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Details for messenger / hormone: TGF-beta 1

EndoNet ID: ENH00212

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Synonyms

  • TGF-beta 1
  • TGF-ss
  • TGF-beta
  • TGFbeta1
  • transforming growth factor beta 1
  • transforming growth factor beta-1
  • TGFB1
  • TGFB
  • TGF beta

General information

  • Several cytokines and related factors are synthesised within adipose tissue, including TGF-β. [1]
  • Cytokines from the TGF-beta family play a role in liver development, by induction of Vg1. [2]
  • TGFbeta1, a potent keratinocyte growth inhibitor, has been shown to be overexpressed in keratinocytes in certain inflammatory skin diseases. [3]
  • The cytokine TGF-β plays a critical role in the resolution of tissue injury in multiple organs, including the lung. [4]
  • Transforming growth factor beta contributes to progressive diabetic nephropathy. [5]
  • Latent TGFbeta1 overexpression in keratinocytes results in a severe psoriasis-like skin disorder. [3]
  • TGF-beta1 may also regulate blood pressure via stimulation of endothelin-1 and/or renin secretion. [6]
  • Hepatic over-expression of TGF-beta1 promotes LPS-induced inflammatory cytokine secretion by liver cells and endotoxemic shock. [7]
  • TGFbeta1 is known for its potent and diverse biological effects, including immune regulation, and cell growth and differentiation. [8]
  • Histamine, cysteinyl-leukotrienes, and tumour necrosis factor alpha was strongly reduced by TGF-beta 1. [9]
  • Transforming growth factor ss (TGF-ss) is an immunosuppressor. [10]
  • The synthesis of IGFs through osteoblasts is down-regulated by many locally produced growth factors, particularly transforming growth factor beta and cortisol, and this probably accounts for the osteoporotic effects of this steroid, whereas PTH is stimulatory. [11]
  • TGF-beta1 is expressed in the healthy human intestine and controls mucosal immune responses and inflammation by regulating the function of lymphocytes, macrophages, dendritic cells, and eosinophils. [9]
  • Prostaglandin D2 generation and cyclooxygenase 1 and 2 expression were upregulated by TGF-ß1. [9]
  • TGF-beta-mediated epithelial-mesenchymal transition of mammary epithelial cells is accompagnied by the loss of laminin-5 production and the upregulation of fibronectin and its alpha-5/beta-1 integrin receptor. [12]
  • Members of the transforming growth factor beta (TGF-beta) family regulate fundamental physiological processes, such as cell growth, differentiation and apoptosis, in almost all cell types. [13]
  • TGF-beta1 induces bone marrow reticulin fibrosis in hairy cell leukemia. [14]
  • TGF-betas are important growth suppressing factors in normal breast epithelium and their activity is mediated by specific receptors, including TGF-beta-RII. [15]
  • Apoptosis is induced by transforming growth factor beta1 (TGFbeta1), the physiological negative regulator of liver growth. [16]
  • TGF-beta1 is the strongest known inducer of fibrogenesis in the effector cells of hepatic fibrosis, i.e. activated hepatic stellate cells and myofibroblasts. [17]
  • A mutation affecting the latency-associated peptide of TGFbeta1 in Camurati-Engelmann disease enhances osteoclast formation in vitro. [18]
  • TGF-beta stimulates osteoblast proliferation and growth, and inhibits the expression of the markers characteristic of the osteoblast phenotype such as osteocalcin. [19]

Classification

Hormone function

  • development and growth
    • growth stimulation
    • immune response
      • activation

      Chemical classification

      • hormone
        • genome-encoded
          • cytokines
            • TGF-beta family

        Composition

        mature protein (2 times)

        Sequence
        ALDTNYCFS STEKNCCVR QLYIDFRKD 
        LGWKWIHEP KGYHANFCL GPCPYIWSL 
        DTQYSKVLA LYNQHNPGA SAAPCCVPQ 
        ALEPLPIVY YVGRKPKVE QLSNMIVRS 
        CKCS

        Links to other resources

        UniProt P01137
        Ensembl ENST00000221930
        • Anatomical structure: mucosa_of_large_intestine

