Abstract
Several chemicals present in cigarette smoke (CS) have been reported to induce heme oxygenase-1 (HO-1) expression, which represents a prime defense mechanism in protecting the cells from stress-dependent adverse effects on peripheral vascular system. However, the effects of cigarette smoke extract (CSE) on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in brain vessels are not completely understood. Here, we used a mouse brain endothelial cell culture (bEnd.3) to investigate the effect of CSE on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in cerebral vessels. We demonstrated that sublethal concentrations of CSE (30-μg/ml) induced submaximal HO-1 expression in bEnd.3 cells. NADPH oxidase-dependent ROS generation played a key role in CSE-induced HO-1 expression. CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was observed by pretreatment with the respective pharmacological inhibitors or transfection with PDGFR shRNA. CSE activated NADPH oxidase through c-Src in bEnd.3 cells. Taken together, these results suggested that, in bEnd.3 cells, CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was regulated by c-Src or c-Src activated-NADPH oxidase/ROS.
| Original language | English |
|---|---|
| Pages (from-to) | 741-750 |
| Number of pages | 10 |
| Journal | Journal of Cellular Physiology |
| Volume | 225 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Dec 1 2010 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Physiology
- Clinical Biochemistry
- Cell Biology
Cite this
Cigarette smoke extract induces HO-1 expression in mouse cerebral vascular endothelial cells : Involvement of c-Src/NADPH oxidase/PDGFR/JAK2/STAT3 pathway. / Shih, Ruey Horng; Lee, I-Ta; Hsieh, Hsi Lung; Kou, Yu Ru; Yang, Chuen Mao.
In: Journal of Cellular Physiology, Vol. 225, No. 3, 01.12.2010, p. 741-750.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cigarette smoke extract induces HO-1 expression in mouse cerebral vascular endothelial cells
T2 - Involvement of c-Src/NADPH oxidase/PDGFR/JAK2/STAT3 pathway
AU - Shih, Ruey Horng
AU - Lee, I-Ta
AU - Hsieh, Hsi Lung
AU - Kou, Yu Ru
AU - Yang, Chuen Mao
PY - 2010/12/1
Y1 - 2010/12/1
N2 - Several chemicals present in cigarette smoke (CS) have been reported to induce heme oxygenase-1 (HO-1) expression, which represents a prime defense mechanism in protecting the cells from stress-dependent adverse effects on peripheral vascular system. However, the effects of cigarette smoke extract (CSE) on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in brain vessels are not completely understood. Here, we used a mouse brain endothelial cell culture (bEnd.3) to investigate the effect of CSE on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in cerebral vessels. We demonstrated that sublethal concentrations of CSE (30-μg/ml) induced submaximal HO-1 expression in bEnd.3 cells. NADPH oxidase-dependent ROS generation played a key role in CSE-induced HO-1 expression. CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was observed by pretreatment with the respective pharmacological inhibitors or transfection with PDGFR shRNA. CSE activated NADPH oxidase through c-Src in bEnd.3 cells. Taken together, these results suggested that, in bEnd.3 cells, CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was regulated by c-Src or c-Src activated-NADPH oxidase/ROS.
AB - Several chemicals present in cigarette smoke (CS) have been reported to induce heme oxygenase-1 (HO-1) expression, which represents a prime defense mechanism in protecting the cells from stress-dependent adverse effects on peripheral vascular system. However, the effects of cigarette smoke extract (CSE) on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in brain vessels are not completely understood. Here, we used a mouse brain endothelial cell culture (bEnd.3) to investigate the effect of CSE on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in cerebral vessels. We demonstrated that sublethal concentrations of CSE (30-μg/ml) induced submaximal HO-1 expression in bEnd.3 cells. NADPH oxidase-dependent ROS generation played a key role in CSE-induced HO-1 expression. CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was observed by pretreatment with the respective pharmacological inhibitors or transfection with PDGFR shRNA. CSE activated NADPH oxidase through c-Src in bEnd.3 cells. Taken together, these results suggested that, in bEnd.3 cells, CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was regulated by c-Src or c-Src activated-NADPH oxidase/ROS.
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UR - http://www.scopus.com/inward/citedby.url?scp=77957850108&partnerID=8YFLogxK
U2 - 10.1002/jcp.22270
DO - 10.1002/jcp.22270
M3 - Article
VL - 225
SP - 741
EP - 750
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
SN - 0021-9541
IS - 3
ER -