Letter by Rus et al Regarding Article, “RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis”
To the Editor:
The recently published article by Cui et al1 sheds new light on the role of RGC-32 (response gene to complement 32) in atherogenesis. This interesting article describes a new mechanism of action of RGC-32 in inducing the expression of the endothelial cell adhesion molecules ICAM-1 and VCAM-1, which are necessary for monocyte recruitment into the atherogenic lesion core. We would like to add a few comments on several findings reported in this article.
We have also examined the expression of RGC-32 in the human aortic atherosclerotic wall.2 We found that RGC-32 was expressed in human aortic atherosclerotic lesions: by endothelial cells, by inflammatory cells (CD4+ and CD68+ cells) in intimal thickenings and fibrous …