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1
Content available remote

Apoptosis and autophagy induced by TGF-beta1 in bovine mammary epithelial BME-UV1 cells

100%
Gajewska M., Gajkowska B., Motyl T.
Journal of Physiology and Pharmacology. Supplement
|
2005
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tom 56
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nr 3
143-157
Mammary gland growth and involution is based on a dynamic equilibrium between proliferation and apoptosis of mammary gland epithelial cells (MEC). TGF-ß1 is an important antiproliferative and apoptogenic factor for mammary gland epithelial cells, acting in auto/paracrine matter and thus considered an important local regulator of mammary tissue involution. So far the studies on mammary gland involution concerned only apoptosis as a type I of MEC programmed cell death (PCD). Autophagy is known to be type II of PCD and this paper is the first, supporting evidence for the TGF-ß1-induced autophagy in bovine mammary epithelial cell line BME-UV1, as a distinct to apoptosis type of PCD. Laser scanning cytometry and confocal microscopy were used for analysis of MAP1 LC3 and Beclin1 expression - two proteins considered being the most reliable biochemical markers of autophagy. The significant increase of MAP1 LC3 and Beclin1 expression in cells treated with TGF-ß1 (2 ng/ml) was observed. Ultrastructural observation in electron microscopy revealed that autophagy is not only alternative, but also complementary to apoptosis type of cell death in TGF-ß1-treated bovine MEC. It was manifested by typical morphological features of apoptosis (cell shrinkage, margination and condensation of chromatin) and autophagy (autophagosomes, autophagic vacuoles) in the same cell.
2
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Dissimilar effects of LY 294002 and PD 098059 in IGF-I- mediated inhibition of TGF-beta1 expression and apoptosis in bovine mammary epithelial cells

100%
Zarzynska J., Motyl T.
Journal of Physiology and Pharmacology. Supplement
|
2005
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tom 56
|
nr 3
181-193
In mammary epithelial cells (MEC) TGF-ß1 is the auto-/paracrine growth inhibitor and inducer of apoptosis and therefore is considered as an important local regulator of mammary tissue involution. However, the mechanisms of controlled TGF-ß1 expression in the course of bovine mammary gland remodelling are still unclear. Recent study performed in this laboratory support the evidence that TGF-ß1 expression in bovine MEC is regulated by hormones of somatotropic axis (GH, IGF-I and somatostatin). Present study was focused on the contribution of IGF-I-induced signaling pathways in anti-TGF-ß1 and anti-apoptotic effects of IGF-I. Laser scanning cytometry was applied for the measurement of TGF-ß1 content and apoptotic cell number in bovine BME-UV1 MEC. Involution of the bovine mammary gland in vitro was modeled by decreasing the availability of FBS for bovine MEC. Reducing FBS content in the medium from 10% to 0.5% evoked highly significant increase of TGF-ß1 expression and increase of apoptotic cell number. IGF-I (50 ng/ml) completely abrogated FBS deficiency-induced TGF-ß1 expression and apoptosis in bovine MEC. In order to establish which of the IGF-I signaling pathways contributed to anti-TGF-ß1 and anti-apoptotic effects, the inhibitors of PI3-kinase - (LY 294002) and MEK- (MAPKK for ERK) (PD 098059) mediated signaling pathways were applied to our model. The results clearly showed that inhibition of PI3-K reverses the ability of IGF-I to suppress TGF-ß1 expression and apoptosis. An inhibition of ERK1/2 pathway even potentiated inhibitory effect of IGF-I on TGF-ß1 expression, but partially abrogated anti-apoptotic effect of IGF-I. In conclusion, the results of the study indicate that PI3-K/Akt pathway contributed significantly to the inhibition of TGF-ß1 expression by IGF-I, whereas both PI3-K/Akt and ERK1/2 pathways are involved in the anti-apoptotic effect of IGF-I in bovine MEC.
3
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Evidence of TWIST1 and transforming growth factor-beta1 aberrant expressions as novel therapeutic targets in modulating the severity of osteoarthritis with focus on biologic agents

100%
Ye C., Ye J., Wu H., Zhang F., Liu Y.
Journal of Physiology and Pharmacology
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2020
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tom 71
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nr 6
4
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Transforming growth factor-beta1 upregulates myostatin expression in mouse C2C12 myoblasts

