The collection of NFATc1-dependent transcripts in the osteoclast includes numerous genes non-essential to physiologic bone resorption
Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including osteoporosis, inflammatory arthritis and cancer metastasis. Differentiation of these multinucleated giant cells from precursors is controlle...
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| Published in | Bone (New York, N.Y.) Vol. 51; no. 5; pp. 902 - 912 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Amsterdam
Elsevier Inc
01.11.2012
Elsevier |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including osteoporosis, inflammatory arthritis and cancer metastasis. Differentiation of these multinucleated giant cells from precursors is controlled by the cytokine RANKL, which through its receptor RANK initiates a signaling cascade culminating in the activation of transcriptional regulators which induce the expression of the bone degradation machinery. The transcription factor nuclear factor of activated T-cells c1 (NFATc1) is the master regulator of this process and in its absence osteoclast differentiation is aborted both in vitro and in vivo. Differential mRNA expression analysis by microarray is used to identify genes of potential physiologic relevance across nearly all biologic systems. We compared the gene expression profile of murine wild-type and NFATc1-deficient osteoclast precursors stimulated with RANKL and identified that the majority of the known genes important for osteoclastic bone resorption require NFATc1 for induction. Here, five novel RANKL-induced, NFATc1-dependent transcripts in the osteoclast are described: Nhedc2, Rhoc, Serpind1, Adcy3 and Rab38. Despite reasonable hypotheses for the importance of these molecules in the bone resorption pathway and their dramatic induction during differentiation, the analysis of mice with mutations in these genes failed to reveal a function in osteoclast biology. Compared to littermate controls, none of these mutants demonstrated a skeletal phenotype in vivo or alterations in osteoclast differentiation or function in vitro. These data highlight the need for rigorous validation studies to complement expression profiling results before functional importance can be assigned to highly regulated genes in any biologic process.
► Microarray profiling was used to identify NFATc1 dependent transcripts in the osteoclast. ► These NFATc1 dependent transcripts encompass 80 genes, including 4 known osteoclast regulators. ► Five candidate regulators were selected for study: Nhedc2, Serpind1, Adcy3, Rhoc and Rab38. ► Mutant mice in each of these genes exhibited normal bone mass and osteoclast function. |
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| AbstractList | Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including osteoporosis, inflammatory arthritis and cancer metastasis. Differentiation of these multinucleated giant cells from precursors is controlled by the cytokine RANKL, which through its receptor RANK initiates a signaling cascade culminating in the activation of transcriptional regulators which induce the expression of the bone degradation machinery. The transcription factor nuclear factor of activated T-cells c1 (NFATc1) is the master regulator of this process and in its absence osteoclast differentiation is aborted both in vitro and in vivo. Differential mRNA expression analysis by microarray is used to identify genes of potential physiologic relevance across nearly all biologic systems. We compared the gene expression profile of murine wild-type and NFATc1-deficient osteoclast precursors stimulated with RANKL and identified that the majority of the known genes important for osteoclastic bone resorption require NFATc1 for induction. Here, five novel RANKL-induced, NFATc1-dependent transcripts in the osteoclast are described: Nhedc2, Rhoc, Serpind1, Adcy3 and Rab38. Despite reasonable hypotheses for the importance of these molecules in the bone resorption pathway and their dramatic induction during differentiation, the analysis of mice with mutations in these genes failed to reveal a function in osteoclast biology. Compared to littermate controls, none of these mutants demonstrated a skeletal phenotype in vivo or alterations in osteoclast differentiation or function in vitro. These data highlight the need for rigorous validation studies to complement expression profiling results before functional importance can be assigned to highly regulated genes in any biologic process.
