RGD Reference Report - Fibroblast growth factor 16 and 18 are expressed in human cardiovascular tissues and induce on endothelial cells migration but not proliferation. - Rat Genome Database

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Fibroblast growth factor 16 and 18 are expressed in human cardiovascular tissues and induce on endothelial cells migration but not proliferation.

Authors: Antoine, M  Wirz, W  Tag, CG  Gressner, AM  Wycislo, M  Muller, R  Kiefer, P 
Citation: Antoine M, etal., Biochem Biophys Res Commun. 2006 Jul 21;346(1):224-33. Epub 2006 May 26.
RGD ID: 10047366
Pubmed: PMID:16756958   (View Abstract at PubMed)
DOI: DOI:10.1016/j.bbrc.2006.05.105   (Journal Full-text)

Endothelial cells line the blood vessel and precursor endothelial cells appear to have a pivotal effect on the organ formation of the heart, the embryonic development of the kidney, and the liver. Several growth factors including the fibroblast growth factors (FGF) seem to be involved in these processes. Ligands such as basic FGF produced and secreted by endothelial cells may also coordinate cellular migration, differentiation, and proliferation under pathological conditions including wound healing, tumorgenesis, and fibrogenesis in the adult. Recently we demonstrated the expression of two secreted FGFs, FGF16, and FGF18, in HUVEC and in rat aortic tissue. In the present report, we confirmed by RT-PCR analysis that FGF18 is wildly expressed in the cardiovascular tissue, while FGF16 showed a more restricted expression pattern. HUVEC clearly demonstrated chemotaxis towards FGF16 and FGF18. Both FGFs also enhanced cell migration in response to mechanical damage. However, recombinant FGF16 and FGF18 failed to induce endothelial cell proliferation or sprouting in a three-dimensional in vitro angiogenesis assay. Fgf18 expression was earlier reported in the liver, and we detected FGF18 expression in liver vascular and liver sinusoidal endothelial cells (LSECs), but not in hepatic parenchymal cells. Recombinant FGF18 stimulated DNA synthesis in primary hepatocytes, suggesting, that endothelial FGF18 might have a paracrine function in promoting growth of the parenchymal tissue. Interestingly, FGF2, which is mitogenic on endothelial cells and hepatocytes stimulates a sustained MAPK activation in both cell types, while FGF18 causes a short transient activation of the MAPK pathway in endothelial cells but a sustained activation in hepatocytes. Therefore, the difference in the time course of MAPK activation by the different FGFs appears to be the cause for the different cellular responses.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Fgf1Ratpositive regulation of hepatocyte proliferation involved_inIDA PMID:16756958UniProt 
Fgf18Ratpositive regulation of hepatocyte proliferation involved_inIDA PMID:16756958UniProt 

Cellular Component

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Fgf18Ratcytoplasm located_inIDA PMID:16756958UniProt 
Fgf18Ratnucleus located_inIDA PMID:16756958UniProt 

Objects Annotated

Genes (Rattus norvegicus)
Fgf1  (fibroblast growth factor 1)
Fgf18  (fibroblast growth factor 18)


Additional Information