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Neuroprotective effect of insulin-like growth factor-1: effects on tyrosine kinase receptor (Trk) expression in dorsal root ganglion neurons with glutamate-induced excitotoxicity in vitro.
Brain Res Bull. 2013 Aug; 97:86-95.BR

Abstract

Insulin-like growth factor-1 (IGF-1) may play an important role in regulating the expression of distinct tyrosine kinase receptor (Trk) in primary sensory dorsal root ganglion (DRG) neurons. Glutamate (Glu) is the main excitatory neurotransmitter and induces neuronal excitotoxicity for primary sensory neurons. It is not known whether IGF-1 influences expression of TrkA, TrkB, and TrkC in DRG neurons with excitotoxicity induced by Glu. In the present study, primary cultured DRG neurons with Glu-induced excitotoxicity were used to determine the effects of IGF-1 on TrkA, TrkB, and TrkC expression. The results showed that IGF-1 increased the expression of TrkA and TrkB and their mRNAs, but not TrkC and its mRNA, in primary cultured DRG neurons with excitotoxicity induced by Glu. Interestingly, neither the extracellular signal-regulated protein kinase (ERK1/2) inhibitor PD98059 nor the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 blocked the effect of IGF-1, but both inhibitors together were effective. IGF-1 may play an important role in regulating different Trk receptor expression in DRG neurons through ERK1/2 and PI3K/Akt signaling pathways. The contribution of distinct Trk receptors might be one of the mechanisms that IGF-1 rescues dying neurons from Glu excitotoxic injury. These data imply that IGF-1 signaling might be a potential target on modifying distinct Trk receptor-mediated biological effects of primary sensory neurons with excitotoxicity.

Authors+Show Affiliations

Department of Anatomy, Shandong University School of Medicine, Jinan 250012, China. lihao462929@163.comNo 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

23769847

Citation

Li, Hao, et al. "Neuroprotective Effect of Insulin-like Growth Factor-1: Effects On Tyrosine Kinase Receptor (Trk) Expression in Dorsal Root Ganglion Neurons With Glutamate-induced Excitotoxicity in Vitro." Brain Research Bulletin, vol. 97, 2013, pp. 86-95.
Li H, Dong H, Li J, et al. Neuroprotective effect of insulin-like growth factor-1: effects on tyrosine kinase receptor (Trk) expression in dorsal root ganglion neurons with glutamate-induced excitotoxicity in vitro. Brain Res Bull. 2013;97:86-95.
Li, H., Dong, H., Li, J., Liu, H., Liu, Z., & Li, Z. (2013). Neuroprotective effect of insulin-like growth factor-1: effects on tyrosine kinase receptor (Trk) expression in dorsal root ganglion neurons with glutamate-induced excitotoxicity in vitro. Brain Research Bulletin, 97, 86-95. https://doi.org/10.1016/j.brainresbull.2013.05.014
Li H, et al. Neuroprotective Effect of Insulin-like Growth Factor-1: Effects On Tyrosine Kinase Receptor (Trk) Expression in Dorsal Root Ganglion Neurons With Glutamate-induced Excitotoxicity in Vitro. Brain Res Bull. 2013;97:86-95. PubMed PMID: 23769847.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective effect of insulin-like growth factor-1: effects on tyrosine kinase receptor (Trk) expression in dorsal root ganglion neurons with glutamate-induced excitotoxicity in vitro. AU - Li,Hao, AU - Dong,Haixia, AU - Li,Jianmin, AU - Liu,Huaxiang, AU - Liu,Zhen, AU - Li,Zhenzhong, Y1 - 2013/06/12/ PY - 2013/03/22/received PY - 2013/05/24/revised PY - 2013/05/28/accepted PY - 2013/6/18/entrez PY - 2013/6/19/pubmed PY - 2014/3/19/medline KW - Dorsal root ganglion KW - Glutamate KW - Insulin-like growth factor-1 KW - Neurotoxicity KW - Tyrosine kinase receptor SP - 86 EP - 95 JF - Brain research bulletin JO - Brain Res. Bull. VL - 97 N2 - Insulin-like growth factor-1 (IGF-1) may play an important role in regulating the expression of distinct tyrosine kinase receptor (Trk) in primary sensory dorsal root ganglion (DRG) neurons. Glutamate (Glu) is the main excitatory neurotransmitter and induces neuronal excitotoxicity for primary sensory neurons. It is not known whether IGF-1 influences expression of TrkA, TrkB, and TrkC in DRG neurons with excitotoxicity induced by Glu. In the present study, primary cultured DRG neurons with Glu-induced excitotoxicity were used to determine the effects of IGF-1 on TrkA, TrkB, and TrkC expression. The results showed that IGF-1 increased the expression of TrkA and TrkB and their mRNAs, but not TrkC and its mRNA, in primary cultured DRG neurons with excitotoxicity induced by Glu. Interestingly, neither the extracellular signal-regulated protein kinase (ERK1/2) inhibitor PD98059 nor the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 blocked the effect of IGF-1, but both inhibitors together were effective. IGF-1 may play an important role in regulating different Trk receptor expression in DRG neurons through ERK1/2 and PI3K/Akt signaling pathways. The contribution of distinct Trk receptors might be one of the mechanisms that IGF-1 rescues dying neurons from Glu excitotoxic injury. These data imply that IGF-1 signaling might be a potential target on modifying distinct Trk receptor-mediated biological effects of primary sensory neurons with excitotoxicity. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/23769847/Neuroprotective_effect_of_insulin_like_growth_factor_1:_effects_on_tyrosine_kinase_receptor__Trk__expression_in_dorsal_root_ganglion_neurons_with_glutamate_induced_excitotoxicity_in_vitro_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(13)00097-X DB - PRIME DP - Unbound Medicine ER -