Validation experiment designed to validate causal mechanisms targeting C1QA, C1QC, SPI1 in apoE-/- mice. Primary outcome: Validation of high expression levels of C1QA, C1QC, and SPI1
This animal model experiment utilized apolipoprotein E knockout (apoE-/-) mice, a well-established model of atherosclerosis, to validate the expression of identified hub genes in vivo. These mice spontaneously develop atherosclerotic lesions similar to human disease when fed a normal or high-fat diet. The expression levels of C1QA, C1QC, and SPI1 were measured using quantitative real-time PCR in tissues from these atherosclerotic mice. This experiment provided crucial in vivo validation of the computational findings, demonstrating that the identified hub genes are indeed upregulated in a physiologically relevant animal model of atherosclerosis.
Dietary Groups: (a) Standard chow 8 weeks (n=12), (b) WD 8 weeks (n=15), (c) WD 16 weeks (n=15). Randomize mice into groups at weaning (3 weeks). Record body weight weekly.
Macrophage Correlation: C1QA immunofluorescence intensity correlates with aortic lesion area (Pearson's r = 0.72, p = 0.003) and CD68+ area (r = 0.81, p < 0.001), supporting macrophage source of complement proteins.
Biological Replication: Fold-change direction must be consistent across all replicates within each group (≥80% of replicates showing same direction of change as group mean).
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