Response by Cui et al to Letter Regarding Article, “RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis”

We welcome the letter from Rus et al commenting on our recent study showing that RGC-32 (response gene to complement 32) mediates the development of atherosclerosis by facilitating monocyte–endothelial cell (EC) interaction through induction of endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1.1 Our conclusion is based on several observations: (1) RGC-32 is induced in ECs in both human and mouse atherosclerotic lesions; (2) RGC-32 deficiency ( Rgc32 −/−) attenuates the spontaneously-developed and high-fat diet–induced atherosclerosis in Apoe −/− mice; (3) Rgc32 −/− mice transplanted with wild-type bone marrow does not significantly alter the Rgc32 −/− phenotype; (4) Rgc32 −/− inhibits endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1expression and monocyte–EC interaction.1 These data strongly suggest that endothelial RGC-32 plays an essential role in atherosclerosis.We understand the concern in the letter about the differences in RGC-32 expression in human atherosclerotic lesions in our and Dr Vlaicu et al’s2 studies and appreciate the insights that the discrepancy may be the result of the differences in the atherosclerotic lesions from different arterial regions. …