Developmental Expression of the Genes Encoding Transforming Growth Factor Alpha and Its Receptor in the Hypothalamus of Female Rhesus Macaques

1994 ◽  
Vol 60 (4) ◽  
pp. 346-359 ◽  
Author(s):  
Ying Jun Ma ◽  
Maria E. Costa ◽  
Sergio R. Ojeda
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Rhesus Macaques ◽  
Developmental Expression ◽  
Transforming Growth Factor Alpha ◽  
Female Rhesus ◽  
Genes Encoding ◽  
Factor Alpha ◽  
Female Rhesus Macaques

scholarly journals Developmental expression of rat transforming growth factor-alpha mRNA.

1985 ◽  
Vol 5 (12) ◽  
pp. 3644-3646 ◽  
Author(s):  
D C Lee ◽  
R Rochford ◽  
G J Todaro ◽  
L P Villarreal
Keyword(s):  
Growth Factor ◽  
Northern Blot Analysis ◽  
Transforming Growth Factor ◽  
Developmental Expression ◽  
Transforming Growth Factor Alpha ◽  
Undetectable Level ◽  
Gene Encoding ◽  
Hybridization Probe ◽  
Factor Alpha ◽  
Developing Rat

Expression of the gene encoding transforming growth factor-alpha (TGF alpha) was examined in developing rat embryos by using a cloned TGF alpha cDNA as a hybridization probe. Northern blot analysis of RNA isolated from whole fetuses revealed that TGF alpha mRNA was present at relatively high levels in 8- through 10-day-old embryos and then declined to the low or undetectable level, which is characteristic of adult tissues before birth. The level of TGF alpha mRNA present during early gestation was similar to that present in retrovirus-transformed cells in culture, suggesting that TGF alpha expression is not highly localized in the embryo. These observations are consistent with the hypothesis that TGF alpha plays a role in development, possibly as a fetal growth factor.

Developmental expression of rat transforming growth factor-alpha mRNA

1985 ◽  
Vol 5 (12) ◽  
pp. 3644-3646
Author(s):  
D C Lee ◽  
R Rochford ◽  
G J Todaro ◽  
L P Villarreal
Keyword(s):  
Growth Factor ◽  
Northern Blot Analysis ◽  
Transforming Growth Factor ◽  
Developmental Expression ◽  
Transforming Growth Factor Alpha ◽  
Undetectable Level ◽  
Gene Encoding ◽  
Hybridization Probe ◽  
Factor Alpha ◽  
Developing Rat

Expression of the gene encoding transforming growth factor-alpha (TGF alpha) was examined in developing rat embryos by using a cloned TGF alpha cDNA as a hybridization probe. Northern blot analysis of RNA isolated from whole fetuses revealed that TGF alpha mRNA was present at relatively high levels in 8- through 10-day-old embryos and then declined to the low or undetectable level, which is characteristic of adult tissues before birth. The level of TGF alpha mRNA present during early gestation was similar to that present in retrovirus-transformed cells in culture, suggesting that TGF alpha expression is not highly localized in the embryo. These observations are consistent with the hypothesis that TGF alpha plays a role in development, possibly as a fetal growth factor.

MOLECULAR CONTROL OF ARTICULAR CARTILAGE DEGENERATION BY TRANSFORMING GROWTH FACTOR ALPHA

2008 ◽  
Vol 31 (4) ◽  
pp. 2
Author(s):  
Tom Appleton ◽  
Shirine Usmani ◽  
John Mort ◽  
Frank Beier
Keyword(s):  
Gene Expression ◽  
Articular Cartilage ◽  
Growth Factor ◽  
P38 Mapk ◽  
Transforming Growth Factor ◽  
Cartilage Degeneration ◽  
Signalling Pathways ◽  
Transforming Growth Factor Alpha ◽  
Factor Alpha ◽  
Articular Cartilage Degeneration

Background: Articular cartilage degeneration is a hallmark of osteoarthritis (OA). We previously identified increased expression of transforming growth factor alpha (TGF?) and chemokine (C-C motif) ligand 2 (CCL2) in articular cartilage from a rat modelof OA (1,2). We subsequently reported that TGF? signalling modified chondrocyte cytoskeletal organization, increased catabolic and decreased anabolic gene expression and suppressed Sox9. Due to other roles in chondrocytes, we hypothesized that the effects ofTGF? on chondrocytes are mediated by Rho/ROCK and MEK/ERK signaling pathways. Methods: Primary cultures of chondrocytes and articularosteochondral explants were treated with pharmacological inhibitors of MEK1/2(U0126), ROCK (Y27632), Rho (C3), p38 MAPK (SB202190) and PI3K (LY294002) to elucidate pathway involvement. Results: Using G-LISA we determined that stimulation of primary chondrocytes with TGF? activates RhoA. Reciprocally, inhibition of RhoA/ROCK but not other signalling pathways prevents modification of the actin cytoskeleton in responseto TGF?. Inhibition of MEK/ERKsignaling rescued suppression of anabolic gene expression by TGF? including SOX9 mRNA and protein levels. Inhibition of MEK/ERK, Rho/ROCK, p38 MAPK and PI3K signalling pathways differentially controlled the induction of MMP13 and TNF? gene expression. TGF? also induced expression of CCL2 specifically through MEK/ERK activation. In turn, CCL2 treatment induced the expression of MMP3 and TNF?. Finally, we assessed cartilage degradation by immunohistochemical detection of type II collagen cleavage fragments generated by MMPs. Blockade of RhoA/ROCK and MEK/ERK signalling pathways reduced the generation of type IIcollagen cleavage fragments in response to TGF? stimulation. Conclusions: Rho/ROCK signalling mediates TGF?-induced changes inchondrocyte morphology, while MEK/ERK signalling mediates the suppression ofSox9 and its target genes, and CCL2 expression. CCL2, in turn, induces the expression of MMP3 and TNF?, two potent catabolic factors known to be involved in OA. These pathways may represent strategic targets for interventional approaches to treating cartilage degeneration in osteoarthritis. References: 1. Appleton CTG et al. Arthritis Rheum 2007;56:1854-68. 2. Appleton CTG et al. Arthritis Rheum 2007; 56:3693-705.

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