Anti-ischemia/reperfusion of C1 inhibitor in myocardial cell injury via regulation of local myocardial C3 activity

Jinrong Fu, Guosheng Lin, Bin Zeng, Zhiwei Wu, Yanxia Wu, Honggang Chu, Gangjian Qin, Gong Liang, Jinan Li, Xiang Gan, Xiaolan Yu, Chunhua Li, Dongxu Liu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


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 languageEnglish (US)
Pages (from-to)162-168
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - Nov 10 2006


  • C1 inhibitor
  • C3
  • Cardiomyocyte
  • Complement
  • Hemolysis
  • Ischemia
  • Reperfusion

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


Dive into the research topics of 'Anti-ischemia/reperfusion of C1 inhibitor in myocardial cell injury via regulation of local myocardial C3 activity'. Together they form a unique fingerprint.

Cite this