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Low dose nicotine attenuates Aβ neurotoxicity through activation early growth response gene 1 pathway.

Xue M, Zhu L, Zhang J, Qiu J, Du G, Qiao Z, Jin G, Gao F, Zhang Q - PLoS ONE (2015)

Bottom Line: In addition, the up-regulation of EGR-1 by nicotine can also increase the phosphorylation of CyclinD1 which contributes to the attenuation of amyloid-β (Aβ(25-35)) -induced neurotoxicity.Although nicotine and Aβ(25-35) can activate EGR-1, the expression of EGR-1 is down-regulated following treatment with nicotine and Aβ(25-35).This study demonstrates that low dose nicotine attenuates Aβ(25-35)-induced neurotoxicity in vitro and in vivo through activating EGR-1 pathway.

View Article: PubMed Central - PubMed

Affiliation: College of Chemistry and Chemical Engineering, Xiamen University, Xiamen, Fujian, 361005, P.R.China; Institute of Biomedical Engineering, Department of Biomaterials, College of Materials, Xiamen University, Xiamen, Fujian, 361005, P.R.China; Department of Basic Medical Science, Medical College, Xiamen University, Xiamen, Fujian, 361005, P.R.China.

ABSTRACT
Epidemiological studies indicate that smoking is negatively correlated with the incidence and development of Alzheimer's disease (AD). Nicotine was reported to be the active factor. However, the detailed mechanisms still remain to be fully elucidated. Early growth response gene 1 (EGR-1) plays important roles in several important biological processes such as promoting cell growth, differentiation, anti oxidative stress, and apoptosis, but few in the pathogenesis of AD. In the present study, we show that nicotine can activate the MAPK/ERK/EGR-1 signaling pathway partially through α7 nAChR. In addition, the up-regulation of EGR-1 by nicotine can also increase the phosphorylation of CyclinD1 which contributes to the attenuation of amyloid-β (Aβ(25-35)) -induced neurotoxicity. Although nicotine and Aβ(25-35) can activate EGR-1, the expression of EGR-1 is down-regulated following treatment with nicotine and Aβ(25-35). This study demonstrates that low dose nicotine attenuates Aβ(25-35)-induced neurotoxicity in vitro and in vivo through activating EGR-1 pathway.

No MeSH data available.


Related in: MedlinePlus

Time course and concentration dependence of nicotine activation of EGR-1 in SH-SY5Y cells.a, b) Nicotine activates EGR-1 in the nanomolar to micromole range when SH-SY5Y cells were treated with nicotine for 30 min; the relative level of EGR1 was quantified and presented in panel b. β-actin serves as control. c-e) The SH-SY5Y cells were with 10-6M nicotine by the indicated time, the relative level of EGR1 was quantified and presented in panel d and f respectively. β-actin serves as control. g) The mRNA level of EGR1 in SH-SY5Y cells after nicotine treatment was measured by RT-PCR. i) Immunofluorescence was shown when SH-SY5Y cells were treated by nicotine compared to control.
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pone.0120267.g001: Time course and concentration dependence of nicotine activation of EGR-1 in SH-SY5Y cells.a, b) Nicotine activates EGR-1 in the nanomolar to micromole range when SH-SY5Y cells were treated with nicotine for 30 min; the relative level of EGR1 was quantified and presented in panel b. β-actin serves as control. c-e) The SH-SY5Y cells were with 10-6M nicotine by the indicated time, the relative level of EGR1 was quantified and presented in panel d and f respectively. β-actin serves as control. g) The mRNA level of EGR1 in SH-SY5Y cells after nicotine treatment was measured by RT-PCR. i) Immunofluorescence was shown when SH-SY5Y cells were treated by nicotine compared to control.

Mentions: EGR-1 is an important transcription factor in AD [14–18, 21]. We detected the time course and concentration dependent effect of nicotine on the activation of EGR-1. As shown in Fig. 1, EGR-1 was dramatically activated by 10–6 M nicotine in 30 minutes (Fig. 1A). EGR-1 was quickly activated during time course, and the peak response occurred at 45 min (Fig. 1C, 1E). The activation of EGR-1 was then decreased with 1 hour treatment. This data confirms others' reports that nicotine could immediately activate EGR-1 and follow to basal level [22, 23]. The quantification data was presented on the right panels (Fig. 1B, 1D, 1F).