100%
Budasz-Swiderska M., Jank M., Motyl T.
Journal of Physiology and Pharmacology. Supplement
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2005
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tom 56
|
nr 3
195-214
Myostatin (MSTN) and transforming growth factor-ß1 (TGF-ß1) belong to the same TGF-ß superfamily of proteins. They are involved in regulation of skeletal muscle growth and development as well as muscle catabolism. The aim of the present study was to investigate the relationship between mstn and TGF-ß1 expression in proliferating and differentiating mouse C2C12 myoblasts cultured in normal and catabolic conditions and to evaluate the effect of exogenous TGF-ß1 as well as "knock down" of TGF-ß1 receptor type II on mstn expression in proliferating and differentiating myogenic cells. The direct effect of TGF-ß1 on myostatin was also examined. Myostatin expression increased gradually with cell confluency in proliferating cultures, while the level of TGF-ß1, detected in the form of a 100 kDa small latent complex diminished. Myostatin expression was accompanied by a partial cell cycle arrest. Three forms of myostatin were found: a 52 kDa precursor, a 40 kDa latency associated propeptide, and a 26 kDa active peptide. A decrease in myostatin and TGF-ß1 levels was observed during the first three days of differentiation, which was subsequently followed by significant increase of their expression during next three to four days of differentiation. Catabolic state induced by dexamethasone significantly increased the level of all forms of myostatin as well as latent (100 kDa) and active (25 kDa) forms of TGF-ß1 in differentiating myoblasts in a dose dependent manner. Exogenous TGF-ß1 (2 ng/ml) significantly increased myostatin levels both in proliferating and differentiating C2C12 myoblasts, whereas silencing of the TGF-ß1 receptor II gene significantly lowered myostatin level in examined cells. The presented results indicate that TGF-ß1 may control myostatin-related regulation of myogenesis through up-regulation of myostatin, predominantly in the course of terminal differentiation and glucocorticoid-dependent catabolic stimulation.
5

Potential role of transforming growth factor beta 1 in drug resistance of tumor cells

100%
Stoika R., Yakymovych M., Souchelnytskyi S., Yakymovych I.
Acta Biochimica Polonica
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2003
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tom 50
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nr 2
Acquired drug resistance of tumor cells is frequently observed in cancer patients un­dergoing chemotherapy. We studied murine leukemia L1210 cells sensitive and resis­tant to the cytotoxic action of cisplatin and showed that cisplatin-resistant leukemia cells were also refractory to TGF /β1-dependent growth inhibition and apoptosis. Ad­dressing the question about the mechanisms responsible for the cross-resistance to cisplatin and TGF /β1, we found that cisplatin- and TGF /β1-resistant L1210 cells pos­sessed a decreased expression of type I TGF /β1 receptor, while the expression of type II TGFβ1 receptor was not affected. Western blot analysis of Smad proteins 2, 3, 4, 6, and 7, which participate in signal transduction pathway down-stream of the TGF /β1 receptors, revealed an increased expression of Smad 6, inhibiting TGF β1 action, only in cisplatin- and TGFβ1-resistant L1210 cells. TGFβ1 and especially the cytotoxic mis­tletoe agglutinin increased Smad 6 expression in TGF β1-sensitive but not in TGF /β1-resistant L1210 cells. TGF /β1-resistant L1210 cells also differed from TGF /β1-sensitive cells by the lack of expression of the pro-apoptotic p53 protein and higher level of expression of the anti-apoptotic Bcl-2 protein. Thus, the described co-expression of tumor cell refractoriness to an anti-cancer drug and to the inhibitory cytokine TGF β1 is accompanied by multiple changes in the TGF β1 signal transduction pathway and in other regulatory systems of the target cells. Besides, we found that various anti-tumor drugs and cytotoxic plant lectins increased the level of TGF β1 expression in both TGF β1-sensitive and -resistant L1210 cells. A hypothesis is proposed that TGF β1 can at least partly mediate the effect of cell-stressing agents and, thus, the development of TGF β1 resistance may be responsible for the appearance of tumor cell refractoriness to the action of some anti-cancer drugs.
6

The immunoreactivity of TGF-beta1 in non-alcoholic fatty liver disease

84%
Kempinski R., Neubauer K., Poniewierka E., Kaczorowski M., Halon A.
Folia Histochemica et Cytobiologica
|
2019
|
tom 57
|
nr 2
7
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Transcriptional pattern of TGF-beta1 inhibitory effect on mouse C2C12 myoblasts differentiation

