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Upregulated expression of transforming growth factor-beta receptors in dermal fibroblasts of skin sections from patients with systemic sclerosis. 2002

Masahide Kubo, and Hironobu Ihn, and Kenichi Yamane, and Kunihiko Tamaki
Faculty of Medicine, University of Tokyo, Japan.

OBJECTIVE To investigate the expression levels of transforming growth factor-beta (TGF-beta) receptors in the skin of patients with systemic sclerosis (SSc). METHODS We examined expressions of TGF-beta type I and type II receptors (TGF-betaRI and TGF-betaRII) in skin sections of 5 patients with SSc and 5 healthy controls using in situ hybridization and immunohistochemical analysis. RESULTS The expression levels of both TGF-betaRI and TGF-betaRII were elevated in the dermal fibroblasts of skin sections from patients with SSc in comparison to control skin sections in in situ hybridization and in immunohistochemical stainings. The numbers of fibroblasts expressing TGF-betaRI and TGF-betaRII in the SSc skin sections were increased in comparison to controls. The inflammatory cells around the vessels also expressed TGF-betaRI and TGF-betaRII intensively in the SSc skin sections. CONCLUSIONS These results suggest that the autocrine TGF-beta signaling due to the overexpression of TGF-betaRI and TGF-betaRII in dermal fibroblasts is involved in the pathogenesis of dermal fibrosis in patients with SSc.

UI MeSH Term Description Entries
D007150 Immunohistochemistry Histochemical localization of immunoreactive substances using labeled antibodies as reagents. Immunocytochemistry,Immunogold Techniques,Immunogold-Silver Techniques,Immunohistocytochemistry,Immunolabeling Techniques,Immunogold Technics,Immunogold-Silver Technics,Immunolabeling Technics,Immunogold Silver Technics,Immunogold Silver Techniques,Immunogold Technic,Immunogold Technique,Immunogold-Silver Technic,Immunogold-Silver Technique,Immunolabeling Technic,Immunolabeling Technique,Technic, Immunogold,Technic, Immunogold-Silver,Technic, Immunolabeling,Technics, Immunogold,Technics, Immunogold-Silver,Technics, Immunolabeling,Technique, Immunogold,Technique, Immunogold-Silver,Technique, Immunolabeling,Techniques, Immunogold,Techniques, Immunogold-Silver,Techniques, Immunolabeling
D002452 Cell Count The number of CELLS of a specific kind, usually measured per unit volume or area of sample. Cell Density,Cell Number,Cell Counts,Cell Densities,Cell Numbers,Count, Cell,Counts, Cell,Densities, Cell,Density, Cell,Number, Cell,Numbers, Cell
D005347 Fibroblasts Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. Fibroblast
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000077293 Receptor, Transforming Growth Factor-beta Type I A transmembrane serine-threonine kinase that forms a heteromeric complex with TYPE II TGF-BETA RECEPTORS to bind TGF-BETA and regulate a variety of physiological and pathological processes including CELL CYCLE ARREST; CELL PROLIFERATION; CELL DIFFERENTIATION; WOUND HEALING; EXTRACELLULAR MATRIX production, immunosuppression and ONCOGENESIS. Activin Receptor-like Kinase 5,Receptor, TGF-beta Type I,Serine-Threonine-Protein Kinase Receptor R4,TGF-beta RPK,TGF-beta Receptor Protein Kinase,TGF-beta Type I Receptor,TGF-beta Type I Receptors,TGFBR1,TbetaR-I Kinase,Transforming Growth Factor beta Receptor I,Transforming Growth Factor, beta Receptor 1,Type I TGF-beta Receptor,Type I TGF-beta Receptors,Activin Receptor like Kinase 5,Kinase, TbetaR-I,Serine Threonine Protein Kinase Receptor R4,TGF beta Receptor Protein Kinase,TGF beta Type I Receptor,TGF beta Type I Receptors,TbetaR I Kinase,Type I TGF beta Receptor,Type I TGF beta Receptors
D000077294 Receptor, Transforming Growth Factor-beta Type II A transmembrane serine-threonine kinase that forms a heteromeric complex with TYPE I TGF-BETA RECEPTORS when bound to TGF-BETA. This receptor complex regulates a variety of physiological and pathological processes including CELL CYCLE ARREST; CELL PROLIFERATION; CELL DIFFERENTIATION; WOUND HEALING; EXTRACELLULAR MATRIX production, immunosuppression and ONCOGENESIS. TGF-beta Type II Receptor,TGF-beta Type II Receptors,TGFBR2,TbetaR-II Kinase,Transforming Growth Factor-beta Type II Receptor,Transforming Growth Factor-beta Type II Receptors,Type II TGF-beta Receptor,Type II TGF-beta Receptors,Kinase, TbetaR-II,Receptor, Transforming Growth Factor beta Type II,TGF beta Type II Receptor,TGF beta Type II Receptors,TbetaR II Kinase,Transforming Growth Factor beta Type II Receptor,Transforming Growth Factor beta Type II Receptors,Type II TGF beta Receptor,Type II TGF beta Receptors
D012333 RNA, Messenger RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm. Messenger RNA,Messenger RNA, Polyadenylated,Poly(A) Tail,Poly(A)+ RNA,Poly(A)+ mRNA,RNA, Messenger, Polyadenylated,RNA, Polyadenylated,mRNA,mRNA, Non-Polyadenylated,mRNA, Polyadenylated,Non-Polyadenylated mRNA,Poly(A) RNA,Polyadenylated mRNA,Non Polyadenylated mRNA,Polyadenylated Messenger RNA,Polyadenylated RNA,RNA, Polyadenylated Messenger,mRNA, Non Polyadenylated
D012595 Scleroderma, Systemic A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA. Sclerosis, Systemic,Systemic Scleroderma,Systemic Sclerosis
D015398 Signal Transduction The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. Cell Signaling,Receptor-Mediated Signal Transduction,Signal Pathways,Receptor Mediated Signal Transduction,Signal Transduction Pathways,Signal Transduction Systems,Pathway, Signal,Pathway, Signal Transduction,Pathways, Signal,Pathways, Signal Transduction,Receptor-Mediated Signal Transductions,Signal Pathway,Signal Transduction Pathway,Signal Transduction System,Signal Transduction, Receptor-Mediated,Signal Transductions,Signal Transductions, Receptor-Mediated,System, Signal Transduction,Systems, Signal Transduction,Transduction, Signal,Transductions, Signal
D015854 Up-Regulation A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins. Receptor Up-Regulation,Upregulation,Up-Regulation (Physiology),Up Regulation

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