Downregulation of osteoblast markers and induction of the glial fibrillary acidic protein by oncostatin M in osteosarcoma cells require PKCdelta and STAT3
The effects of OSM on proliferation and differentiation of osteosarcoma and nontransformed osteoblasts were analyzed. OSM downregulates osteoblast markers but induces the glial fibrillary acidic protein by the combined activation of PKCdelta and STAT3, offering new lines of therapeutic investigation...
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Veröffentlicht in: | Journal of bone and mineral research 2004-11, Vol.19 (11), p.1850-1861 |
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creator | Chipoy, Céline Berreur, Martine Couillaud, Séverine Pradal, Gilbert Vallette, François Colombeix, Caroline Rédini, Françoise Heymann, Dominique Blanchard, Frédéric |
description | The effects of OSM on proliferation and differentiation of osteosarcoma and nontransformed osteoblasts were analyzed. OSM downregulates osteoblast markers but induces the glial fibrillary acidic protein by the combined activation of PKCdelta and STAT3, offering new lines of therapeutic investigations.
Oncostatin M (OSM) is a multifunctional cytokine of the interleukin-6 family implicated in embryonic development, differentiation, inflammation, and regeneration of various tissues, mainly the liver, bone, and the central nervous and hematopoietic systems. One particularity of OSM relies on its growth inhibitory and pro-differentiating effects on a variety of tumor cell lines such as melanoma, providing arguments for a therapeutic application of OSM. The objective of this study was to analyze the effects of OSM on osteosarcoma cell lines proliferation and differentiation.
Proliferation was analyzed by 3H thymidine incorporation. Differentiation was analyzed by semiquantitative RT-PCR and immunocytochemistry for various markers. Alizarin red S staining was used to evaluate bone nodule formation. Morphological changes were studied by confocal and electron microscopy. Western blotting, kinases inhibitors, and dominant negative STAT3 were used to identified the signaling pathways implicated.
OSM inhibits the growth of rat osteosarcoma cell lines as well as normal osteoblasts, in correlation with induction of the cyclin-dependent kinases inhibitor p21WAF1. However, OSM reduces osteoblast markers such as alkaline phosphatase, osteocalcin, and bone sialoprotein, leading to strong inhibition of mineralized nodule formation. This inhibitory effect is restricted to mature osteoblasts and differentiated osteosarcoma because OSM effectively stimulates osteoblast markers and bone nodule formation in early, but not late, bone marrow mesenchymal stem cell (BMSC) cultures. In osteosarcoma cells or BMSC, OSM induces expression of the glial fibrillary acidic protein (GFAP) as well as morphological and ultrastructural changes, for example, elongated shape and bundles of microfilaments in cell processes. Rottlerin (PKCdelta inhibitor), and to a lesser degree UO126 (MEK/ERK inhibitor), prevents the loss of osteoblastic markers by OSM, whereas dominant negative STAT3 prevents GFAP induction.
These results highlight the particular gene expression profile of OSM-treated osteosarcoma cells and BMSCs, suggesting either a osteocytic or a glial-like phenotype. Together with the implicat |
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Oncostatin M (OSM) is a multifunctional cytokine of the interleukin-6 family implicated in embryonic development, differentiation, inflammation, and regeneration of various tissues, mainly the liver, bone, and the central nervous and hematopoietic systems. One particularity of OSM relies on its growth inhibitory and pro-differentiating effects on a variety of tumor cell lines such as melanoma, providing arguments for a therapeutic application of OSM. The objective of this study was to analyze the effects of OSM on osteosarcoma cell lines proliferation and differentiation.
Proliferation was analyzed by 3H thymidine incorporation. Differentiation was analyzed by semiquantitative RT-PCR and immunocytochemistry for various markers. Alizarin red S staining was used to evaluate bone nodule formation. Morphological changes were studied by confocal and electron microscopy. Western blotting, kinases inhibitors, and dominant negative STAT3 were used to identified the signaling pathways implicated.