Low dose nicotine attenuates Aβ neurotoxicity through activation early growth response gene 1 pathway.

Xue M, Zhu L, Zhang J, Qiu J, Du G, Qiao Z, Jin G, Gao F, Zhang Q - PLoS ONE (2015)

Time course and concentration dependence of nicotine activation of EGR-1 in SH-SY5Y cells.a, b) Nicotine activates EGR-1 in the nanomolar to micromole range when SH-SY5Y cells were treated with nicotine for 30 min; the relative level of EGR1 was quantified and presented in panel b. β-actin serves as control. c-e) The SH-SY5Y cells were with 10-6M nicotine by the indicated time, the relative level of EGR1 was quantified and presented in panel d and f respectively. β-actin serves as control. g) The mRNA level of EGR1 in SH-SY5Y cells after nicotine treatment was measured by RT-PCR. i) Immunofluorescence was shown when SH-SY5Y cells were treated by nicotine compared to control.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4376385&req=5

pone.0120267.g001: Time course and concentration dependence of nicotine activation of EGR-1 in SH-SY5Y cells.a, b) Nicotine activates EGR-1 in the nanomolar to micromole range when SH-SY5Y cells were treated with nicotine for 30 min; the relative level of EGR1 was quantified and presented in panel b. β-actin serves as control. c-e) The SH-SY5Y cells were with 10-6M nicotine by the indicated time, the relative level of EGR1 was quantified and presented in panel d and f respectively. β-actin serves as control. g) The mRNA level of EGR1 in SH-SY5Y cells after nicotine treatment was measured by RT-PCR. i) Immunofluorescence was shown when SH-SY5Y cells were treated by nicotine compared to control.
Mentions: EGR-1 is an important transcription factor in AD [14–18, 21]. We detected the time course and concentration dependent effect of nicotine on the activation of EGR-1. As shown in Fig. 1, EGR-1 was dramatically activated by 10–6 M nicotine in 30 minutes (Fig. 1A). EGR-1 was quickly activated during time course, and the peak response occurred at 45 min (Fig. 1C, 1E). The activation of EGR-1 was then decreased with 1 hour treatment. This data confirms others' reports that nicotine could immediately activate EGR-1 and follow to basal level [22, 23]. The quantification data was presented on the right panels (Fig. 1B, 1D, 1F).

Bottom Line: In addition, the up-regulation of EGR-1 by nicotine can also increase the phosphorylation of CyclinD1 which contributes to the attenuation of amyloid-β (Aβ(25-35)) -induced neurotoxicity.Although nicotine and Aβ(25-35) can activate EGR-1, the expression of EGR-1 is down-regulated following treatment with nicotine and Aβ(25-35).This study demonstrates that low dose nicotine attenuates Aβ(25-35)-induced neurotoxicity in vitro and in vivo through activating EGR-1 pathway.

View Article: PubMed Central - PubMed

Affiliation: College of Chemistry and Chemical Engineering, Xiamen University, Xiamen, Fujian, 361005, P.R.China; Institute of Biomedical Engineering, Department of Biomaterials, College of Materials, Xiamen University, Xiamen, Fujian, 361005, P.R.China; Department of Basic Medical Science, Medical College, Xiamen University, Xiamen, Fujian, 361005, P.R.China.

ABSTRACT
Epidemiological studies indicate that smoking is negatively correlated with the incidence and development of Alzheimer's disease (AD). Nicotine was reported to be the active factor. However, the detailed mechanisms still remain to be fully elucidated. Early growth response gene 1 (EGR-1) plays important roles in several important biological processes such as promoting cell growth, differentiation, anti oxidative stress, and apoptosis, but few in the pathogenesis of AD. In the present study, we show that nicotine can activate the MAPK/ERK/EGR-1 signaling pathway partially through α7 nAChR. In addition, the up-regulation of EGR-1 by nicotine can also increase the phosphorylation of CyclinD1 which contributes to the attenuation of amyloid-β (Aβ(25-35)) -induced neurotoxicity. Although nicotine and Aβ(25-35) can activate EGR-1, the expression of EGR-1 is down-regulated following treatment with nicotine and Aβ(25-35). This study demonstrates that low dose nicotine attenuates Aβ(25-35)-induced neurotoxicity in vitro and in vivo through activating EGR-1 pathway.

No MeSH data available.


Related in: MedlinePlus