Ischemia and reperfusion cause myocardial edema. Myocardial edema itself impairs heart function and is therefore potentially important in the pathophysiology of ischemia-reperfusion injury.
Aquaporins (AQPs) are a family of water channel proteins (all together there are 12 AQPs) that facilitate movement of water by increasing membrane water permeability, increasing water flux in response to osmotic gradients. Very little is known about AQPs in the human heart, but in some noncardiac tissues, such as brain and cornea, the involvement of AQPs in the development and resolution of tissue edema has been demonstrated.
Our group have earlier found that AQP4-KO mice had increased resistance to ischemia-reperfusion injury, but we also found that AQP1-mRNA was increased in AQP4-KO, whereas Western blot showed no difference at protein-level of AQP1 in AQP4-KO compared mice which where not altered genetically.
We have therefore, by transmission immuno electron microscopy, investigated the subcellular distribution and localization of AQP1 in mice hearts, and whether it is upregulated in AQP4-KO as a compensatory mechanism.
We found that AQP1 is concentrated along capillaries in the heart, and that it seems to be more AQP1 on the nearest surface (23,5 nm) of the endothelial cells compared to the basal membrane, but this difference is not present if we count along AQP1 located 100 nm away from each of the membranes, wich may indicate that AQP1 is present in caveolae in the cardiac capillaries. There is not more AQP1 in t-tubuli as compared to the cardiomyocyte cell membrane (plasma membrane). AQP-1 is not upregulated in AQP4-KO.