Hypoxia and antioxidants enhance soluble ICAM-1 release from cardiac fibroblasts
| dc.contributor | Sapna, S. | |
| dc.contributor | Shivakumar, K. | |
| dc.date.accessioned | 2012-12-04T11:44:17Z | |
| dc.date.available | 2012-12-04T11:44:17Z | |
| dc.date.issued | 2007 | |
| dc.description.abstract | Intercellular adhesion molecule-1 plays a key role in mediating inflammatory and immune responses. There is also increasing appreciation of the role of its soluble form, sICAM-1, in regulating inflammation. This study evaluated the effects of hypoxia and N-acetyl-L-cysteine on sICAM-1 production by adult rat cardiac fibroblasts. By ELISA, hypoxia was found to cause a 61% increase in sICAM-1 in cardiac fibroblast culture supernates. However, RT-PCR did not reveal a concomitant increase in cell surface ICAM-1 transcript levels, suggesting that the increase in sICAM-1 may involve post-transcriptional and/or post-translational mechanisms. Using pharmacological inhibitors, it was observed that p42/44 MAPK and PKC mediate the stimulatory effect of hypoxia on sICAM-1 production. Remarkably, N-acetyl-L-cysteine caused a 3-fold increase in sICAM-1 by p42/44 MAPK-, p38 MAPK- and PKC-independent mechanisms. Pyrrolidine dithiocarbamate, another potent antioxidant, also augmented sICAM-1. The findings presented in this communication underscore the link between redox status and sICAM-1 release from cardiac fibroblasts. Further, because hypoxia is a major component of myocardial ischemia and is pro-inflammatory, and both N-acetylcysteine and pyrrolidine dithiocarbamate are clinically used antioxidants, the observations may have clinical significance. | |
| dc.identifier.citation | MOLECULAR AND CELLULAR BIOCHEMISTRY. 303; 40910; 259-262 | en_US |
| dc.identifier.uri | http://dx.doi.org/10.1007/s11010-007-9475-9 | |
| dc.identifier.uri | http://www.ncbi.nlm.nih.gov/pubmed/17458516 | |
| dc.identifier.uri | https://dspace.sctimst.ac.in/handle/123456789/589 | |
| dc.publisher | MOLECULAR AND CELLULAR BIOCHEMISTRY | |
| dc.subject | Cardiology | |
| dc.title | Hypoxia and antioxidants enhance soluble ICAM-1 release from cardiac fibroblasts |