► Microarray profiling was used to identify NFATc1 dependent transcripts in the osteoclast. ► These NFATc1 dependent transcripts encompass 80 genes, including 4 known osteoclast regulators. ► Five candidate regulators were selected for study: Nhedc2, Serpind1, Adcy3, Rhoc and Rab38. ► Mutant mice in each of these genes exhibited normal bone mass and osteoclast function. Abstract Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including osteoporosis, inflammatory arthritis and cancer metastasis. Differentiation of these multinucleated giant cells from precursors is controlled by the cytokine RANKL, which through its receptor RANK initiates a signaling cascade culminating in the activation of transcriptional regulators which induce the expression of the bone degradation machinery. The transcription factor nuclear factor of activated T-cells c1 (NFATc1) is the master regulator of this process and in its absence osteoclast differentiation is aborted both in vitro and in vivo. Differential mRNA expression analysis by microarray is used to identify genes of potential physiologic relevance across nearly all biologic systems. We compared the gene expression profile of murine wild-type and NFATc1-deficient osteoclast precursors stimulated with RANKL and identified that the majority of the known genes important for osteoclastic bone resorption require NFATc1 for induction. Here, five novel RANKL-induced, NFATc1-dependent transcripts in the osteoclast are described: Nhedc2 , Rhoc , Serpind1 , Adcy3 and Rab38 . Despite reasonable hypotheses for the importance of these molecules in the bone resorption pathway and their dramatic induction during differentiation, the analysis of mice with mutations in these genes failed to reveal a function in osteoclast biology. Compared to littermate controls, none of these mutants demonstrated a skeletal phenotype in vivo or alterations in osteoclast differentiation or function in vitro. These data highlight the need for rigorous validation studies to complement expression profiling results before functional importance can be assigned to highly regulated genes in any biologic process. Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including osteoporosis, inflammatory arthritis and cancer metastasis. Differentiation of these multinucleated giant cells from precursors is controlled by the cytokine RANKL, which through its receptor RANK initiates a signaling cascade culminating in the activation of transcriptional regulators which induce the expression of the bone degradation machinery. The transcription factor nuclear factor of activated T-cells c1 (NFATc1) is the master regulator of this process and in its absence osteoclast differentiation is aborted both in vitro and in vivo . Differential mRNA expression analysis by microarray is used to identify genes of potential physiologic relevance across nearly all biologic systems. We compared the gene expression profile of murine wild-type and NFATc1-deficient osteoclast precursors stimulated with RANKL and identified that the majority of the known genes important for osteoclastic bone resorption require NFATc1 for induction. Here, five novel RANKL-induced, NFATc1-dependent transcripts in the osteoclast are described: Nhedc2 , Rhoc , Serpind1, Adcy3 and Rab38 . Despite reasonable hypotheses for the importance of these molecules in the bone resorption pathway and their dramatic induction during differentiation, the analysis of mice with mutations in these genes failed to reveal a function in osteoclast biology. Compared to littermate controls, none of these mutants demonstrated a skeletal phenotype in vivo or alterations in osteoclast differentiation or function in vitro . These data highlight the need for rigorous validation studies to complement expression profiling results before functional importance can be assigned to highly regulated genes in any biologic process. Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including osteoporosis, inflammatory arthritis and cancer metastasis. Differentiation of these multinucleated giant cells from precursors is controlled by the cytokine RANKL, which through its receptor RANK initiates a signaling cascade culminating in the activation of transcriptional regulators which induce the expression of the bone degradation machinery. The transcription factor nuclear factor of activated T-cells c1 (NFATc1) is the master regulator of this process and in its absence osteoclast differentiation is aborted both in vitro and in vivo. Differential mRNA expression analysis by microarray is used to identify genes of potential physiologic relevance across nearly all biologic systems. We compared the gene expression profile of murine wild-type and NFATc1-deficient osteoclast precursors stimulated with RANKL and identified that the majority of the known genes important for osteoclastic bone resorption require NFATc1 for induction. Here, five novel RANKL-induced, NFATc1-dependent transcripts in the osteoclast are described: Nhedc2, Rhoc, Serpind1, Adcy3 and Rab38. Despite reasonable hypotheses for the importance of these molecules in the bone resorption pathway and their dramatic induction during differentiation, the analysis of mice with mutations in these genes failed to reveal a function in osteoclast biology. Compared to littermate controls, none of these mutants demonstrated a skeletal phenotype in vivo or alterations in osteoclast differentiation or function in vitro. These data highlight the need for rigorous validation studies to complement expression profiling results before functional importance can be assigned to highly regulated genes in any biologic process. Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including osteoporosis, inflammatory arthritis and cancer metastasis. Differentiation of these multinucleated giant cells from precursors is controlled by the cytokine RANKL, which through its receptor RANK initiates a signaling cascade culminating in the activation of transcriptional regulators which induce the expression of the bone degradation machinery. The transcription factor nuclear factor of activated T-cells c1 (NFATc1) is the master regulator of this process and in its absence osteoclast differentiation is aborted both in vitro and in vivo. Differential mRNA expression analysis by microarray is used to identify genes of potential physiologic relevance across nearly all biologic systems. We compared the gene expression profile of murine wild-type and NFATc1-deficient osteoclast precursors stimulated with RANKL and identified that the majority of the known genes important for osteoclastic bone resorption require NFATc1 for induction. Here, five novel RANKL-induced, NFATc1-dependent transcripts in the osteoclast are described: Nhedc2, Rhoc, Serpind1, Adcy3 and Rab38. Despite reasonable hypotheses for the importance of these molecules in the bone resorption pathway and their dramatic induction during differentiation, the analysis of mice with mutations in these genes failed to reveal a function in osteoclast biology. Compared to littermate controls, none of these mutants demonstrated a skeletal phenotype in vivo or alterations in osteoclast differentiation or function in vitro. These data highlight the need for rigorous validation studies to complement expression profiling results before functional importance can be assigned to highly regulated genes in any biologic process.Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including osteoporosis, inflammatory arthritis and cancer metastasis. Differentiation of these multinucleated giant cells from precursors is controlled by the cytokine RANKL, which through its receptor RANK initiates a signaling cascade culminating in the activation of transcriptional regulators which induce the expression of the bone degradation machinery. The transcription factor nuclear factor of activated T-cells c1 (NFATc1) is the master regulator of this process and in its absence osteoclast differentiation is aborted both in vitro and in vivo. Differential mRNA expression analysis by microarray is used to identify genes of potential physiologic relevance across nearly all biologic systems. We compared the gene expression profile of murine wild-type and NFATc1-deficient osteoclast precursors stimulated with RANKL and identified that the majority of the known genes important for osteoclastic bone resorption require NFATc1 for induction. Here, five novel RANKL-induced, NFATc1-dependent transcripts in the osteoclast are described: Nhedc2, Rhoc, Serpind1, Adcy3 and Rab38. Despite reasonable hypotheses for the importance of these molecules in the bone resorption pathway and their dramatic induction during differentiation, the analysis of mice with mutations in these genes failed to reveal a function in osteoclast biology. Compared to littermate controls, none of these mutants demonstrated a skeletal phenotype in vivo or alterations in osteoclast differentiation or function in vitro. These data highlight the need for rigorous validation studies to complement expression profiling results before functional importance can be assigned to highly regulated genes in any biologic process. |
| Author | Sitara, Despina Wu, Jing Aliprantis, Antonios O. Sulyanto, Rosalyn Charles, Julia F. Brady, Nicholas Sigrist, Kirsten Storm, Daniel Tsang, Kelly Coury, Fabienne Tollefsen, Douglas M. He, Li |
| AuthorAffiliation | d Division of Hematology, Washington University School of Medicine, St. Louis, MO, USA c Department of Oral Medicine Infection and Immunity, Harvard Dental School, Boston, Massachusetts, USA b Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA a Department of Medicine, Division of Rheumatology, Allergy and Immunology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA 6 Department of Laboratory Medicine and Pathology and Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA 2 Institut de Génomique Fonctionnelle de Lyon, Ecole Normale Supérieure de Lyon, Lyon, France 3 OCC Dentistry, Columbus, OH, USA 5 China Novartis Institutes for BioMedical Research Co., Shanghai 201203, China e Department of Pharmacology, University of Washington Medical School, Seattle, WA, USA 4 New York University College of Dentistry, New York, NY, USA 7 Department of Molecular Biology, Cell Biology and Biochemistry, |
