Tags

Type your tag names separated by a space and hit enter

The Effects of IGF-1 on Trk Expressing DRG Neurons with HIV-gp120- Induced Neurotoxicity.
Curr HIV Res. 2016; 14(2):154-64.CH

Abstract

BACKGROUND

HIV envelope glycoprotein gp120 is the main protein that causes HIVassociated sensory neuropathy. However, the underlying mechanisms of gp120-induced neurotoxicity are still unclear. There are lack effective treatments for relieving HIV-related neuropathic symptoms caused by gp120-induced neurotoxicity.

METHODS

In the present study, tyrosine kinase receptor (Trk)A, TrkB, and TrkC expression in primary cultured dorsal root ganglion (DRG) neurons with gp120-induced neurotoxicity was investigated. The effects of IGF-1 on distinct Trk-positive DRG neurons with gp120-induced neurotoxicity were also determined.

RESULTS

The results showed that gp120 not only dose-dependently induced DRG neuronal apoptosis and inhibited neuronal survival and neurite outgrowth, but also decreased distinct Trk expression levels. IGF-1 rescued DRG neurons from apoptosis and improved neuronal survival of gp120 neurotoxic DRG neurons in vitro. IGF-1 also improved TrkA and TrkB, but not TrkC, expression in gp120 neurotoxic conditions. The effects of IGF-1 could be blocked by preincubation with the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002.

CONCLUSION

These results suggested that gp120 may have a wide range of neurotoxicity on different subpopulations of DRG neurons, while IGF-1 might only relieve some subpopulations of DRG neurons with gp120-induced neurotoxicity. These data provide novel information of mechanisms of gp120 neurotoxicity on primary sensory neurons and the potential therapeutic effects of IGF-1 on gp120-induced neurotoxicity.

Authors+Show Affiliations

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableDepartment of Rheumatology, Shandong University Qilu Hospital, 107 Wenhua Xi Road, Jinan, Shandong Province 250012, China. huaxiangliu@hotmail.com.

Pub Type(s)

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

Language

eng

PubMed ID

26652865

Citation

Li, Hao, et al. "The Effects of IGF-1 On Trk Expressing DRG Neurons With HIV-gp120- Induced Neurotoxicity." Current HIV Research, vol. 14, no. 2, 2016, pp. 154-64.
Li H, Liu Z, Chi H, et al. The Effects of IGF-1 on Trk Expressing DRG Neurons with HIV-gp120- Induced Neurotoxicity. Curr HIV Res. 2016;14(2):154-64.
Li, H., Liu, Z., Chi, H., Bi, Y., Song, L., & Liu, H. (2016). The Effects of IGF-1 on Trk Expressing DRG Neurons with HIV-gp120- Induced Neurotoxicity. Current HIV Research, 14(2), 154-64.
Li H, et al. The Effects of IGF-1 On Trk Expressing DRG Neurons With HIV-gp120- Induced Neurotoxicity. Curr HIV Res. 2016;14(2):154-64. PubMed PMID: 26652865.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The Effects of IGF-1 on Trk Expressing DRG Neurons with HIV-gp120- Induced Neurotoxicity. AU - Li,Hao, AU - Liu,Zhen, AU - Chi,Heng, AU - Bi,Yanwen, AU - Song,Lijun, AU - Liu,Huaxiang, PY - 2015/06/20/received PY - 2015/11/22/revised PY - 2015/12/10/accepted PY - 2015/12/15/entrez PY - 2015/12/15/pubmed PY - 2016/10/21/medline SP - 154 EP - 64 JF - Current HIV research JO - Curr. HIV Res. VL - 14 IS - 2 N2 - BACKGROUND: HIV envelope glycoprotein gp120 is the main protein that causes HIVassociated sensory neuropathy. However, the underlying mechanisms of gp120-induced neurotoxicity are still unclear. There are lack effective treatments for relieving HIV-related neuropathic symptoms caused by gp120-induced neurotoxicity. METHODS: In the present study, tyrosine kinase receptor (Trk)A, TrkB, and TrkC expression in primary cultured dorsal root ganglion (DRG) neurons with gp120-induced neurotoxicity was investigated. The effects of IGF-1 on distinct Trk-positive DRG neurons with gp120-induced neurotoxicity were also determined. RESULTS: The results showed that gp120 not only dose-dependently induced DRG neuronal apoptosis and inhibited neuronal survival and neurite outgrowth, but also decreased distinct Trk expression levels. IGF-1 rescued DRG neurons from apoptosis and improved neuronal survival of gp120 neurotoxic DRG neurons in vitro. IGF-1 also improved TrkA and TrkB, but not TrkC, expression in gp120 neurotoxic conditions. The effects of IGF-1 could be blocked by preincubation with the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002. CONCLUSION: These results suggested that gp120 may have a wide range of neurotoxicity on different subpopulations of DRG neurons, while IGF-1 might only relieve some subpopulations of DRG neurons with gp120-induced neurotoxicity. These data provide novel information of mechanisms of gp120 neurotoxicity on primary sensory neurons and the potential therapeutic effects of IGF-1 on gp120-induced neurotoxicity. SN - 1873-4251 UR - https://www.unboundmedicine.com/medline/citation/26652865/The_Effects_of_IGF_1_on_Trk_Expressing_DRG_Neurons_with_HIV_gp120__Induced_Neurotoxicity_ L2 - http://www.eurekaselect.com/138001/article DB - PRIME DP - Unbound Medicine ER -