Universität zu Köln

Andres, Christine, Hasenauer, Jan ORCID: 0000-0002-4935-3312, Ahn, Hye-Sook, Joseph, Elizabeth K., Isensee, Joerg ORCID: 0000-0002-3390-0051, Theis, Fabian J., Allgoewer, Frank, Levine, Jon D., Dib-Hajj, Sulayman D., Waxman, Stephen G. and Hucho, Tim ORCID: 0000-0002-4147-9308 (2013). Wound-healing growth factor, basic FGF, induces Erk1/2-dependent mechanical hyperalgesia. Pain, 154 (10). S. 2216 - 2227. PHILADELPHIA: LIPPINCOTT WILLIAMS & WILKINS. ISSN 1872-6623

Full text not available from this repository.

Abstract

Growth factors such as nerve growth factor and glial cell line-derived neurotrophic factor are known to induce pain sensitization. However, a plethora of other growth factors is released during inflammation and tissue regeneration, and many of them are essential for wound healing. Which wound-healing factors also alter the sensitivity of nociceptive neurons is not well known. We studied the wound-healing factor, basic fibroblast growth factor ( bFGF), for its role in pain sensitization. Reverse transcription polymerase chain reaction showed that the receptor of bFGF, FGFR1, is expressed in lumbar rat dorsal root ganglia (DRG). We demonstrated presence of FGFR1 protein in DRG neurons by a recently introduced quantitative automated immunofluorescent microscopic technique. FGFR1 was expressed in all lumbar DRG neurons as quantified by mixture modeling. Corroborating the mRNA and protein expression data, bFGF induced Erk1/2 phosphorylation in nociceptive neurons, which could be blocked by inhibition of FGF receptors. Furthermore, bFGF activated Erk1/2 in a dose- and time-dependent manner. Using single-cell electrophysiological recordings, we found that bFGF treatment of DRG neurons increased the current-density of Na(V)1.8 channels. Erk1/2 inhibitors abrogated this increase. Importantly, intradermal injection of bFGF in rats induced Erk1/2-dependent mechanical hyperalgesia. Perspective: Analyzing intracellular signaling dynamics in nociceptive neurons has proven to be a powerful approach to identify novel modulators of pain. In addition to describing a new sensitizing factor, our findings indicate the potential to investigate wound-healing factors for their role in nociception. (C) 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Andres, Christine UNSPECIFIED UNSPECIFIED UNSPECIFIED Hasenauer, Jan UNSPECIFIED orcid.org/0000-0002-4935-3312 UNSPECIFIED Ahn, Hye-Sook UNSPECIFIED UNSPECIFIED UNSPECIFIED Joseph, Elizabeth K. UNSPECIFIED UNSPECIFIED UNSPECIFIED Isensee, Joerg UNSPECIFIED orcid.org/0000-0002-3390-0051 UNSPECIFIED Theis, Fabian J. UNSPECIFIED UNSPECIFIED UNSPECIFIED Allgoewer, Frank UNSPECIFIED UNSPECIFIED UNSPECIFIED Levine, Jon D. UNSPECIFIED UNSPECIFIED UNSPECIFIED Dib-Hajj, Sulayman D. UNSPECIFIED UNSPECIFIED UNSPECIFIED Waxman, Stephen G. UNSPECIFIED UNSPECIFIED UNSPECIFIED Hucho, Tim UNSPECIFIED orcid.org/0000-0002-4147-9308 UNSPECIFIED
URN:	urn:nbn:de:hbz:38-475109
DOI:	10.1016/j.pain.2013.07.005
Journal or Publication Title:	Pain
Volume:	154
Number:	10
Page Range:	S. 2216 - 2227
Date:	2013
Publisher:	LIPPINCOTT WILLIAMS & WILKINS
Place of Publication:	PHILADELPHIA
ISSN:	1872-6623
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language PROTEIN-KINASE-C; SENSORY NEURONS; RHEUMATOID-ARTHRITIS; SODIUM-CHANNELS; MESSENGER-RNA; PAIN; EXPRESSION; GDNF; TRKA; RAT Multiple languages Anesthesiology; Clinical Neurology; Neurosciences Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/47510