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  • 1
    Electronic Resource
    Electronic Resource
    Insulin-like Growth Factor-II (IGF-II) and IGF Binding Proteins in Human Endometrium (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 626 (1991), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb37924.x
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  • 2
    Electronic Resource
    Electronic Resource
    Insulin-like growth factor I/somatomedin-C (IGF-I/SM-C) and glucocorticoids synergistically regulate mitosis in competent human fibroblasts (1983)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 116 (1983), S. 191-197 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In serum-free medium, insulin-like growth factor-I/somatomedin-C (IGF-I/SM-C) was weakly mitogenic for adult human fibroblasts in culture. However, in the presence of 0.5% human hypopituitary serum (HHS), which by itself had little effect, there was a marked dose-dependent response to IGF-I/SM-C with a 10- to 20-fold increase in [3H]thymidine incorporation at 25 ng/ml IFG-I/SM-C. With the further addition of dexamethasone or hydrocortisone to the combination of IGF-I/SM-C + 0.5% HHS, there was a dramatic synergistic effect resulting in a 60- to 70-fold increase in [3H]thymidine incorporation. This stimulation was two times greater than that seen with 20% FCS. In contrast, glucocorticoids had no effect in serum-free medium or with HHS alone. These [3H]thymidine incorporation results were clearly supported by cell replication studies. Dose-response curves for 125I IGF-I/SM-C binding and IGF-I/SM-C stimulation of [3H]thymidine incorporation were similar with 1/2 maximal effects for both at 5 ng/ml. However, the striking synergism seen with glucocorticoids occurred in the absence of any glucocorticoid-induced change in IGF-I/SM-C binding, indicating that the interaction of IGF-I/SM-C and glucocorticoids occurs at a postreceptor level. These data demonstrate that in the presence of a low concentration of HHS, IGF-I/SM-C and glucocorticoids stimulate complete cell cycle traverse and replication of human fibroblasts.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041160210
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  • 3
    Electronic Resource
    Electronic Resource
    Hormonal control of the replication of human fetal fibroblasts: Role of somatomedin C/insulin-like growth factor I (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 128 (1986), S. 47-54 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Sparse cultures of fetal and postnatal human fibroblasts were equivalent in their responsiveness to the mitogenic action of somatomedin C/insulin-like growth factor I (SM-C/IGF-I). At both developmental stages, the addition of SM-C/IGF-I (100 ng/ml) increased cell number at day 3 1.4-fold in serum-free medium and 2-fold in the presence of 0.25% human hypopituitary serum. Furthermore, dose-response curves indicated that there was no difference in the sensitivity of fetal and postnatal fibroblasts to the growth-promoting effects of SM-C/IGF-I, with a half-maximal response occuring at 6 ng/ml SM-C/IGF I. This biological action of SM-C/IGF-I correlated with SM-C/IGF-I binding to fetal and postnatal fibroblast monolayers. Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) also stimulated replication of fetal and postnatal fibroblasts. The mitogenic effects of SM-C/IGF-I, EGF, and PDGF were additive. Dexamethasone, which alone had no effect, was synergistic with SM-C/IGF-I in stimulating replication of postnatal fibroblasts. The combination of SM-C/IGF-I (100 ng/ml), dexamethasone (10-7 M), EGF (10 ng/ml), and PDGF (5 ng/ml) had the same mitogenic effectiveness as 10% calf serum (CS) in postnatal cells. In marked contrast, there was no mitogenic interaction between SM-C/IGF-I and dexamethasone in fetal fibroblasts. In fetal cells, SM-C/IGF-I + EGF + PDGF ± dexamethasone could only account for 50% of the activity of 10% CS. Moreover, fetal cells were 50-100% more responsive than postnatal cells to the proliferative effect of serum.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041280109
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  • 4
    Electronic Resource
    Electronic Resource
    Density-associated loss of functional receptors for somatomedin-C/insulinlike growth factor I (SM-C/IGF-I) on cultured human fibroblast monolayers (1984)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 121 (1984), S. 419-424 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The mitogenic activity of somatomedin-C/insulinlike growth factor-I (SM-C/IGF-I) appears to be greatly influenced by cell culture conditions, especially the presence of other growth factors and nutrients in the culture medium. To investigate the effect of cell density on SM-C/IGF-I activity, we have evaluated SM-C/IGF-I binding and stimulation of DNA synthesis and cell replication as a function of cell density in cultured human fibroblast monolayers. At fibroblast concentrations of 2.7 × 105 and 1.48 × 106 cells per 60-mm dish, specific binding of [125I]SM-C/IGF-I per 106 cells