OSM inhibits the growth of rat osteosarcoma cell lines as well as normal osteoblasts, in correlation with induction of the cyclin-dependent kinases inhibitor p21WAF1. However, OSM reduces osteoblast markers such as alkaline phosphatase, osteocalcin, and bone sialoprotein, leading to strong inhibition of mineralized nodule formation. This inhibitory effect is restricted to mature osteoblasts and differentiated osteosarcoma because OSM effectively stimulates osteoblast markers and bone nodule formation in early, but not late, bone marrow mesenchymal stem cell (BMSC) cultures. In osteosarcoma cells or BMSC, OSM induces expression of the glial fibrillary acidic protein (GFAP) as well as morphological and ultrastructural changes, for example, elongated shape and bundles of microfilaments in cell processes. Rottlerin (PKCdelta inhibitor), and to a lesser degree UO126 (MEK/ERK inhibitor), prevents the loss of osteoblastic markers by OSM, whereas dominant negative STAT3 prevents GFAP induction.
These results highlight the particular gene expression profile of OSM-treated osteosarcoma cells and BMSCs, suggesting either a osteocytic or a glial-like phenotype. Together with the implication of PKCdelta, ERK1/2, and STAT3, these results offer new lines of investigations for neural cell transplantation and osteosarcoma therapy.</description><identifier>ISSN: 0884-0431</identifier><identifier>PMID: 15476586</identifier><language>eng</language><publisher>United States</publisher><subject>Alkaline Phosphatase - metabolism ; Animals ; Anthraquinones - pharmacology ; Blotting, Western ; Bone and Bones - metabolism ; Bone Marrow Cells - cytology ; Butadienes - pharmacology ; Cell Cycle Proteins - metabolism ; Cell Differentiation ; Cell Line, Tumor ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p21 ; DNA - metabolism ; DNA-Binding Proteins - physiology ; Dose-Response Relationship, Drug ; Down-Regulation ; Enzyme Inhibitors - pharmacology ; Glial Fibrillary Acidic Protein - biosynthesis ; Immunohistochemistry ; Inflammation ; Integrin-Binding Sialoprotein ; Interleukin-6 - metabolism ; Mesoderm - cytology ; Microscopy, Confocal ; Microscopy, Electron ; Models, Biological ; Nitriles - pharmacology ; Osteoblasts - cytology ; Osteoblasts - metabolism ; Osteocalcin - metabolism ; Osteosarcoma - metabolism ; Protein Kinase C - physiology ; Protein Kinase C-delta ; Rats ; Regeneration ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Sialoglycoproteins - metabolism ; Signal Transduction ; STAT3 Transcription Factor ; Stem Cells - cytology ; Thymidine - chemistry ; Time Factors ; Trans-Activators - physiology ; Transfection</subject><ispartof>Journal of bone and mineral research, 2004-11, Vol.19 (11), p.1850-1861</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15476586$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chipoy, Céline</creatorcontrib><creatorcontrib>Berreur, Martine</creatorcontrib><creatorcontrib>Couillaud, Séverine</creatorcontrib><creatorcontrib>Pradal, Gilbert</creatorcontrib><creatorcontrib>Vallette, François</creatorcontrib><creatorcontrib>Colombeix, Caroline</creatorcontrib><creatorcontrib>Rédini, Françoise</creatorcontrib><creatorcontrib>Heymann, Dominique</creatorcontrib><creatorcontrib>Blanchard, Frédéric</creatorcontrib><title>Downregulation of osteoblast markers and induction of the glial fibrillary acidic protein by oncostatin M in osteosarcoma cells require PKCdelta and STAT3</title><title>Journal of bone and mineral research</title><addtitle>J Bone Miner Res</addtitle><description>The effects of OSM on proliferation and differentiation of osteosarcoma and nontransformed osteoblasts were analyzed. OSM downregulates osteoblast markers but induces the glial fibrillary acidic protein by the combined activation of PKCdelta and STAT3, offering new lines of therapeutic investigations.
