Transforming Growth Factor-β1 Suppresses Thyrotropin-Induced Na+/I- Symporter Messenger RNA and Protein Levels in FRTL-5 Rat Thyroid Cells

Thyroid ◽  
1997 ◽  
Vol 7 (5) ◽  
pp. 789-794 ◽  
Author(s):  
AKIO KAWAGUCHI ◽  
MASATO IKEDA ◽  
TOYOSHI ENDO ◽  
TAKAHIKO KOGAI ◽  
ASAKO MIYAZAKI ◽  
...  
Keyword(s):  
Growth Factor ◽  
Messenger Rna ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Thyroid Cells ◽  
Protein Levels ◽  
Rat Thyroid

Immune imbalance of regulatory T/type 2 helper cells in the pathogenesis of allergic rhinitis in children

2015 ◽  
Vol 130 (1) ◽  
pp. 89-94 ◽  
Author(s):  
R Sun ◽  
X-Y Tang ◽  
Y Yang
Keyword(s):  
Allergic Rhinitis ◽  
Growth Factor ◽  
Messenger Rna ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Clinical Severity ◽  
Helper Cell ◽  
Helper Cells ◽  
Immune Imbalance

AbstractObjectives:To determine the role of regulatory T/type 2 helper cell-mediated immune imbalance in the pathogenesis of allergic rhinitis and examine the association between clinical severity and regulatory T/type 2 helper cell-mediated immune imbalance.Methods:Levels of interleukins 4 and 5 and transforming growth factor β1, and expression of FOXP3 and GATA3 (which are functionally related to regulatory T and type 2 helper cells, respectively), were evaluated in 46 allergic rhinitis patients and 42 healthy subjects.Results:Compared to controls, allergic rhinitis patients showed significantly higher interleukin 4 and 5 levels, but lower transforming growth factor β1 levels. Furthermore, FOXP3 messenger RNA expression was lower in allergic rhinitis patients, while GATA3 messenger RNA and protein expression was significantly higher. Regulatory T/type 2 helper cell ratio was inversely correlated with clinical symptom scores.Conclusion:Regulatory T/type 2 helper cell immune imbalance may contribute to allergic rhinitis development. These findings provide a new insight into disease pathogenesis and potential therapeutic approaches.

scholarly journals Requirement of Cyclin D1 in Mesangial Cell Mitogenesis

2000 ◽  
Vol 11 (8) ◽  
pp. 1398-1408
Author(s):  
STEFAN LANG ◽  
ANDREA HARTNER ◽  
R. BERND STERZEL ◽  
HARALD O. SCHÖCKLMANN
Keyword(s):  
Growth Factor ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Transforming Growth Factor ◽  
D1 Protein ◽  
Transforming Growth Factor Β1 ◽  
Protein Levels ◽  
Cyclin D1 Protein

Abstract. Hyperplasia of mesangial cells (MC) is a frequent finding in glomerulonephritis. The control and function of cyclin D1, a regulator of cell cycle progression, in MC proliferation in vivo and in vitro were investigated. In a rat model of mesangioproliferative glomerulonephritis, increases in the number of cyclin D1-positive MC nuclei were prominent on day 5 of the disease, preceding the peak of MC hyperplasia. In growth-arrested rat MC in culture, mitogenic stimulation with serum or platelet-derived growth factor (PDGF) led to rapid increases in cyclin D1 protein expression. Transforming growth factor-β1 inhibited PDGF induction of cyclin D1 protein at 12 h. In an examination of the subcellular distribution of cyclin D1, it was observed that stimulation of MC with PDGF for 6 h caused translocation of cyclin D1 from the cytoplasm into the nucleus. Coincubation with PDGF and transforming growth factor-β1 completely inhibited this effect, without altering the cellular cyclin D1 protein abundance at that time point. To test whether reduction of cyclin D1 protein levels was sufficient to inhibit mitogenesis, MC were transfected with antisense oligonucleotides (ODN) complementary to rat cyclin D1 mRNA. Antisense ODN against cyclin D1 reduced the serum- or PDGF-induced protein expression of cyclin D1 to 27 or 10% of control levels, respectively. These inhibitory effects were correlated with diminished cyclin-dependent kinase 4 activity. Antisense ODN against cyclin D1 also decreased the PDGF-induced increase in p21Waf-1 protein levels. The MC proliferation caused by serum or PDGF was markedly inhibited by antisense ODN against cyclin D1, as measured by [3H]thymidine uptake and cell counts. It is concluded that increased cyclin D1 protein expression of MC is required for MC proliferation. Targeting cyclin D1 expression may represent an effective means to inhibit MC proliferation in vitro and in vivo.