84%
Wicik Z., Sadkowski T., Jank M., Motyl T.
Polish Journal of Veterinary Sciences
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2010
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tom 13
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nr 4
The aim of the present study was to define the effect of TGF-β1 on C2C12 myoblasts myogenesis. TGF-β1 together with its receptor is a negative auto-paracrine regulator of myogenesis, which influences the proliferation, differentiation, and functions of muscle cells. TGF-β1 exerts highly significant inhibitory effect on differentiation of C2C12 mouse myoblasts manifested by the impairment of cell fusion and very low expression of myosin heavy chain. The study of differentiating C2C12 mouse myoblasts treated with TGF-β1 revealed 502 genes (436 down-regulated and 66 up-regulated) with statistically different expression. TGF-β1-regulated genes were identified to be involved in 29 biological processes, 29 molecular functions groups and 59 pathways. The strongest inhibiting effect of TGF-β1 was observed in the cadherin and Wnt pathways. The key-genes that could play the role of TGF-β1 targets during myoblasts differentiation was identified such as: Max, Creb1, Ccna2, Bax, MdfI, Tef, Tubg1, Cxcl5, Rho, Calca and Lgals4.
8
Content available remote

Transforming growth factor-beta1 and tumor necrosis factor-a concentration in serum during disturbed lymph flow from a liver in rats

84%
Beck B.
Journal of Physiology and Pharmacology
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2017
|
tom 68
|
nr 1
9

Clinical parameters of inflammatory bowel disease in children do not correlate with four common polymorphisms of the transforming growth factor beta1 gene

84%
Liberek A., Jakobkiewicz-Banecka J., Kloska A., Swiderska J., Kmiec Z., Luczak G., Wierzbicki P., Liberek T., Marek K., Plata-Nazar K., Sikorska-Wisniewska G., Kaminska B., Wegrzyn G.
Acta Biochimica Polonica
|
2011
|
tom 58
|
nr 4
Transforming growth factor β1 (TGF-β1) is a cytokine affecting cell proliferation and development, which also has an immunomodulatory activity. Correlations between polymorphisms of the TGF-β1 gene and clinical parameters of inflammatory bowel disease (IBD) were reported previously in adults. Here, we tested whether such correlations occur in pediatric patients suffering from IBD. One hundred and four pediatric IBD patients were involved in this study. Among them, 36 were diagnosed with Crohn's Disease (CD) and 68 were diagnosed with ulcerative colitis (UC). The control group consisted of 103 children, in which IBD was excluded. TGF-β1 levels were determined in plasma and intestinal mucosa samples. The presence of the TGF β1 protein and the amount of TGF β1 mRNA were estimated in intestinal mucosa by immunohistochemistry and reverse transcription Real-Time PCR, respectively. Four common polymorphisms of the TGF-β1 gene were investigated: -800G/A, -509C/T, 869T/C and 915G/C. No significant correlation between TGF-β1 genotypes and (i) TGF-β1 levels in plasma and tissue samples, (ii) TGF-β1 gene expression efficiency in intestinal mucosa, (iii) IBD clinical parameters and (iv) inflammatory activity could be detected in children suffering from IBD. We conclude that, contrary to previous suggestions, the four common polymorphisms of the TGF-β1 gene do not influence the susceptibility to or clinical parameters of IBD in the tested population of children.
10

Elevated level of ambient glucose stimulates the synthesis of high-molecular-weight hyaluronic acid by human mesangial cells. The involvement of transforming growth factor beta1 and its activation by thrombospondin-1