Oncostatin M (OSM) is a multifunctional cytokine of the interleukin-6 family implicated in embryonic development, differentiation, inflammation, and regeneration of various tissues, mainly the liver, bone, and the central nervous and hematopoietic systems. One particularity of OSM relies on its growth inhibitory and pro-differentiating effects on a variety of tumor cell lines such as melanoma, providing arguments for a therapeutic application of OSM. The objective of this study was to analyze the effects of OSM on osteosarcoma cell lines proliferation and differentiation.
Proliferation was analyzed by 3H thymidine incorporation. Differentiation was analyzed by semiquantitative RT-PCR and immunocytochemistry for various markers. Alizarin red S staining was used to evaluate bone nodule formation. Morphological changes were studied by confocal and electron microscopy. Western blotting, kinases inhibitors, and dominant negative STAT3 were used to identified the signaling pathways implicated.
OSM inhibits the growth of rat osteosarcoma cell lines as well as normal osteoblasts, in correlation with induction of the cyclin-dependent kinases inhibitor p21WAF1. However, OSM reduces osteoblast markers such as alkaline phosphatase, osteocalcin, and bone sialoprotein, leading to strong inhibition of mineralized nodule formation. This inhibitory effect is restricted to mature osteoblasts and differentiated osteosarcoma because OSM effectively stimulates osteoblast markers and bone nodule formation in early, but not late, bone marrow mesenchymal stem cell (BMSC) cultures. In osteosarcoma cells or BMSC, OSM induces expression of the glial fibrillary acidic protein (GFAP) as well as morphological and ultrastructural changes, for example, elongated shape and bundles of microfilaments in cell processes. Rottlerin (PKCdelta inhibitor), and to a lesser degree UO126 (MEK/ERK inhibitor), prevents the loss of osteoblastic markers by OSM, whereas dominant negative STAT3 prevents GFAP induction.
These results highlight the particular gene expression profile of OSM-treated osteosarcoma cells and BMSCs, suggesting either a osteocytic or a glial-like phenotype. Together with the implication of PKCdelta, ERK1/2, and STAT3, these results offer new lines of investigations for neural cell transplantation and osteosarcoma therapy.</description><subject>Alkaline Phosphatase - metabolism</subject><subject>Animals</subject><subject>Anthraquinones - pharmacology</subject><subject>Blotting, Western</subject><subject>Bone and Bones - metabolism</subject><subject>Bone Marrow Cells - cytology</subject><subject>Butadienes - pharmacology</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell Differentiation</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>DNA - metabolism</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Down-Regulation</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Glial Fibrillary Acidic Protein - biosynthesis</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Integrin-Binding Sialoprotein</subject><subject>Interleukin-6 - metabolism</subject><subject>Mesoderm - cytology</subject><subject>Microscopy, Confocal</subject><subject>Microscopy, Electron</subject><subject>Models, Biological</subject><subject>Nitriles - pharmacology</subject><subject>Osteoblasts - cytology</subject><subject>Osteoblasts - metabolism</subject><subject>Osteocalcin - metabolism</subject><subject>Osteosarcoma - metabolism</subject><subject>Protein Kinase C - physiology</subject><subject>Protein Kinase C-delta</subject><subject>Rats</subject><subject>Regeneration</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Sialoglycoproteins - metabolism</subject><subject>Signal Transduction</subject><subject>STAT3 Transcription Factor</subject><subject>Stem Cells - cytology</subject><subject>Thymidine - chemistry</subject><subject>Time Factors</subject><subject>Trans-Activators - physiology</subject><subject>Transfection</subject><issn>0884-0431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kMtOwzAQRbMA0VL4BTQrdpFsHDvJsiqviiKQyD5y7EkxOHZrJ0L9Fb6WlLarWczRuVf3LJmSoshSkjE6SS5j_CKECC7ERTKhPMsFL8Q0-b33Py7gerCyN96Bb8HHHn1jZeyhk-EbQwTpNBinB3Vi-k-EtTXSQmuaYKyVYQdSGW0UbILv0ThoduCdGm2j2cHrKDioowzKdxIUWhsh4HYwAeH9ZaHR9vI_66OaV-wqOW-ljXh9vLOkenyoFs_p6u1puZiv0g3PRKozrTTeEc50wzJNWt2KIie5LKnirCRIdM7p_i8EaQWjvGlJWSJvKDJBOZsltwft2Hs7YOzrzsR9N-nQD7EWouRlUdIRvDmCQ9OhrjfBjPvs6tOY7A9PNnIB</recordid><startdate>200411</startdate><enddate>200411</enddate><creator>Chipoy, Céline</creator><creator>Berreur, Martine</creator><creator>Couillaud, Séverine</creator><creator>Pradal, Gilbert</creator><creator>Vallette, François</creator><creator>Colombeix, Caroline</creator><creator>Rédini, Françoise</creator><creator>Heymann, Dominique</creator><creator>Blanchard, Frédéric</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200411</creationdate><title>Downregulation of osteoblast markers and induction of the glial fibrillary acidic protein by oncostatin M in osteosarcoma cells require PKCdelta and STAT3</title><author>Chipoy, Céline ; Berreur, Martine ; Couillaud, Séverine ; Pradal, Gilbert ; Vallette, François ; Colombeix, Caroline ; Rédini, Françoise ; Heymann, Dominique ; Blanchard, Frédéric</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p546-d4dcde2053db34d0fdf68707a91c5390e0d7512053660f6315bf099e5b1e36153</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Alkaline Phosphatase - metabolism</topic><topic>Animals</topic><topic>Anthraquinones - pharmacology</topic><topic>Blotting, Western</topic><topic>Bone and Bones - metabolism</topic><topic>Bone Marrow Cells - cytology</topic><topic>Butadienes - pharmacology</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell Differentiation</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>DNA - metabolism</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Down-Regulation</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Glial Fibrillary Acidic Protein - biosynthesis</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Integrin-Binding Sialoprotein</topic><topic>Interleukin-6 - metabolism</topic><topic>Mesoderm - cytology</topic><topic>Microscopy, Confocal</topic><topic>Microscopy, Electron</topic><topic>Models, Biological</topic><topic>Nitriles - pharmacology</topic><topic>Osteoblasts - cytology</topic><topic>Osteoblasts - metabolism</topic><topic>Osteocalcin - metabolism</topic><topic>Osteosarcoma - metabolism</topic><topic>Protein Kinase C - physiology</topic><topic>Protein Kinase C-delta</topic><topic>Rats</topic><topic>Regeneration</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Sialoglycoproteins - metabolism</topic><topic>Signal Transduction</topic><topic>STAT3 Transcription Factor</topic><topic>Stem Cells - cytology</topic><topic>Thymidine - chemistry</topic><topic>Time Factors</topic><topic>Trans-Activators - physiology</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chipoy, Céline</creatorcontrib><creatorcontrib>Berreur, Martine</creatorcontrib><creatorcontrib>Couillaud, Séverine</creatorcontrib><creatorcontrib>Pradal, Gilbert</creatorcontrib><creatorcontrib>Vallette, François</creatorcontrib><creatorcontrib>Colombeix, Caroline</creatorcontrib><creatorcontrib>Rédini, Françoise</creatorcontrib><creatorcontrib>Heymann, Dominique</creatorcontrib><creatorcontrib>Blanchard, Frédéric</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of bone and mineral research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chipoy, Céline</au><au>Berreur, Martine</au><au>Couillaud, Séverine</au><au>Pradal, Gilbert</au><au>Vallette, François</au><au>Colombeix, Caroline</au><au>Rédini, Françoise</au><au>Heymann, Dominique</au><au>Blanchard, Frédéric</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulation of osteoblast markers and induction of the glial fibrillary acidic protein by oncostatin M in osteosarcoma cells require PKCdelta and STAT3</atitle><jtitle>Journal of bone and mineral research</jtitle><addtitle>J Bone Miner Res</addtitle><date>2004-11</date><risdate>2004</risdate><volume>19</volume><issue>11</issue><spage>1850</spage><epage>1861</epage><pages>1850-1861</pages><issn>0884-0431</issn><abstract>The effects of OSM on proliferation and differentiation of osteosarcoma and nontransformed osteoblasts were analyzed. OSM downregulates osteoblast markers but induces the glial fibrillary acidic protein by the combined activation of PKCdelta and STAT3, offering new lines of therapeutic investigations.
