NDLI: Effects of diadenosine tetraphosphate on FGF9-induced chloride flux changes in achondroplastic chondrocytes

Content Provider	Springer Nature Link
Author	Huete, Fernando Guzman Aranguez, Ana Ortín, Javier Hoyle, Charles H. V. Pintor, Jesús
Copyright Year	2011
Abstract	Achondroplasia, the most common type of dwarfism, is characterized by a mutation in the fibroblast growth factor receptor 3 (FGFR3). Achondroplasia is an orphan pathology with no pharmacological treatment so far. However, the possibility of using the dinucleotide diadenosine tetraphosphate (Ap$_{4}$A) with therapeutic purposes in achondroplasia has been previously suggested. The pathogenesis involves the constitutive activation of FGFR3, resulting in altered biochemical and physiological processes in chondrocytes. Some of these altered processes can be influenced by changes in cell volume and ionic currents. In this study, the action of mutant FGFR3 on chondrocyte size and chloride flux in achondroplastic chondrocytes was investigated as well as the effect of the Ap$_{4}$A on these processes triggered by mutant FGFR3. Stimulation with the fibroblast growth factor 9 (FGF9), the preferred ligand for FGFR3, induced an enlarged achondroplastic chondrocyte size and an increase in the intracellular chloride concentration, suggesting the blockade of chloride efflux. Treatment with the Ap$_{4}$A reversed the morphological changes triggered by FGF9 and restored the chloride efflux. These data provide further evidence for the therapeutic potential of this dinucleotide in achondroplasia treatment.
Starting Page	243
Ending Page	249
Page Count	7
File Format	PDF
ISSN	15739538
Journal	Purinergic Signalling
Volume Number	7
Issue Number	2
e-ISSN	15739546
Language	English
Publisher	Springer Netherlands
Publisher Date	2011-05-11
Publisher Institution	International Purine Club
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Diadenosine tetraphosphate Dinucleotides Achondroplasia Chondrocytes Chloride flux Fibroblast growth factor receptor 3 Pharmacology/Toxicology Biomedicine general Cancer Research Neurosciences Human Physiology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology Cellular and Molecular Neuroscience

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