Transforming growth factor β1 and fibronectin messenger RNA in rat brain: Responses to injury and cell-type localization

Neuroscience ◽  
1993 ◽  
Vol 54 (4) ◽  
pp. 893-907 ◽  
Author(s):  
G.M. Pasinetti ◽  
N.R. Nichols ◽  
G. Tocco ◽  
T. Morgan ◽  
N. Laping ◽  
...  
Keyword(s):  
Growth Factor ◽  
Rat Brain ◽  
Messenger Rna ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Cell Type ◽  
Brain Responses

scholarly journals Interleukin-13 augments transforming growth factor-β1-induced tissue inhibitor of metalloproteinase-1 expression in primary human airway fibroblasts

2005 ◽  
Vol 288 (2) ◽  
pp. C435-C442 ◽  
Author(s):  
XiuXia Zhou ◽  
John B. Trudeau ◽  
Kathryn J. Schoonover ◽  
Jessica I. Lundin ◽  
Steve M. Barnes ◽  
...  
Keyword(s):  
Growth Factor ◽  
Protein Expression ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Tissue Inhibitor ◽  
Mrna Stabilization ◽  
Protein Levels ◽  
Human Airway ◽  
Tgf Β1

Tissue inhibitor of metalloproteinase (TIMP)-1 is a potent inhibitor of activated matrix metalloproteinases (MMPs) such as gelatinases and collagenases. TIMP-1 is induced by transforming growth factor-β1 (TGF-β1), but details regarding signaling pathways remain unclear. T-helper-2 cytokines also have profibrotic properties and can interact with TGF-β. In the present study, we examined the effects of interleukin (IL)-13 (2,500 pM) on TGF-β1 (200 pM)-induced expression of TIMP-1 mRNA and protein in primary human airway fibroblasts obtained from 57 human subjects. IL-13 alone had no effect on TIMP-1 mRNA or protein expression. However, IL-13 synergistically augmented TGF-β1-induced TIMP-1 mRNA and protein expression ( P < 0.001 vs. TGF-β1 alone). The upregulation of TIMP-1 by the combination of TGF-β1 and IL-13 involved increased transcription, with little effect on mRNA stabilization. Initial exploration of the pathways leading to the synergy determined that activation of the phosphatidylinositol 3-kinase (PI3K)-Akt pathway by IL-13 may have a negative effect on TIMP-1 production. The specific PI3K inhibitor LY-294002 in the presence of TGF-β1, IL-13, or the combination of the two caused significant increases in TIMP-1 mRNA expression, while LY-294002 increased TIMP-1 protein levels in the presence of IL-13 alone. These results suggest that IL-13 augments TGF-β1-induced profibrotic responses at both the mRNA and protein levels. Although IL-13 induced activation of PI3K-Akt, the activation did not contribute to the synergy observed with TGF-β1 plus IL-13 in TIMP-1 expression and in fact may dampen it. The mechanisms behind the synergy remain to be determined.

Enhanced expression of transforming growth factor-β1 during thyroid hyperplasia in rats

1994 ◽  
Vol 141 (1) ◽  
pp. 45-57 ◽  
Author(s):  
A Logan ◽  
C Smith ◽  
G P Becks ◽  
A M Gonzalez ◽  
I D Phillips ◽  
...  
Keyword(s):  
Growth Rate ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Total Serum ◽  
Ribonuclease Protection Assay ◽  
Mrna Levels ◽  
Rat Thyroid ◽  
Thyroid Hyperplasia ◽  
Tgf Β1

Abstract Transforming growth factor-β1 (TGF-β1) has been reported to influence the growth rate and iodine uptake and organification in vitro by isolated thyrocytes. We have determined changes in the expression and presence of TGF-β1 within the rat thyroid during goitre induction, and subsequent involution following goitrogen withdrawal. Hyperplastic goitres were induced in adult rats by administration of methimazole together with a low iodine diet for up to 12 weeks. Goitrogen-treated rats quickly became hypothyroid compared with controls, and exhibited thyroid hyperplasia and hypertrophy assessed by thyroid weight, and DNA and protein content (control: total serum thyroxine (T4) 66 ± 4 nmol/l, thyroid weight 5 ± 1 mg/100 g body weight, mean ± s.d., n = 10; 2 weeks goitrogen: T4 undetectable, thyroid weight 27 ± 4 mg/100 g, n = 10). Thyroid growth rate slowed subsequently between 2 and 10 weeks. Messenger RNA for TGF-β1 was compared in the thyroids and livers of control and goitrous rats by ribonuclease protection assay. Low levels of mRNA for TGF-β1 were detected in thyroids from control rats at all time-points, while TGF-β1 mRNA was barely detectable in liver. Thyroid TGF-β1 mRNA levels substantially and progressively increased at 1 and 2 weeks of goitrogen treatment respectively, and remained above control levels at 4 and 10 weeks. As thyroid involution occurred 4 weeks following goitrogen withdrawal, so thyroid TGF-β1 mRNA levels declined. In control animals, the cellular localization of TGF-β1 mRNA, determined by in situ hybridization, was found to be a subpopulation of follicular epithelial cells, and immunohistochemical co-localization of TGF-β1 and calcitonin identified these tentatively as parafollicular or C-cells. During goitre formation, abundant TGF-β1 mRNA and peptide were found to be widely distributed within the entire follicular epithelium. While this ubiquitous distribution had largely disappeared in the involuting gland, TGF-β1 peptide was retained within the parafollicular cells, which appeared more abundant than in thyroids from control animals. These results suggest that an increased local expression of TGF-β1, a putative growth inhibitor, during thyroid hyperplasia may contribute to the temporal stabilization of goitre size. Journal of Endocrinology (1994) 141, 45–57

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