Document Detail

Transforming growth factor-β1 regulates Cdk5 activity in primary sensory neurons.
MedLine Citation:
PMID:  22451679     Owner:  NLM     Status:  MEDLINE    
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.
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    
Functional Genomics Section, Laboratory of Cell and Developmental Biology, NIDCR, National Institutes of Health, Bethesda, Maryland 20892, USA.
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MeSH Terms
Calcium / metabolism
Cell Line, Tumor
Cyclin-Dependent Kinase 5 / genetics,  metabolism*
Ganglia, Spinal / metabolism*,  pathology
Hyperalgesia / genetics,  metabolism,  pathology
MAP Kinase Signaling System*
Mice, Knockout
Mitogen-Activated Protein Kinase 3 / genetics,  metabolism
Pain / genetics,  metabolism,  pathology
Phosphorylation / genetics
Sensory Receptor Cells / metabolism*,  pathology
TRPV Cation Channels / genetics,  metabolism
Transforming Growth Factor beta1 / genetics,  metabolism*
Trigeminal Ganglion / metabolism*,  pathology
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 protein, mouse; EC protein, rat; EC Kinase 5; EC Protein Kinase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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