| AuthorAffiliation_xml | – name: e Department of Pharmacology, University of Washington Medical School, Seattle, WA, USA – name: b Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA – name: 2 Institut de Génomique Fonctionnelle de Lyon, Ecole Normale Supérieure de Lyon, Lyon, France – name: 4 New York University College of Dentistry, New York, NY, USA – name: 6 Department of Laboratory Medicine and Pathology and Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA – name: a Department of Medicine, Division of Rheumatology, Allergy and Immunology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA – name: 3 OCC Dentistry, Columbus, OH, USA – name: d Division of Hematology, Washington University School of Medicine, St. Louis, MO, USA – name: 5 China Novartis Institutes for BioMedical Research Co., Shanghai 201203, China – name: 7 Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA – name: c Department of Oral Medicine Infection and Immunity, Harvard Dental School, Boston, Massachusetts, USA |
| Author_xml | – sequence: 1 givenname: Julia F. surname: Charles fullname: Charles, Julia F. organization: Department of Medicine, Division of Rheumatology, Allergy and Immunology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA – sequence: 2 givenname: Fabienne surname: Coury fullname: Coury, Fabienne organization: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA – sequence: 3 givenname: Rosalyn surname: Sulyanto fullname: Sulyanto, Rosalyn organization: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA – sequence: 4 givenname: Despina surname: Sitara fullname: Sitara, Despina organization: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA – sequence: 5 givenname: Jing surname: Wu fullname: Wu, Jing organization: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA – sequence: 6 givenname: Nicholas surname: Brady fullname: Brady, Nicholas organization: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA – sequence: 7 givenname: Kelly surname: Tsang fullname: Tsang, Kelly organization: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA – sequence: 8 givenname: Kirsten surname: Sigrist fullname: Sigrist, Kirsten organization: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA – sequence: 9 givenname: Douglas M. surname: Tollefsen fullname: Tollefsen, Douglas M. organization: Division of Hematology, Washington University School of Medicine, St. Louis, MO, USA – sequence: 10 givenname: Li surname: He fullname: He, Li organization: Division of Hematology, Washington University School of Medicine, St. Louis, MO, USA – sequence: 11 givenname: Daniel surname: Storm fullname: Storm, Daniel organization: Department of Pharmacology, University of Washington Medical School, Seattle, WA, USA – sequence: 12 givenname: Antonios O. surname: Aliprantis fullname: Aliprantis, Antonios O. email: aaliprantis@partners.org organization: Department of Medicine, Division of Rheumatology, Allergy and Immunology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA |
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| Keywords | Bone resorption Gene array OCPs Adcy3 Rab38 Serpind1 Nhedc2 Osteoclast Nfatc1 Rhoc ras homolog gene family member C nuclear factor of activated T-cells c1 serpin peptidase inhibitor, clade D, member 1 adenylate cyclase 3 ras-related protein Na +/H + exchanger-like domain-containing protein 2 osteoclast precursors Messenger RNA Morphology NHEDC2 NFATc1 |
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| Snippet | Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone including... Abstract Osteoclasts are specialized secretory cells of the myeloid lineage important for normal skeletal homeostasis as well as pathologic conditions of bone... |
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| SubjectTerms | Adenylyl Cyclases - genetics Adenylyl Cyclases - metabolism Animals Arthritis Biological and medical sciences Blotting, Western Bone cancer Bone resorption Bone Resorption - genetics Cancer Cell Differentiation - genetics Cell Differentiation - physiology Cells, Cultured Cytokines Data processing DNA microarrays Fundamental and applied biological sciences. Psychology Gene array Gene expression Giant cells Homeostasis Lymphocytes T Mice Mutation NFATC Transcription Factors - genetics NFATC Transcription Factors - metabolism NFATc1 NHEDC2 Oligonucleotide Array Sequence Analysis Orthopedics Osteoclast Osteoclastogenesis Osteoclasts Osteoclasts - cytology Osteoclasts - drug effects Osteoclasts - metabolism Osteoprogenitor cells rab GTP-Binding Proteins - genetics rab GTP-Binding Proteins - metabolism RANK Ligand - pharmacology ras Proteins - genetics ras Proteins - metabolism Real-Time Polymerase Chain Reaction rhoC GTP-Binding Protein Signal transduction Skeleton and joints Sodium-Hydrogen Exchangers - genetics Sodium-Hydrogen Exchangers - metabolism TRANCE protein Transcription activation Transcription factors Vertebrates: anatomy and physiology, studies on body, several organs or systems Vertebrates: osteoarticular system, musculoskeletal system |
| Title | The collection of NFATc1-dependent transcripts in the osteoclast includes numerous genes non-essential to physiologic bone resorption |
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