scholarly journals Long Term Stabilization of Expanding Aortic Aneurysms by a Short Course of Cyclosporine A through Transforming Growth Factor-Beta Induction

PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e28903 ◽  
Author(s):  
Jianping Dai ◽  
Stéphanie Michineau ◽  
Grégory Franck ◽  
Pascal Desgranges ◽  
Jean-Pierre Becquemin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cyclosporine A ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Aortic Aneurysms ◽  
Short Course ◽  
Growth Factor Beta

The Effects of Cyclosporine on Protein Expression of P53 and Transforming Growth Factor-Beta in Human Renal Tubular Cells

2000 ◽  
Vol 6 (S2) ◽  
pp. 604-605
Author(s):  
H. Song ◽  
C. Wei
Keyword(s):  
Growth Factor ◽  
Cyclosporine A ◽  
Transforming Growth Factor Beta ◽  
Renal Cell ◽  
Transforming Growth Factor ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Cellular Apoptosis ◽  
Growth Factor Beta ◽  
Renal Tubular

Cyclosporine-A (CsA) is the widely used immunosuppressant drug in renal transplantation. However, the effects of cyclosporine-A are limited by a significant nephrotoxicity. The mechanisms of CsA-induced allograft nephropathy are remaining controversial. Recent study indicated that cellular apoptosis may contribute to the cyclosporine A-mediated cytotoxic action. To date, regarding the effects of cyclosporine A on renal cell apoptosis-related gene expression remain poorly defined. p53 is an important gene in control of renal cell growth and death. Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that has anti-proliferative as well as fibrogenic properties.We hypothesized that cyclosporine-A may increase p53 and TGF-β expression in renal tubular cells. These actions of cyclosporine-A may contribute to the cellular apoptosis, fibrosis and CsA-induced nephrotoxicity. Therefore, current study was designed to determine the effects of cyclosporine-A on the p53 and TGF-βl protein expression by immunohistochemical staining (IHCS) in cultured human tubular cells.

The isolation and long-term culture of normal human endometrial epithelium and stroma. Expression of mRNAs for angiogenic polypeptides basally and on oestrogen and progesterone challenges

1995 ◽  
Vol 108 (1) ◽  
pp. 323-331 ◽  
Author(s):  
L. Zhang ◽  
M.C. Rees ◽  
R. Bicknell
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Vascular Endothelial ◽  
Long Term Culture ◽  
Normal Human ◽  
Growth Factor Beta ◽  
Endometrial Epithelial Cells

A highly reproducible and technically straightforward technique for the isolation and long-term culture of normal human endometrial epithelial cells is described. The essential conditions for long-term culture are that the cells be seeded onto a gelatin matrix and that ‘endothelial cell growth supplement’ be present in the culture medium. Normal endometrial epithelial cells express cytokeratins and oestrogen receptors. They may be passaged five to six times without change in properties. Growth of normal endometrial epithelial cells was stimulated by 17-beta-oestradiol and epidermal growth factor. Expression of the mRNA coding for seven polypeptide angiogenic factors, by normal endometrial epithelial, stromal and three endometrial carcinoma lines, was examined. The endometrial epithelial and stromal cells express mRNA for the polypeptide angiogenic factors, basic fibroblast growth factor, vascular endothelial cell growth factor, transforming growth factor-beta 1 and pleiotrophin, as well as the cytokine midkine. Expression of the mRNA for both vascular endothelial growth factor and midkine by normal endometrial epithelial cells showed a 2-fold increase on treatment with a physiological dose of 17-beta-oestradiol (10(−10) M) while, in contrast, the mRNA of transforming growth factor-beta 1 decreased 4-fold on treatment with 17-beta-oestradiol (10(−10) M) and was abolished by exposure to progesterone (5 × 10(−9) M). Expression of the mRNAs for angiogenic polypeptides by the endometrial carcinoma lines was more restricted.

A phorbol ester-regulated ribonuclease system controlling transforming growth factor beta 1 gene expression in hematopoietic cells

1990 ◽  
Vol 10 (11) ◽  
pp. 5983-5990
Author(s):  
R E Wager ◽  
R K Assoian
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Fold Increase ◽  
Mrna Levels ◽  
Tgf Beta ◽  
Growth Factor Beta

12-Tetradecanoylphorbol-13-acetate (TPA)-induced differentiation of U937 promonocytes leads to a 30-fold increase in transforming growth factor beta 1 (TGF-beta 1) gene expression, and this effect results from a stabilized mRNA. Similar up-regulation was detected in TPA-treated K562 erythroblasts but was absent from cell lines that do not differentiate in response to TPA. Related studies in vitro showed that postnuclear extracts of U937 promonocytes contain a ribonuclease system that degrades TGF-beta 1 mRNA selectively and that this system is completely blocked by prior treatment of the cells with TPA. These data identify a new mechanism for regulating TGF-beta 1 mRNA levels and allow us to establish the overall basis for control of TGF-beta 1 gene expression by activation of protein kinase C. Our results also provide a new basis for understanding the long-term up-regulation of TGF-beta 1 gene expression that can accompany hematopoietic cell differentiation.

scholarly journals A phorbol ester-regulated ribonuclease system controlling transforming growth factor beta 1 gene expression in hematopoietic cells.

