Stress Fibers - genetics</topic><topic>Stress Fibers - metabolism</topic><topic>Stress Fibers - ultrastructure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Titushkin, Igor</creatorcontrib><creatorcontrib>Cho, Michael</creatorcontrib><collection>Pascal-Francis</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Mechanical & Transportation Engineering Abstracts</collection><collection>Physical Education Index</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>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>Biotechnology Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biomechanics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Titushkin, Igor</au><au>Cho, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered osteogenic commitment of human mesenchymal stem cells by ERM protein-dependent modulation of cellular biomechanics</atitle><jtitle>Journal of biomechanics</jtitle><addtitle>J Biomech</addtitle><date>2011-10-13</date><risdate>2011</risdate><volume>44</volume><issue>15</issue><spage>2692</spage><epage>2698</epage><pages>2692-2698</pages><issn>0021-9290</issn><eissn>1873-2380</eissn><abstract>Abstract Cellular mechanics is known to play an important role in many cellular functions including adhesion, migration, proliferation, and differentiation. Human mesenchymal stem cells (hMSCs) demonstrate unique mechanical properties distinct from fully differentiated cells. This observation suggests that the stem cell mechanics may be modulated to regulate the hMSCs' lineage commitment. Specifically, ERM (ezrin, radixin, moesin) proteins are known to mediate the membrane–cytoskeleton adhesion, cell elasticity, actin cytoskeleton organization, and therefore could serve as potential targets for modulation of the cellular mechanics. Combining silencing RNA, atomic force microscopy, and laser optical tweezers, the role of the ERM proteins involved in the regulation of stem cell biomechanics and osteogenic differentiation was quantitatively determined. Transient ERM knockdown by RNAi causes disassembly of actin stress fibers and focal adhesions, a decrease in the cell stiffness, and membrane separation from the cytoskeleton. The silencing RNA treatment not only induced mechanical changes in stem cells but impaired biochemically-directed osteogenic differentiation. The intact actin cytoskeleton and focal adhesions of hMSCs appear critical for the osteogenic induction. Thus, ERM knockdown modulates the dynamics of cell mechanical changes during hMSC differentiation and regulates the expression of tissue specific molecular markers. These findings are of particular interest for modulation of the cellular biomechanics to control hMSCs' activities and fate in tissue engineering, regenerative medicine, and other stem cell-based therapeutic applications.</abstract><cop>Kidlington</cop><pub>Elsevier Ltd</pub><pmid>21864840</pmid><doi>10.1016/j.jbiomech.2011.07.024</doi><tpages>7</tpages></addata></record> |
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| subjects | Actin AFM Antigens, Differentiation - metabolism Biological and medical sciences Biotechnology Cell Differentiation - physiology Cell Membrane - genetics Cell Membrane - metabolism Cell Membrane - ultrastructure Cell physiology Cells, Cultured Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Cytoskeleton ERM proteins Fundamental and applied biological sciences. Psychology Gene Silencing Humans LOT Membrane Proteins - genetics Membrane Proteins - metabolism Mesenchymal Stromal Cells - metabolism Mesenchymal Stromal Cells - ultrastructure Microfilament Proteins - genetics Microfilament Proteins - metabolism Microscopy, Atomic Force Molecular and cellular biology Osteogenesis - physiology Physical Medicine and Rehabilitation Proteins SiRNA Stem cell biomechanics Stem cells Stress Fibers - genetics Stress Fibers - metabolism Stress Fibers - ultrastructure |
| title | Altered osteogenic commitment of human mesenchymal stem cells by ERM protein-dependent modulation of cellular biomechanics |
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