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Alterations in tyrosine kinase receptor (Trk) expression induced by insulin-like growth factor-1 in cultured dorsal root ganglion neurons.
Brain Res Bull. 2013 Jan; 90:25-34.BR

Abstract

Insulin-like growth factor-1 (IGF-1) is a neurotrophic factor expressed in small dorsal root ganglion (DRG) neurons. IGF-1 promotes neuronal survival by activating its receptor (IGF-1R). Whether IGF-1 and its signaling pathways influence the expression of tyrosine kinase receptors TrkA, TrkB and TrkC in DRG neurons remains unknown. In the present study, primary cultured DRG neurons were used to determine the effects of IGF-1 on TrkA, TrkB and TrkC expression. The involvement of extracellular signal-regulated protein kinase (ERK1/2) and the effects of phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways on IGF-1 were also evaluated. DRG neurons were cultured for 48h and then exposed to IGF-1, PD98059 plus IGF-1, LY294002 plus IGF-1, and PD98059 plus LY294002 plus IGF-1 for an additional 24h. The DRG neurons were continuously exposed to culture medium as a control. All cultures were then processed for detection of mRNA levels of TrkA, TrkB and TrkC using real-time PCR analysis. Protein levels of TrkA, TrkB and TrkC were detected using a Western blot assay. The expression of TrkA, TrkB and TrkC in situ was determined by a fluorescent labeling technique. The levels of phosphorylated ERK1/2 (pERK1/2) and phosphorylated Akt (pAkt) were detected using a Western blot assay. The results indicated that in primary cultured DRG neurons, IGF-1 increased the expression of TrkA and TrkB and their mRNAs but not TrkC or its mRNA. Neither the ERK1/2 inhibitor PD98059 nor the PI3K inhibitor LY294002 alone blocked the effect of IGF-1, but the use of both inhibitors together was effective. IGF-1 may play an important role in regulating the expression of different Trk receptors in DRG neurons through the ERK1/2 and PI3K/Akt signaling pathways. These results suggest that IGF-1 signaling might be a potential target on modifying distinct Trk receptor-mediated biological effects.

Authors+Show Affiliations

Department of Anatomy, Shandong University School of Medicine, Jinan 250012, China. lihao462929@yahoo.com.cnNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23022575

Citation

Li, Hao, et al. "Alterations in Tyrosine Kinase Receptor (Trk) Expression Induced By Insulin-like Growth Factor-1 in Cultured Dorsal Root Ganglion Neurons." Brain Research Bulletin, vol. 90, 2013, pp. 25-34.
Li H, Zhang P, Fu G, et al. Alterations in tyrosine kinase receptor (Trk) expression induced by insulin-like growth factor-1 in cultured dorsal root ganglion neurons. Brain Res Bull. 2013;90:25-34.
Li, H., Zhang, P., Fu, G., Li, J., Liu, H., & Li, Z. (2013). Alterations in tyrosine kinase receptor (Trk) expression induced by insulin-like growth factor-1 in cultured dorsal root ganglion neurons. Brain Research Bulletin, 90, 25-34. https://doi.org/10.1016/j.brainresbull.2012.09.011
Li H, et al. Alterations in Tyrosine Kinase Receptor (Trk) Expression Induced By Insulin-like Growth Factor-1 in Cultured Dorsal Root Ganglion Neurons. Brain Res Bull. 2013;90:25-34. PubMed PMID: 23022575.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Alterations in tyrosine kinase receptor (Trk) expression induced by insulin-like growth factor-1 in cultured dorsal root ganglion neurons. AU - Li,Hao, AU - Zhang,Ping, AU - Fu,Guangchun, AU - Li,Jianmin, AU - Liu,Huaxiang, AU - Li,Zhenzhong, Y1 - 2012/09/26/ PY - 2012/05/10/received PY - 2012/09/12/revised PY - 2012/09/17/accepted PY - 2012/10/2/entrez PY - 2012/10/2/pubmed PY - 2013/6/1/medline SP - 25 EP - 34 JF - Brain research bulletin JO - Brain Res. Bull. VL - 90 N2 - Insulin-like growth factor-1 (IGF-1) is a neurotrophic factor expressed in small dorsal root ganglion (DRG) neurons. IGF-1 promotes neuronal survival by activating its receptor (IGF-1R). Whether IGF-1 and its signaling pathways influence the expression of tyrosine kinase receptors TrkA, TrkB and TrkC in DRG neurons remains unknown. In the present study, primary cultured DRG neurons were used to determine the effects of IGF-1 on TrkA, TrkB and TrkC expression. The involvement of extracellular signal-regulated protein kinase (ERK1/2) and the effects of phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways on IGF-1 were also evaluated. DRG neurons were cultured for 48h and then exposed to IGF-1, PD98059 plus IGF-1, LY294002 plus IGF-1, and PD98059 plus LY294002 plus IGF-1 for an additional 24h. The DRG neurons were continuously exposed to culture medium as a control. All cultures were then processed for detection of mRNA levels of TrkA, TrkB and TrkC using real-time PCR analysis. Protein levels of TrkA, TrkB and TrkC were detected using a Western blot assay. The expression of TrkA, TrkB and TrkC in situ was determined by a fluorescent labeling technique. The levels of phosphorylated ERK1/2 (pERK1/2) and phosphorylated Akt (pAkt) were detected using a Western blot assay. The results indicated that in primary cultured DRG neurons, IGF-1 increased the expression of TrkA and TrkB and their mRNAs but not TrkC or its mRNA. Neither the ERK1/2 inhibitor PD98059 nor the PI3K inhibitor LY294002 alone blocked the effect of IGF-1, but the use of both inhibitors together was effective. IGF-1 may play an important role in regulating the expression of different Trk receptors in DRG neurons through the ERK1/2 and PI3K/Akt signaling pathways. These results suggest that IGF-1 signaling might be a potential target on modifying distinct Trk receptor-mediated biological effects. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/23022575/Alterations_in_tyrosine_kinase_receptor__Trk__expression_induced_by_insulin_like_growth_factor_1_in_cultured_dorsal_root_ganglion_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(12)00211-0 DB - PRIME DP - Unbound Medicine ER -