1990 ◽  
Vol 10 (11) ◽  
pp. 5983-5990 ◽  
Author(s):  
R E Wager ◽  
R K Assoian
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Fold Increase ◽  
Mrna Levels ◽  
Tgf Beta ◽  
Growth Factor Beta

12-Tetradecanoylphorbol-13-acetate (TPA)-induced differentiation of U937 promonocytes leads to a 30-fold increase in transforming growth factor beta 1 (TGF-beta 1) gene expression, and this effect results from a stabilized mRNA. Similar up-regulation was detected in TPA-treated K562 erythroblasts but was absent from cell lines that do not differentiate in response to TPA. Related studies in vitro showed that postnuclear extracts of U937 promonocytes contain a ribonuclease system that degrades TGF-beta 1 mRNA selectively and that this system is completely blocked by prior treatment of the cells with TPA. These data identify a new mechanism for regulating TGF-beta 1 mRNA levels and allow us to establish the overall basis for control of TGF-beta 1 gene expression by activation of protein kinase C. Our results also provide a new basis for understanding the long-term up-regulation of TGF-beta 1 gene expression that can accompany hematopoietic cell differentiation.

scholarly journals Transforming Growth Factor Beta-Activated Kinase 1–Dependent Microglial and Macrophage Responses Aggravate Long-Term Outcomes After Ischemic Stroke

Stroke ◽  
2020 ◽  
Vol 51 (3) ◽  
pp. 975-985 ◽  
Author(s):  
Rongrong Wang ◽  
Hongjian Pu ◽  
Qing Ye ◽  
Ming Jiang ◽  
Jie Chen ◽  
...  
Keyword(s):  
Brain Injury ◽  
White Matter ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Ischemia Reperfusion ◽  
Rna Seq ◽  
Stroke Outcomes ◽  
Growth Factor Beta

Background and Purpose— Microglia/macrophages (Mi/MΦ) can profoundly influence stroke outcomes by acquiring functionally dominant phenotypes (proinflammatory or anti-inflammatory; deleterious or salutary). Identification of the molecular mechanisms that dictate the functional status of Mi/MΦ after brain ischemia/reperfusion may reveal novel therapeutic targets for stroke. We hypothesized that activation of TAK1 (transforming growth factor beta-activated kinase 1), a key MAP3K upstream of multiple inflammation-regulating pathways, drives Mi/MΦ toward a proinflammatory phenotype and potentiates ischemia/reperfusion brain injury. Methods— Young adult mice were subjected to 1 hour of middle cerebral artery occlusion (MCAO) followed by reperfusion. TAK1 was targeted by tamoxifen-induced Mi/MΦ-specific knockout or administration of a selective inhibitor 5Z-7-Oxozeaenol after MCAO. Neurobehavioral deficits and long-term gray matter and white matter injury were assessed up to 35 days after MCAO. Mi/MΦ functional status and brain inflammatory profiles were assessed 3 days after MCAO by RNA-seq, flow cytometry, and immunohistochemistry. Results— TAK1 Mi/MΦ-specific knockout markedly ameliorated neurological deficits in the rotarod and cylinder tests for at least 35 days after MCAO. Mechanistically, RNA-seq of purified brain Mi/MΦ demonstrated that proinflammatory genes and their predicted biological functions were downregulated or inhibited in microglia and macrophages from TAK1 Mi/MΦ-specific knockout mice versus WT mice 3 days after MCAO. Consistent with the anti-inflammatory phenotype of Mi/MΦ-specific knockout, oxozeaenol treatment mitigated neuroinflammation 3 days after MCAO, manifested by less Iba1 + /CD16 + proinflammatory Mi/MΦ and suppressed brain invasion of various peripheral immune cells. Oxozeaenol treatment beginning 2 hours after MCAO improved long-term sensorimotor and cognitive functions in the foot fault, rotarod, and water maze tests. Furthermore, Oxozeaenol promoted both gray matter and white matter integrity 35 days after MCAO. Conclusions— TAK1 promotes ischemia/reperfusion-induced inflammation, brain injury, and maladaptive behavior by enhancing proinflammatory and deleterious Mi/MΦ responses. Therefore, TAK1 inhibition is a promising therapy to improve long-term stroke outcomes.

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