Nicotine upregulates nerve growth factor expression and prevents apoptosis of cultured spinal cord neurons

Rosario Garrido; Kelley King-Pospisil; Kwang Won Son; Bernhard Hennig; Michal Toborek

doi:10.1016/S0168-0102(03)00222-0

Nicotine upregulates nerve growth factor expression and prevents apoptosis of cultured spinal cord neurons

Rosario Garrido, Kelley King-Pospisil, Kwang Won Son, Bernhard Hennig, Michal Toborek

Research output: Contribution to journal › Article › peer-review

45 Scopus citations

Abstract

Modulation of neurotrophic factor expression may constitute an important part of neuroprotective effects of nicotine. Therefore, the effects of nicotine on expression of nerve growth factor (NGF) and its receptor, tyrosine receptor kinase A (trkA), were studied in cultured spinal cord neurons treated with arachidonic acid. Because injury to spinal cord is associated with elevated levels of arachidonic acid, this cell culture system has been developed in our laboratory as an in vitro model of neuronal injury in spinal cord trauma. Treatment with nicotine markedly upregulated NGF mRNA and protein expression in spinal cord neurons. In addition, a 12h treatment with nicotine increased mRNA levels of trkA. Both nicotine and exogenous NGF inhibited arachidonic acid induced apoptosis of spinal cord neurons. However, the blockage of the trkA receptor prevented nicotine-mediated anti-apoptotic effects. The present results indicate that increased expression of NGF may be an important element of the neuroprotective effects of nicotine in injured spinal cord neurons.

Original language	English
Pages (from-to)	349-355
Number of pages	7
Journal	Neuroscience Research
Volume	47
Issue number	3
DOIs	https://doi.org/10.1016/S0168-0102(03)00222-0
State	Published - Nov 1 2003

Bibliographical note

Funding Information:
This work was supported in part by the Kentucky Spinal Cord and Head Injury Research Trust (KSCHIRT) and Philip Morris External Research Program.

Funding

This work was supported in part by the Kentucky Spinal Cord and Head Injury Research Trust (KSCHIRT) and Philip Morris External Research Program.

Funders	Funder number
Philip Morris External Research Program
National Institutes of Health/National Institute of Environmental Health Sciences	P42ES007380
National Institutes of Health/National Institute of Environmental Health Sciences
Kentucky Spinal Cord and Head Injury Research Trust

Keywords

Fatty acids
Neuroprotection
Nicotine
Spinal cord neurons
Spinal cord trauma

ASJC Scopus subject areas

General Neuroscience

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10.1016/S0168-0102(03)00222-0

Cite this

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title = "Nicotine upregulates nerve growth factor expression and prevents apoptosis of cultured spinal cord neurons",

abstract = "Modulation of neurotrophic factor expression may constitute an important part of neuroprotective effects of nicotine. Therefore, the effects of nicotine on expression of nerve growth factor (NGF) and its receptor, tyrosine receptor kinase A (trkA), were studied in cultured spinal cord neurons treated with arachidonic acid. Because injury to spinal cord is associated with elevated levels of arachidonic acid, this cell culture system has been developed in our laboratory as an in vitro model of neuronal injury in spinal cord trauma. Treatment with nicotine markedly upregulated NGF mRNA and protein expression in spinal cord neurons. In addition, a 12h treatment with nicotine increased mRNA levels of trkA. Both nicotine and exogenous NGF inhibited arachidonic acid induced apoptosis of spinal cord neurons. However, the blockage of the trkA receptor prevented nicotine-mediated anti-apoptotic effects. The present results indicate that increased expression of NGF may be an important element of the neuroprotective effects of nicotine in injured spinal cord neurons.",

keywords = "Fatty acids, Neuroprotection, Nicotine, Spinal cord neurons, Spinal cord trauma",

author = "Rosario Garrido and Kelley King-Pospisil and Son, \{Kwang Won\} and Bernhard Hennig and Michal Toborek",

note = "Funding Information: This work was supported in part by the Kentucky Spinal Cord and Head Injury Research Trust (KSCHIRT) and Philip Morris External Research Program.",

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AU - King-Pospisil, Kelley

AU - Son, Kwang Won

AU - Hennig, Bernhard

AU - Toborek, Michal

N1 - Funding Information: This work was supported in part by the Kentucky Spinal Cord and Head Injury Research Trust (KSCHIRT) and Philip Morris External Research Program.

PY - 2003/11/1

Y1 - 2003/11/1

N2 - Modulation of neurotrophic factor expression may constitute an important part of neuroprotective effects of nicotine. Therefore, the effects of nicotine on expression of nerve growth factor (NGF) and its receptor, tyrosine receptor kinase A (trkA), were studied in cultured spinal cord neurons treated with arachidonic acid. Because injury to spinal cord is associated with elevated levels of arachidonic acid, this cell culture system has been developed in our laboratory as an in vitro model of neuronal injury in spinal cord trauma. Treatment with nicotine markedly upregulated NGF mRNA and protein expression in spinal cord neurons. In addition, a 12h treatment with nicotine increased mRNA levels of trkA. Both nicotine and exogenous NGF inhibited arachidonic acid induced apoptosis of spinal cord neurons. However, the blockage of the trkA receptor prevented nicotine-mediated anti-apoptotic effects. The present results indicate that increased expression of NGF may be an important element of the neuroprotective effects of nicotine in injured spinal cord neurons.

AB - Modulation of neurotrophic factor expression may constitute an important part of neuroprotective effects of nicotine. Therefore, the effects of nicotine on expression of nerve growth factor (NGF) and its receptor, tyrosine receptor kinase A (trkA), were studied in cultured spinal cord neurons treated with arachidonic acid. Because injury to spinal cord is associated with elevated levels of arachidonic acid, this cell culture system has been developed in our laboratory as an in vitro model of neuronal injury in spinal cord trauma. Treatment with nicotine markedly upregulated NGF mRNA and protein expression in spinal cord neurons. In addition, a 12h treatment with nicotine increased mRNA levels of trkA. Both nicotine and exogenous NGF inhibited arachidonic acid induced apoptosis of spinal cord neurons. However, the blockage of the trkA receptor prevented nicotine-mediated anti-apoptotic effects. The present results indicate that increased expression of NGF may be an important element of the neuroprotective effects of nicotine in injured spinal cord neurons.

KW - Fatty acids

KW - Neuroprotection

KW - Nicotine

KW - Spinal cord neurons

KW - Spinal cord trauma

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Nicotine upregulates nerve growth factor expression and prevents apoptosis of cultured spinal cord neurons

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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