Oncostatin M (OSM) is a multifunctional cytokine of the interleukin-6 family implicated in embryonic development, differentiation, inflammation, and regeneration of various tissues, mainly the liver, bone, and the central nervous and hematopoietic systems. One particularity of OSM relies on its growth inhibitory and pro-differentiating effects on a variety of tumor cell lines such as melanoma, providing arguments for a therapeutic application of OSM. The objective of this study was to analyze the effects of OSM on osteosarcoma cell lines proliferation and differentiation.
Proliferation was analyzed by 3H thymidine incorporation. Differentiation was analyzed by semiquantitative RT-PCR and immunocytochemistry for various markers. Alizarin red S staining was used to evaluate bone nodule formation. Morphological changes were studied by confocal and electron microscopy. Western blotting, kinases inhibitors, and dominant negative STAT3 were used to identified the signaling pathways implicated.
OSM inhibits the growth of rat osteosarcoma cell lines as well as normal osteoblasts, in correlation with induction of the cyclin-dependent kinases inhibitor p21WAF1. However, OSM reduces osteoblast markers such as alkaline phosphatase, osteocalcin, and bone sialoprotein, leading to strong inhibition of mineralized nodule formation. This inhibitory effect is restricted to mature osteoblasts and differentiated osteosarcoma because OSM effectively stimulates osteoblast markers and bone nodule formation in early, but not late, bone marrow mesenchymal stem cell (BMSC) cultures. In osteosarcoma cells or BMSC, OSM induces expression of the glial fibrillary acidic protein (GFAP) as well as morphological and ultrastructural changes, for example, elongated shape and bundles of microfilaments in cell processes. Rottlerin (PKCdelta inhibitor), and to a lesser degree UO126 (MEK/ERK inhibitor), prevents the loss of osteoblastic markers by OSM, whereas dominant negative STAT3 prevents GFAP induction.
These results highlight the particular gene expression profile of OSM-treated osteosarcoma cells and BMSCs, suggesting either a osteocytic or a glial-like phenotype. Together with the implication of PKCdelta, ERK1/2, and STAT3, these results offer new lines of investigations for neural cell transplantation and osteosarcoma therapy.</abstract><cop>United States</cop><pmid>15476586</pmid><tpages>12</tpages></addata></record> |
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subjects | Alkaline Phosphatase - metabolism Animals Anthraquinones - pharmacology Blotting, Western Bone and Bones - metabolism Bone Marrow Cells - cytology Butadienes - pharmacology Cell Cycle Proteins - metabolism Cell Differentiation Cell Line, Tumor Cell Proliferation Cyclin-Dependent Kinase Inhibitor p21 DNA - metabolism DNA-Binding Proteins - physiology Dose-Response Relationship, Drug Down-Regulation Enzyme Inhibitors - pharmacology Glial Fibrillary Acidic Protein - biosynthesis Immunohistochemistry Inflammation Integrin-Binding Sialoprotein Interleukin-6 - metabolism Mesoderm - cytology Microscopy, Confocal Microscopy, Electron Models, Biological Nitriles - pharmacology Osteoblasts - cytology Osteoblasts - metabolism Osteocalcin - metabolism Osteosarcoma - metabolism Protein Kinase C - physiology Protein Kinase C-delta Rats Regeneration Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Sialoglycoproteins - metabolism Signal Transduction STAT3 Transcription Factor Stem Cells - cytology Thymidine - chemistry Time Factors Trans-Activators - physiology Transfection |
title | Downregulation of osteoblast markers and induction of the glial fibrillary acidic protein by oncostatin M in osteosarcoma cells require PKCdelta and STAT3 |
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