        • Anatomical structure: mucosa_of_small_intestine

        • Anatomical structure: fat_cell

          • Several cytokines and related factors are synthesised within adipose tissue, including TGF-β. [1]

          Influenced by:

          • vasorin
            in smooth_muscle_cell
            • We found that vasorin directly binds to transforming growth factor (TGF)-β and attenuates TGF-β signaling in vitro. [20]
        • Anatomical structure: adipose_tissue

          • Several cytokines and related factors are synthesised within adipose tissue, including TGF-β. [1]
        • Anatomical structure: keratinocyte

          • TGFbeta1, a potent keratinocyte growth inhibitor, has been shown to be overexpressed in keratinocytes in certain inflammatory skin diseases. [3]
        • Anatomical structure: osteoblast

          • Osteoblasts expresses mRNA transcripts of TGF-beta1, TGF-beta2, TGF-beta 3, TGF-beta type I and type II receptors. [21]
        • Anatomical structure: adrenal_cortex

          • TGF-beta1 is an important regulator of human adrenal development. [22]
          • TGF-beta1 and its receptor (type II) are expressed in human adrenocortical cells. [22]
          • TGF-beta1 reduces the proliferation of the adrenocortical cancer cell line in vitro. [22]

          Influenced by:

          • AR
            in adrenal_cortex
            • In a human adrenocortical cell line, DHT is capable of up-regulating both TGF-beta1 mRNA and protein. [22]
        • Anatomical structure: hepatocyte

          • Cytokines from the TGF-beta family play a role in liver development, by induction of Vg1. [2]
          • In the normal adult liver,sinusoidal endothelial cells and Kupffer cells have relatively high, constitutive levels of mRNA for TGF-beta1 and lower but detectable levels for TGF-beta2 and TGF-beta3, whereas stellate cells express very little TGF-beta in the normal state,and hepatocytes essentially none. [23]
        • Anatomical structure: Kupffer_cell_stellate_cell_of_liver

        • Anatomical structure: cell_of_endometrium_of_uterus

          • TGF-beta 1 treatment in vitro acts directly on isolated endometrial epithelial cells, independently suppressing promatrilysin protein expression. [24]
          • TGF-b1 expression is known to be autoinductive and influenced by other growth factors in several cell types, including human endometrial stromal cells. [25]
          • In women, expression of TGF-b1, -b2 and -b3 and the type II receptor occurs in all cell types of the endometrium. [25]

          Influenced by:

          • TGF-beta type II receptor
            in cell_of_endometrium_of_uterus
            • TGF-beta 1 has been shown to decrease TGF-beta 2 and TGF-beta 3 expression while enhancing its own expression. [24]
        • Anatomical structure: osteoclast

        • Anatomical structure: peritoneal_mesothelial_cell

          Influenced by:

          • leptin receptor
            in peritoneal_mesothelial_cell
            • The TGF-beta synthesis induced by leptin was amplified by glucose through increased leptin receptor expression. [26]
        • Anatomical structure: lipocyte_of_liver

          Influenced by:

          • angiotensin II type 1 receptor
            in lipocyte_of_liver
            • Angiotensin II receptor antagonist may also suppress the HSC activation through the decrease of TGF-beta1. [27]
        • Anatomical structure: sinusoidal_endothelial_cell

        • Anatomical structure: macrophage

          • Subtype THP-1 cells secrete TGF-beta1 into the medium by forming a functional complex with the latent TGF-beta1-binding protein. We conclude that subtype THP-1 cells could not take up Ac-LDL because ScR was inhibited (leading to a loss of function) caused by the secreted TGF-beta1. [28]

        Targets

        CellTGF-beta type II receptorvasorin
        adrenal cortex Present
        aorta Present
        brain Present
        cell of endometrium of uterus Present
        Influences
        • TGF-beta 1
        • LIF
        • interleukin 6
        dendritic cell in lymphoid tissues follicular Present
        heart Present
        kidney Present
        lung Present
        mammary gland Present
        osteoblast Present
        placenta Present
        Present
        skeleton muscle Present
        smooth muscle cell Present
        Phenotypes
        • negative regulation of transforming growth factor beta receptor signaling pathway
        Influences
        • TGF-beta 1
        umbilical cord Present
        umbilical vein Present
        umbilical vein endothelial cells Present
        Reference