was 170% higher in sparse than dense monolayers (9.3% vs. 3.4%). Increased binding in sparse monolayers was attributable to approximately twice as many receptors in sparse as in dense cells (31,000 vs. 16,000 sites per cell), as well as to a modest increase in the affinity constant. Similarly, half-maximal stimulation of [methyl-3H]thymidine incorporation was achieved at SM-C/IGF-I concentrations of 2.5 ng/ml in sparse cells but required 20 ng/ml in dense cells. Although this required only 45% occupancy of membrane receptors on sparse cells, and almost 80% occupancy on dense cells, the total number of occupied receptors was similar in both sparse and dense cells (approximately 13,000 receptors/cell for half-maximal stimulation). The presence of increased numbers of “functional receptors” on sparse fibroblasts thus results in enhanced sensitivity to SM-C/IGF-I stimulation of DNA synthesis and cell replication. Progressive decreases in the number of functional receptors, secondary to cell crowding, may contribute to density-dependent inhibition of fibroblast growth.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041210221
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  • 5
    Electronic Resource
    Electronic Resource
    Comparative effects of somatomedin C and insulin on the metabolism and growth of cultured human fibroblasts (1985)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 122 (1985), S. 133-141 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: At concentrations of 25 ng/ml in serum-free medium, somatomedin C (SM-C) and insulin stimulated 3H-thymidine incorporation in adult human fibroblasts 4- and 1.5-fold, respectively. The presence of 0.25% human hypopituitary serum (HHS), which by itself had little effect, enhanced the mitogenicity of both SM-C and insulin. Furthermore, 10-7 M dexamethasone dramatically potentiated SM-C stimulation (70-fold) and insulin stimulation (28-fold) of 3H-thymidine incorporation. With dexamethasone and 0.25% HHS, significant stimulation of DNA synthesis was seen at 2.5 ng/ml for both SM-C and insulin. The effects of SM-C and insulin on 3H-thymidine incorporation were additive. These 3H-thymidine incorporation results were clearly supported by cell replication studies. On the other hand, SM-C and insulin had equivalent, non-additive effects on RNA and protein synthesis and protein degradation. Half-maximal effects were seen for both peptides on all three metabolic processes at 2-5 ng/ml. In contrast to their synergism with SM-C in the stimulation of DNA synthesis and cell replication, HHS and dexamethasone did not enhance SM-C stimulation of RNA or protein synthesis or protein degradation. These data indicate that SM-C and insulin stimulate DNA, RNA, and protein synthesis, protein degradation, and cell replication in adult human fibroblasts at nanomolar concentrations, suggesting that each peptide is capable of acting through its own receptor. Both SM-C and insulin are also capable of synergism with low concentrations of serum and dexamethasone in the stimulation of DNA synthesis and cell replication. It is proposed that SM-C and insulin both participate in the regulation of cell growth and metabolism in vivo.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041220120
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  • 6
    Electronic Resource
    Electronic Resource
    Insulin-like growth factor II binding and action in human fetal fibroblasts (1987)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 133 (1987), S. 560-566 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: To investigate the role of insulin-like growth factor II (IGF-II) in human prenatal growth, IGF-II binding and biological action were studied in four lines of fetal and three lines of postnatal human fibroblasts. Specific biniding of IGF-II was similar in both groups: 15.7% and 14.9% for fetal and postnatal fibroblasts, respectively. This was 5-10 times the amount of IGF-I binding found in these cells. IGF-I and IGF-II caused dose-dependent increases in [14C]aminoisobutyric acid (AIB) uptake. IGF-II was sevenfold less potent than IGF-I in stimulating this metabolic response in both fetal and postnatal fibroblasts. The maximal effect of IGF-II in stimulating [14C]AIB uptake approached that of IGF-I. Similar results were obtained when IGF-I and IGF-II stimulation of [3H]thymidine incorporation was compared in fetal and postnatal fibroblasts. Incubation in the presence of alphalR-3, a monoclonal antibody to the type I IGF receptor, inhibited the ability of both IGF-I and IGF-II to stimulate [14C]AIB uptake and [3H]thymidine incorporation in fetal and postnatal cells. A monoclonal antibody to the insulin receptor did not affect IGF action. These data indicate that IGF-II is a potent metabolic and mitogenic stimulus for human fetal firoblasts. However, despite the presence of abundant type II IGF receptors on both fetal and postnatal human fibroblasts, IGF-II stimulation of amino acid transport and DNA synthesis appears to be mediated through the type I rather than through its own type II IGF receptor.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041330318
