Document Detail


Transforming growth factor-β1 regulates Cdk5 activity in primary sensory neurons.
MedLine Citation:
PMID:  22451679     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In addition to many important roles for Cdk5 in brain development and synaptic function, we reported previously that Cdk5 regulates inflammatory pain signaling, partly through phosphorylation of transient receptor potential vanilloid 1 (TRPV1), an important Na(+)/Ca(2+) channel expressed in primary nociceptive afferent nerves. Because TGF-β regulates inflammatory processes and its receptor is expressed in TRPV1-positive afferents, we studied the cross-talk between these two pathways in sensory neurons during experimental peripheral inflammation. We demonstrate that TGF-β1 increases transcription and protein levels of the Cdk5 co-activator p35 through ERK1/2, resulting in an increase in Cdk5 activity in rat B104 neuroblastoma cells. Additionally, TGF-β1 enhances the capsaicin-induced Ca(2+) influx in cultured primary neurons from dorsal root ganglia (DRG). Importantly, Cdk5 activity was reduced in the trigeminal ganglia and DRG of 14-day-old TGF-β1 knock-out mice, resulting in reduced Cdk5-dependent phosphorylation of TRPV1. The decreased Cdk5 activity is associated with attenuated thermal hyperalgesia in TGF-β1 receptor conditional knock-out mice, where TGF-β signaling is significantly reduced in trigeminal ganglia and DRG. Collectively, our results indicate that active cross-talk between the TGF-β and Cdk5 pathways contributes to inflammatory pain signaling.
Authors:
Elias Utreras; Jason Keller; Anita Terse; Michaela Prochazkova; Michael J Iadarola; Ashok B Kulkarni
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural     Date:  2012-03-28
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  287     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-14     Completed Date:  2012-07-13     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  16917-29     Citation Subset:  IM    
Affiliation:
Functional Genomics Section, Laboratory of Cell and Developmental Biology, NIDCR, National Institutes of Health, Bethesda, Maryland 20892, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / metabolism
Cell Line, Tumor
Cyclin-Dependent Kinase 5 / genetics,  metabolism*
Ganglia, Spinal / metabolism*,  pathology
Hyperalgesia / genetics,  metabolism,  pathology
MAP Kinase Signaling System*
Mice
Mice, Knockout
Mitogen-Activated Protein Kinase 3 / genetics,  metabolism
Pain / genetics,  metabolism,  pathology
Phosphorylation / genetics
Rats
Sensory Receptor Cells / metabolism*,  pathology
TRPV Cation Channels / genetics,  metabolism
Transforming Growth Factor beta1 / genetics,  metabolism*
Trigeminal Ganglion / metabolism*,  pathology
Chemical
Reg. No./Substance:
0/TRPV Cation Channels; 0/TRPV1 protein, mouse; 0/Transforming Growth Factor beta1; 0/Trpv1 protein, rat; 7440-70-2/Calcium; EC 2.7.11.22/Cdk5 protein, mouse; EC 2.7.11.22/Cdk5 protein, rat; EC 2.7.11.22/Cyclin-Dependent Kinase 5; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3
Comments/Corrections

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