Related Experiment Videos
Complement gene expression by rabbit heart: upregulation by ischemia and reperfusion
K Yasojima1, K S Kilgore, R A Washington
1Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, Canada.
Circulation Research
|June 20, 1998
Summary
The heart produces complement proteins C3 and C9, challenging the liver-centric view. Ischemia and reperfusion significantly increase these complement gene expressions in the heart.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Biology
Background:
- The complement system plays a role in myocardial ischemia/reperfusion injury.
- The liver is traditionally considered the primary source of complement components.
Purpose of the Study:
- To investigate the expression of complement proteins C3 and C9 in the rabbit heart.
- To determine if ischemia and reperfusion affect complement gene expression in the heart.
Main Methods:
- Reverse-transcriptase polymerase chain reaction (RT-PCR) to detect mRNA for C3 and C9.
- Western blotting to confirm protein expression.
- Langendorff-perfused isolated rabbit hearts subjected to ischemia and reperfusion.
Main Results:
- Heart tissue expresses mRNAs for complement proteins C3 and C9, which are translated into proteins.
- Ischemia and reperfusion significantly upregulate C3 and C9 mRNA levels in the heart.
- Upregulation of C3 and C9 mRNA in the heart under stress exceeds levels found in normal liver.
Conclusions:
- The heart is capable of expressing complement system genes and proteins.
- Local complement production in the heart may significantly contribute to ischemic injury.
- Reperfusion augments complement expression, exacerbating myocardial damage.