84%
Yevdokimova N. Y.
Acta Biochimica Polonica
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2006
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tom 53
|
nr 2
The dysregulation of the metabolism of glycosaminoglycan and protein components of extracellular matrix (ECM) is a typical feature of diabetic complications. High glucose-induced enrichment of ECM with hyaluronan (HA) not only affects tissue structural integrity, but influences cell metabolic response due to the variety of effects depending on the HA polymer molecular weight. TSP-1-dependent activation of TGFβ1 axis is known to mediate numerous matrix disorders in diabetes, but its role concerning HA has not been studied so far. In this work we demonstrated that 30 mM d-glucose increased the incorporation of [3H]glucosamine in high-molecular-weight ( > 2000 kDa) HA of medium and matrix compartments of human mesangial cultures. Simultaneously, the synthesis of HA with lower molecular weight and HA degradation were not altered. The cause of the increased high-molecular-weight HA synthesis consisted in the up-regulation of hyaluronan synthase (HAS) 2 mRNA without alterations of the expression of HAS3, which generates HA of lower molecular weight. d-Glucose at 30 mM also stimulated the production of transforming growth factor β1 (TGFβ1), the excessive activation of which was determined by the up-regulation of thrombospondin-1 (TSP-1). The blockage of TGFβ1 action either by neutralizing anti-TGFβ1 antibodies or by quenching the TGFβ1 activation (with TSP-1-derived synthetic GGWSHW peptide) abolished the effect of high glucose on HAS2 mRNA expression and normalized the synthesis of HA. Exogenous human TGFβ1 had the same effect on HAS2 expression and HA synthesis as high glucose treatment. Therefore, we supposed that TSP-1-dependent TGFβ1 activation is involved in the observed high glucose effect on HA metabolism. Since high-molecular-weight HA polymers, unlike middle- and low-molecular weight HA oligosaccharides, are known to possess anti-inflammatory and anti-fibrotic functions, we suppose that the enrichment of mesangial matrix with high-molecular-weight HA may represent an endogenous mechanism to limit renal injury in diabetes.
11

TGF-beta1, IL-10 and IL-4 in colostrum of allergic and nonallergic mothers

67%
Marek A., Zagierski M., Liberek A., Aleksandrowicz E., Korzon M., Krzykowski G., Kaminska B., Szlagatys-Sidorkiewicz A.
Acta Biochimica Polonica
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2009
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tom 56
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nr 3
411-414
Objective: To determine transforming growth factor (TGF) β1, interleukin (IL) 4, and IL-10 concentrations in human milk and to assess the relationship between allergic disorders in mothers and the content of the interleukins in their milk. Material and methods: Thirty allergic and 46 healthy mothers were included in the study. Colostrum was collected 2-3 days after delivery. Cytokine concentrations were determined with commercial enzyme-linked immunosorbent systems. Results: TGF-β1was found in milk from 23 women in the control group (53.49%) and 11 in the allergy group (37.93%). When TGF-β1 was present, the median concentration was higher in the allergy group than in the control (61.5 and 30.4 pg/mL, respectively; P < 0.004). IL-10 was present in the colostrum of all the women and the median IL-10 concentration did not differ between the allergy (50.5 pg/mL) and control (51.5 pg/mL) groups. The probability of occurrence of a positive IL-4 value in the allergy group was greater than in the control group (chi-squared [df = 1] = 2.60, P < 0.053). Median IL-4 level did not differ significantly between the two groups (0.5 and 0.5 pg/mL respectively). Conclusions: TGF-β1 was detected less often in the colostrum of allergic mothers than in that of mothers without allergy (but the difference was not statistically significant). IL-4 was found more often in the colostrum of allergic mothers than nonallergic ones. The allergy status did not correlate with IL-10 concentration.
12
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Local regulators of seasonal reproduction processes in uterus masculinus of an adult male European bison (Bison bonasus, Linnaeus 1758)

67%
Tabecka-Lonczynska A., Mytych J., Solek P., Abrachamowicz A., Welz M., Koziorowski M.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 5
13

Acetylcholine receptor-induced experimental myasthenia gravis: what have we learned from animal models after three decades?

67%
Baggi F., Antozzi C., Toscani C., Cordiglieri C.
Archivum Immunologiae et Therapiae Experimentalis
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2012
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tom 60
|
nr 1
14

Influence of IGF-1, TGF-beta1 and bFGF on gene expression in cruciate ligament and dermal fibroblasts

67%
Hyc A., Zeberkiewicz M., Osiecka-Iwan A.
Folia Biologica
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2018
|
tom 66
|
nr 2
15

Influence of cartilage interstitial fluid on gene expression in dermal fibroblasts

67%
Hyc A., Moskalewski S., Stankevic D., Osiecka-Iwan A.
Folia Biologica
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2017
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tom 65
|
nr 1
16

Influence of IGF1, TGFbeta1, bFGF and G-CSF/M-CSF on the mRNA levels of selected matrix proteins, cytokines, metalloproteinase 3 and TIMP1 in rat synovial membrane cells

67%
Osiecka-Iwan A., Moskalewski S., Hyc A.
Folia Histochemica et Cytobiologica
|
2016
|
tom 54
|
nr 3
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