Chronic ethanol exposure enhances activating protein-1 transcriptional activity in human neuroblastoma cells
(2001) In Alcohol 24(3). p.189-195- Abstract
- This study demonstrates a method for studying the effects of ethanol on transcription mediated by activating protein-1 (AP-1). The effects of ethanol on AP-1 activity and on the signaling cascades in this process were investigated by using a reporter gene technique with secreted alkaline phosphatase as the reporter gene coupled to nine DNA AP-1-binding elements. Long-term ethanol exposure (48-72 h) dose dependently enhanced AP-1 transcriptional activity in SH-SY5Y cells. Shorter exposure periods with ethanol did not influence AP-1 transcriptional activity compared with findings for control cells. Inhibition of protein kinase C (PKC) dramatically decreased AP-1 activity in both control and ethanol-exposed cells and abolished the ethanol... (More)
- This study demonstrates a method for studying the effects of ethanol on transcription mediated by activating protein-1 (AP-1). The effects of ethanol on AP-1 activity and on the signaling cascades in this process were investigated by using a reporter gene technique with secreted alkaline phosphatase as the reporter gene coupled to nine DNA AP-1-binding elements. Long-term ethanol exposure (48-72 h) dose dependently enhanced AP-1 transcriptional activity in SH-SY5Y cells. Shorter exposure periods with ethanol did not influence AP-1 transcriptional activity compared with findings for control cells. Inhibition of protein kinase C (PKC) dramatically decreased AP-1 activity in both control and ethanol-exposed cells and abolished the ethanol enhancement. This finding suggests a pivotal role for PKC-coupled signaling in AP-1 transcriptional activity. Phorbol ester stimulation of AP-1 transcriptional activity was not influenced by long-term ethanol exposure. This finding indicates that signaling events upstream of PKC are the targets for ethanol. Mitogen-activated protein kinases ERK and p38 may play a role in ethanol-enhanced AP-1 activity because inhibitors of both enzymes partly reduced the enhancement. The inhibitors also partly blocked phorbol ester-induced AP-1 activation, which demonstrates a function of these mitogen-activated protein kinases downstream of PKC. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1119920
- author
- Fried, Ulrik LU ; Kotarsky, Knut LU and Alling, Christer LU
- organization
- publishing date
- 2001
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- SH-SY5Y, Reporter gene, Mitogen-activated protein kinases, Protein kinase C, Activating protein-1, Ethanol
- in
- Alcohol
- volume
- 24
- issue
- 3
- pages
- 189 - 195
- publisher
- Elsevier
- external identifiers
-
- pmid:11557304
- scopus:0034857234
- ISSN
- 0741-8329
- DOI
- 10.1016/S0741-8329(01)00151-3
- language
- English
- LU publication?
- yes
- id
- e0b87221-94a8-4639-8742-a67813aab0cf (old id 1119920)
- date added to LUP
- 2016-04-01 12:09:37
- date last changed
- 2022-01-26 23:41:49
@article{e0b87221-94a8-4639-8742-a67813aab0cf,
abstract = {{This study demonstrates a method for studying the effects of ethanol on transcription mediated by activating protein-1 (AP-1). The effects of ethanol on AP-1 activity and on the signaling cascades in this process were investigated by using a reporter gene technique with secreted alkaline phosphatase as the reporter gene coupled to nine DNA AP-1-binding elements. Long-term ethanol exposure (48-72 h) dose dependently enhanced AP-1 transcriptional activity in SH-SY5Y cells. Shorter exposure periods with ethanol did not influence AP-1 transcriptional activity compared with findings for control cells. Inhibition of protein kinase C (PKC) dramatically decreased AP-1 activity in both control and ethanol-exposed cells and abolished the ethanol enhancement. This finding suggests a pivotal role for PKC-coupled signaling in AP-1 transcriptional activity. Phorbol ester stimulation of AP-1 transcriptional activity was not influenced by long-term ethanol exposure. This finding indicates that signaling events upstream of PKC are the targets for ethanol. Mitogen-activated protein kinases ERK and p38 may play a role in ethanol-enhanced AP-1 activity because inhibitors of both enzymes partly reduced the enhancement. The inhibitors also partly blocked phorbol ester-induced AP-1 activation, which demonstrates a function of these mitogen-activated protein kinases downstream of PKC.}},
author = {{Fried, Ulrik and Kotarsky, Knut and Alling, Christer}},
issn = {{0741-8329}},
keywords = {{SH-SY5Y; Reporter gene; Mitogen-activated protein kinases; Protein kinase C; Activating protein-1; Ethanol}},
language = {{eng}},
number = {{3}},
pages = {{189--195}},
publisher = {{Elsevier}},
series = {{Alcohol}},
title = {{Chronic ethanol exposure enhances activating protein-1 transcriptional activity in human neuroblastoma cells}},
url = {{http://dx.doi.org/10.1016/S0741-8329(01)00151-3}},
doi = {{10.1016/S0741-8329(01)00151-3}},
volume = {{24}},
year = {{2001}},
}