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1

A targeted multiple antigenic peptide vaccine augments the immune response to self TGF-beta1 and suppresses ongoing hepatic fibrosis

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Li Y., Wang W., Jia X., Zhai S., Wang X., Wang Y., Dang S.
Archivum Immunologiae et Therapiae Experimentalis
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2015
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tom 63
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nr 4
2

IL-6 contributes to the TGF-beta1-mediated epithelial to mesenchymal transition in human salivary gland epithelial cells

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Sisto M., Tamma R., Ribatti D., Lisi S.
Archivum Immunologiae et Therapiae Experimentalis
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2020
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tom 68
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nr 5
3

Polymorphisms in the genes encoding TGF-beta1, TNF-alpha, and IL-6 show association with type 1 diabetes mellitus in the Slovak population

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Javor J., Ferencik S., Bucova M., Stuchlikova M., Martinka E., Barak L., Strbova L., Grosse-Wilde H., Buc M.
Archivum Immunologiae et Therapiae Experimentalis
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2010
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tom 58
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nr 5
385-393
4
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The effect of acute and prolonged endurance exercise on transforming growth factor-ß1 generation in rat skeletal and heart muscle

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Czarkowska-Paczek B., Zendzian-Piotrowska M., Bartlomiejczyk I., Przybylski J., Gorski J.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 4
157-162
The serum level of the transforming growth factor-beta1 (TGF-ß1) is elevated after acute bouts of exercise and prolonged training, as well as after myocardial infarction. However, the source of this increase remains unclear. Contracting skeletal muscles are known to be the source of many cytokines. To determine whether skeletal or heart muscles produce TGF-ß1 during exercise, we investigated the effect of a single bout of acute exercise on TGF-ß1 generation in skeletal and heart muscles in untrained rats (UT, n=30) and in rats subjected to prolonged (6-week) endurance training (T, n=29). The UT and T (a day after final training) groups were subjected to an acute bout of exercise with the same work load. Rats from both groups were sacrificed and skeletal and heart muscle samples were collected before (pre), immediately after (0 h), or 3 hours (3 h) after acute exercise. TGF-ß1 mRNA was quantified by RT-PCR in these samples, and basal TGF-ß1 protein levels were determined in skeletal muscle in the UTpre and Tpre subgroups by ELISA. Acute exercise caused a non-significant increase in TGF-ß1 mRNA in skeletal muscle in UT0h rats, in compare to UTpre rats. There was a significant decrease of TGF-ß1 mRNA in the T0h group (p=0.0013) in compare to Tpre rats. Prolonged training caused a significant increase in TGF-ß1 mRNA (p=0.02); however, the TGF-ß1 protein level decreased (p=0.02). In heart muscle, there was a significant decrease of TGF-ß1 mRNA in UT0h (p=0.01) and UT3h (p=0.04) compared to UTpre rats. TGF-ß1 mRNA levels were unchanged in T0h and T3h compared to Tpre; basal TGF-ß1 mRNA expression after training was also unchanged (UTpre vs. Tpre). We conclude that physical exercise is a potent stimulus for inducing TGF-ß1 gene expression in skeletal muscle, but does not increase the protein level. Thus, skeletal and heart muscle do not contribute to increased serum levels of TGF-ß1 after physical exercise.
5

Monocytic MDSC as a source of immunosuppressive cytokines in chronic lymphocytic leukemia (CLL) microenvironment

100%
Kowalska W., Bojarska-Junak A.
Folia Histochemica et Cytobiologica
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2020
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tom 58
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nr 1
6

The effect of TGF-beta1 and Smad7 gene transfer on the phenotypic changes of rat alveolar epithelial cells

100%
Xu G. P., Li Q. Q., Cao X. X., Chen Q., Zhao Z. H., Diao Z. Q., Xu Z. D.
Cellular and Molecular Biology Letters
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2007
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tom 12
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nr 3
The aim of this study was to investigate whether transforming growth factor-β1 (TGF-β1) could induce alveolar epithelial-mesenchymal transition (EMT) in vitro, and whether Smad7 gene transfer could block this transition. We also aimed to elucidate the possible mechanisms of these processes. The Smad7 gene was transfected to the rat type II alveolar epithelial cell line (RLE-6TN). Expression of the EMT-associated markers was assayed by Western Blot and Real-time PCR. Morphological alterations were examined via phase-contrast microscope and fluorescence microscope, while ultrastructural changes were examined via electron microscope. TGF-β1 treatment induced a fibrotic phenotype of RLE-6TN with increased expression of fibronectin (FN), α-smooth muscle actin (α-SMA) and vimentin, and decreased expression of E-cadherin (E-cad) and cytokeratin19 (CK19). After transfecting the RLE-6TN with the Smad7 gene, the expression of the mesenchymal markers was downregulated while that of the epithelial markers was upregulated. TGF-β1 treatment for 48 h resulted in the separation of RLE-6TN from one another and a change into elongated, myofibroblast-like cells. After the RLE-6TN had been transfected with the Smad7 gene, TGF-β1 treatment had no effect on the morphology of the RLE-6TN. TGF-β1 treatment for 48 h resulted in an abundant expression of α-SMA in the RLE-6TN. If the RLE-6TN were transfected with the Smad7 gene, TGF-β1 treatment for 48 h could only induce a low level of α-SMA expression. Furthermore, TGF-β1 treatment for 12 h resulted in the degeneration and swelling of the osmiophilic multilamellar bodies, which were the markers of type II alveolar epithelial cells. TGF-β1 can induce alveolar epithelialmesenchymal transition in vitro, which is dependent on the Smads signaling pathway to a certain extent. Overexpression of the Smad7 gene can partially block this process.
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