Differential gene expression of flexor tenocytes and synovial sheath cells in vitro: the role of transforming growth factor-beta isoforms

2000 ◽  
Vol 191 (4) ◽  
pp. S90-S91
Author(s):  
Mytien Ngo ◽  
Hung Pham ◽  
Peter Lorenz ◽  
Prosper Benhaim ◽  
Marc Hedrick ◽  
...  
1990 ◽  
Vol 10 (11) ◽  
pp. 5983-5990
Author(s):  
R E Wager ◽  
R K Assoian

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.


1990 ◽  
Vol 10 (11) ◽  
pp. 5983-5990 ◽  
Author(s):  
R E Wager ◽  
R K Assoian

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.


2008 ◽  
Vol 36 (5) ◽  
pp. 941-945 ◽  
Author(s):  
Madeline Murphy ◽  
John Crean ◽  
Derek P. Brazil ◽  
Denise Sadlier ◽  
Finian Martin ◽  
...  

DN (diabetic nephropathy) is the leading cause of end-stage renal disease worldwide and develops in 25–40% of patients with Type 1 or Type 2 diabetes mellitus. Elevated blood glucose over long periods together with glomerular hypertension leads to progressive glomerulosclerosis and tubulointerstitial fibrosis in susceptible individuals. Central to the pathology of DN are cytokines and growth factors such as TGF-β (transforming growth factor β) superfamily members, including BMPs (bone morphogenetic protein) and TGF-β1, which play key roles in fibrogenic responses of the kidney, including podocyte loss, mesangial cell hypertrophy, matrix accumulation and tubulointerstitial fibrosis. Many of these responses can be mimicked in in vitro models of cells cultured in high glucose. We have applied differential gene expression technologies to identify novel genes expressed in in vitro and in vivo models of DN and, importantly, in human renal tissue. By mining these datasets and probing the regulation of expression and actions of specific molecules, we have identified novel roles for molecules such as Gremlin, IHG-1 (induced in high glucose-1) and CTGF (connective tissue growth factor) in DN and potential regulators of their bioactions.


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