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Nicotine enhances angiotensin II-induced mitogenic response in vascular smooth muscle cells and fibroblasts.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Li, Jian-Mei Cui, T. A. Shiuchi, Tetsuya Liu, Hong-Wei Min, Li-Juan Okumura, Midori Jinno, Toyohisa Wu, Lan Iwai, Masaru Horiuchi, Masatsugu |
| Copyright Year | 2004 |
| Abstract | OBJECTIVE The pathogenetic mechanism of tobacco-related cardiovascular diseases is still not well defined. We examined the potential possibility of an interaction between nicotine, a major component of cigarette smoke, and angiotensin II (Ang II), which plays an important role in the pathogenesis of cardiovascular diseases characterized by Ang II type 1 (AT1) receptor-mediated abnormal growth of vascular smooth muscle cells (VSMC) and fibroblasts. METHODS AND RESULTS Nicotine or Ang II-stimulated [3H]thymidine incorporation and c-fos expression in adult rat aortic VSMC and adventitial fibroblast. The nicotine-induced DNA synthesis was not affected by valsartan, an AT1 receptor-specific blocker, or PD123319, an Ang II type 2 (AT2) receptor-specific antagonist. Nicotine or Ang II stimulation rapidly increased extracellular signal-regulated kinase (ERK) activation, tyrosine- and serine-phosphorylation of signal transducer and activator of transcription (STAT)1 and STAT3, and p38 mitogen-activated protein kinase (p38 MAPK), in both cell types. Interestingly, co-administration of nicotine and Ang II at lower doses, which did not affect cell growth, induced DNA synthesis and c-fos expression accompanied by enhancement of ERK, STAT, and p38MAPK activity. PD98059, a mitogen-activated protein kinase/ERK kinase inhibitor, or SB23058, a p38MAPK inhibitor, significantly attenuated the vasotrophic effect of nicotine and Ang II. CONCLUSIONS These results suggest that nicotine exerts a growth-promoting effect on vascular cells and enhances the Ang II-induced vasotrophic effect, which is at least partly mediated by the activation of ERK, STAT, and p38MAPK. |
| Starting Page | 1 |
| Ending Page | 6 |
| Page Count | 6 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://atvb.ahajournals.org/content/atvbaha/early/2003/10/30/01.ATV.0000104007.17365.1c.full.pdf?legid=atvbaha%3B01.ATV.0000104007.17365.1cv1&related-urls=yes |
| Alternate Webpage(s) | http://atvb.ahajournals.org/content/atvbaha/24/1/80.full.pdf |
| Alternate Webpage(s) | http://atvb.ahajournals.org/content/24/1/80.full.pdf |
| Alternate Webpage(s) | http://atvb.ahajournals.org/content/atvbaha/early/2003/10/30/01.ATV.0000104007.17365.1c.full.pdf |
| Alternate Webpage(s) | http://atvb.ahajournals.org/content/atvbaha/24/1/80.full.pdf?download=true |
| PubMed reference number | 14592853v1 |
| Volume Number | 24 |
| Issue Number | 1 |
| Journal | Arteriosclerosis, thrombosis, and vascular biology |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Angiotensin II Angiotensins Cardiovascular Diseases DNA Replication Diabetes Mellitus, Non-Insulin-Dependent FOS gene Mitogen-Activated Protein Kinases Mitogens Muscle, Smooth, Vascular Myocytes, Smooth Muscle Nicotine PD 98059 Promotion (action) STAT protein Smooth muscle (tissue) Stat3 protein Transducers cell growth cell type eIF-2 Kinase valsartan |
| Content Type | Text |
| Resource Type | Article |
