Abstract
C3 is common to all pathways of complement activation augmenting ischemia/reperfusion (I/R)-induced myocardial injury and cardiac dysfunction. Complement inhibition with the complement regulatory protein, C1 inhibitor (C1INH), obviously exerts cardioprotective effects. Here, we examine whether C1INH regulates C3 activity in the ischemic myocardial tissue. C1INH markedly suppressed C3 mRNA expression and protein synthesis in both a model of I/R-induced rat acute myocardial infarction (AMI) and the cultured rat H9c2 heart myocytes. At least, this regulation was at the transcriptional level in response to oxygen tension. In vitro, C3 deposition on, and binding to, the surface of rat myocardial cells were significantly blocked by C1INH treatment. C1INH could inhibit classical complement-mediated cell lysis via suppressing the biological activity of C3. Therefore, C1INH, in addition to inhibition of the systemic complement activation, prevents myocardial cell injury via a direct inhibitory role in the local myocardial C3 activity.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 162-168 |
| Number of pages | 7 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 350 |
| Issue number | 1 |
| DOIs | |
| State | Published - Nov 10 2006 |
Funding
We thank Jun Cai, Difei Sheng, Teng Wang, and Ping Hu (Department of Cardiology, Renmin Hospital, Wuhan University School of Medicine, Wuhan, China) for great assistance. This work was supported by Grants from Chutian Xuezhe Plan of Hubei in China and Hubei University Foundation in China to Dongxu Liu.
Keywords
- C1 inhibitor
- C3
- Cardiomyocyte
- Complement
- Hemolysis
- Ischemia
- Reperfusion
ASJC Scopus subject areas
- Molecular Biology
- Biophysics
- Biochemistry
- Cell Biology