scholarly journals Progressive interdigital cell death: regulation by the antagonistic interaction between fibroblast growth factor 8 and retinoic acid

Development ◽  
2009 ◽  
Vol 136 (21) ◽  
pp. 3669-3678 ◽  
Author(s):  
R. Hernandez-Martinez ◽  
S. Castro-Obregon ◽  
L. Covarrubias
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor 8 ◽  
Antagonistic Interaction ◽  
Interdigital Cell Death

Local retinoid signaling coordinates forebrain and facial morphogenesis by maintaining FGF8 and SHH

Development ◽  
2001 ◽  
Vol 128 (14) ◽  
pp. 2755-2767 ◽  
Author(s):  
Richard A. Schneider ◽  
Diane Hu ◽  
John L. R. Rubenstein ◽  
Malcolm Maden ◽  
Jill A. Helms
Keyword(s):  
Retinoic Acid ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Sonic Hedgehog ◽  
Local Source ◽  
Fibroblast Growth ◽  
Retinoid Signaling ◽  
Retinoid Receptors ◽  
Fibroblast Growth Factor 8 ◽  
Regulatory Cascade

Correlations between facial anomalies and brain defects are well characterized throughout the clinical literature, yet a developmental basis for this association has not been identified. We demonstrate that the frontonasal process, which gives rise to the mid- and upper face, and the forebrain are linked early in their morphogenesis by a local retinoid signaling event that maintains the expression of key regulatory molecules. First, we show that aldehyde dehydrogenase 6, which synthesizes the ligand, retinoic acid, is localized to the ventral epithelium of the presumptive frontonasal process of chick embryos. At least two retinoid receptors are expressed in adjacent populations of mesenchyme. Second, using synthetic pan-specific retinoid antagonists, we transiently inhibit the ability of retinoid receptors to bind retinoic acid in the rostral head and we generate embryos with a hypoplastic forebrain, fused eyes, and no frontonasal process-derived structures such as the upper beak. These defects are not due to eliminating mesenchymal progenitors, as neural crest cells still migrate into the frontonasal process, despite disruptions to retinoid signaling. Rather, these malformations result from loss of fibroblast growth factor 8 and sonic hedgehog expression, which leads to increased programmed cell death and decreased proliferation in the forebrain and frontonasal process. Most significantly, we can rescue the morphological defects by re-introducing retinoic acid, or fibroblast growth factor and sonic hedgehog proteins into antagonist-treated embryos. We propose that the local source of retinoic acid in the rostral head initiates a regulatory cascade that coordinates forebrain and frontonasal process morphogenesis.

Up-regulation of the fibroblast growth factor 8 subfamily in human hepatocellular carcinoma for cell survival and neoangiogenesis

Hepatology ◽  
2011 ◽  
Vol 53 (3) ◽  
pp. 854-864 ◽  
Author(s):  
Christine Gauglhofer ◽  
Sandra Sagmeister ◽  
Waltraud Schrottmaier ◽  
Carina Fischer ◽  
Chantal Rodgarkia-Dara ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Growth Factor ◽  
Cell Survival ◽  
Fibroblast Growth Factor ◽  
Human Hepatocellular Carcinoma ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor 8
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