| Description: |
Background: Angiogenesis, the formation of new blood vessels, plays a key role in development and cancer. In mice, we identified a critical role for Large Ribosomal Subunit Protein 17 (RpL17) in suppressing endothelial cell (EC) proliferation and migration, integral processes for angiogenesis. RNA sequencing of RpL17 knockdown (RpL17-KD) ECs revealed Early Growth Response 1 (EGR1), a known proangiogenic factor, as a key gene following RpL17-KD. In-silico , Breast Cancer gene 1 (BRCA1) was predicted as an RpL17 regulator, suggesting a novel signaling pathway. Hypothesis: BRCA1 regulates RpL17, which elevates EGR1 to increase angiogenesis in ECs. Goal: Investigate the role of the BRCA1-RpL17-EGR1 axis in angiogenesis. Methods: We performed RNA-sequencing on mouse ECs, whole retina staining, and tube formation assays in ECs to examine the effects of RpL17, BRCA1, and EGR1 knockdowns. Mouse models, bioinformatics, RT-qPCR, immunoblotting, and immunofluorescence were used to validate findings and assess gene/protein expression. Results: RpL17 deficient (RpL17+/-) mouse retinas showed increased angiogenesis (n=10, p |