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  • 7
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    Screening a large pediatric cohort with GH deficiency for mutations in genes regulating pituitary development and GH secretion: Frequencies, phenotypes and growth outcomes (2018)
    Elsevier
    Details
    Publication Date: 2018-10-01
    Electronic ISSN: 2352-3964
    Topics: Biology , Medicine
    Published by Elsevier
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  • 8
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    Immunodeficiency Associated with a STAT-5b Mutation and Growth Hormone Insensitivity. (2004)
    American Society of Hematology
    Details
    Publication Date: 2004-11-16
    Description: We recently identified a homozygous mutation in the STAT-5b (signaling transducer and activator of transcription 5b) gene in a female patient with growth hormone insensitivity. The patient had significant growth retardation (height -7.5 SD), despite normal levels of growth hormone (GH) and GH binding protein. Analysis of the GH receptor signaling pathways indicated that the mutation (Ala630 to Pro630) resulted in a protein that could not be activated by GH, and subsequent dysregulation of STAT-5b-dependent genes, such as IGF-I and IGFBP-3. This abstract details an immunodeficiency due to a lack of functional STAT5b. Clinically, the patient had chronic diarrhea as an infant, and suffered several severe infections, including persistent lymphocytic interstitial pneumonia (LIP), a condition associated with children who are HIV-positive or immunodeficient. Laboratory studies showed hypergammaglobulinemia, T-cell lymphopenia with a normal CD4:CD8 T-cell ratio, and total B and NK cells within the normal range. Immunologic analysis showed decreased interleukin (IL)-2 receptor α expression in response to IL-2 on both CD4 and CD8 T cells, despite normal proliferation to mitogens, and normal anti-CD3 proliferation by CFSE analysis. IL-2 mediated γc (common gamma chain) upregulation, induction of CD40-ligand and interferon-γ production by intracellular cytokine analysis in response to either the bacterial superantigen SEB or anti-CD3/anti-CD28 mAb stimulation were normal, suggesting that STAT5b is not necessary for these functions. Importantly, perforin expression in response to IL-2 was decreased in CD8 T cells suggesting that both decreased CD8 number and function contribute to this immunodeficiency. Interestingly, NK cells failed to increase adhesion molecules CD54 or CD58 in response to IL-2 suggesting impaired NK cell function. Lastly, EBV transformed B cell lines were unable to phosphorylate STAT5b in response to IL-2 and IL-7 suggesting an intrinsic B cell defect that may affect immunoglobulin production. Thus, the STAT5b −/ − mutation appears to limit the effects of important γc-containing cytokines on CD4, CD8, NK and B cells, resulting in increased susceptibility to infection.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 9
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    In Vitro and in Vivo Characterization of MOD-4023, a Long-Acting Carboxy-Terminal Peptide (CTP)-Modified Human Growth Hormone (2016)
    American Chemical Society
    Details
    Publication Date: 2016-01-18
    Print ISSN: 1543-8384
    Electronic ISSN: 1543-8392
    Topics: Chemistry and Pharmacology
    Published by American Chemical Society
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  • 10
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    Decreased Generation and Function of CD4+CD25hi T Regulatory Cells in Human STAT5b Deficiency. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: CD4+ CD25+ regulatory T cells (Tregs) are a well characterized population of cells that play an important role in limiting inflammation and in the maintenance of tolerance to self. Here we describe a patient with a homozygous missense mutation (A630P) in the STAT5b gene who clinically displays immune dysregulation in association with decreased numbers and function of Tregs. Freshly isolated or in vitro-derived CD4+CD25high Treg cells from this patient had low Foxp3 expression, did not suppress non Treg T-cell proliferation, and were unable to kill autologous CD4+CD25neg T cells compared to controls. CD25 expression in response to IL-2 did not increase on freshly isolated CD4 T cells and was decreased on T-cell blasts derived from the patient. The patients mother who was heterozygous for this mutation had an intermediate phenotype for all of these immune abnormalities, indicating a gene dosage effect. In contrast, IL-2 upregulated expression of the common gamma chain (γc) cytokine receptor and perforin by T cells normally. Activation-induced T-cell expression of CD40-ligand (CD154) and interferon-gamma (IFN-γ) were also normal in the patient. These results suggest that the STAT5 pathway propagates an important IL-2 mediated signal that is necessary for Treg generation and function in humans in vivo.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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