FGF18 Represses Noggin Expression and Is Induced by Calcineurin
| Autor: | Makoto Abe, Ravi M. Kapadia, Martina I. Reinhold, Michael C. Naski, Zhixiang Liao |
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| Rok vydání: | 2004 |
| Předmět: |
Time Factors
Bone morphogenetic protein 8A Bone Morphogenetic Protein 2 Ligands Biochemistry Mice Transforming Growth Factor beta Aggrecans Fluorescent Antibody Technique Indirect Chelating Agents Extracellular Matrix Proteins Reverse Transcriptase Polymerase Chain Reaction Chemistry Calcineurin Ionomycin Nuclear Proteins Cell Differentiation Cell biology DNA-Binding Proteins Bone morphogenetic protein 7 Bone morphogenetic protein 6 Bone morphogenetic protein 5 GDF6 Bone Morphogenetic Proteins Proteoglycans Signal Transduction Transcriptional Activation medicine.medical_specialty Blotting Western Bone morphogenetic protein Models Biological Bone morphogenetic protein 2 Adenoviridae Transforming Growth Factor beta1 Chondrocytes Internal medicine medicine Animals Humans Lectins C-Type Molecular Biology Cell Nucleus NFATC Transcription Factors Ubiquitin Proteins Bone morphogenetic protein 10 Cell Biology Blotting Northern Precipitin Tests Rats Fibroblast Growth Factors Mice Inbred C57BL Endocrinology Gene Expression Regulation Calcium Carrier Proteins Transcription Factors |
| Zdroj: | Journal of Biological Chemistry. 279:38209-38219 |
| ISSN: | 0021-9258 |
| DOI: | 10.1074/jbc.m404855200 |
| Popis: | Fibroblast growth factors (FGFs) and bone morphogenetic proteins strongly regulate chondrogenesis and chondrocyte gene expression. The interactions of the signaling pathways initiated by these factors are central to the control of chondrocyte differentiation. Here we show that calcium-dependent signals induce expression of FGF18, an essential regulator of bone and cartilage differentiation. The induction of FGF18 expression required the calcium-dependent phosphatase, calcineurin. The activated forms of calcineurin or the calcineurin-dependent transcription factor, NFAT4 (nuclear factor of activated T-cell 4), induced FGF18 expression. FGF18 or a constitutive active FGF receptor suppressed noggin gene induction and thereby increased chondrocyte gene expression and chondrogenesis by facilitating bone morphogenetic protein-dependent signals. These findings reinforce the interdependence of bone morphogenetic protein and FGF signaling and provide a rational explanation for abnormal bone development occurring in humans or mice with constitutively active FGF receptors. |
| Databáze: | OpenAIRE |
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