Fig. 7

Hematopoietic NOD1 deficiency mitigates the increase in neutrophil chemoattractants and NETosis markers in Akita mice. A Quantitative PCR analysis of proinflammatory and anti-inflammatory gene expression in the retinas of NOD1^−/−-Akita → Akita mice and their cohorts (n = 8 per group). B, C Measurement of CXCL1 and CXCL2 production in the culture supernatant of BMDMs treated with peptidoglycan for 24 h (ELISA, n = 8 per group). D, E Detection of neutrophil elastase and myeloperoxidase in the retina (ELISA, n = 6 per group). F Assessment of NOD1 stimulatory activity in serum samples from human subjects using a HEK293T cell-based reporter assay (HC, n = 12; DM-NC, n = 8; NPDR, n = 8). G Schematic diagram of the mechanisms of hematopoietic NOD1-mediated DR progression. Data are presented as the mean ± SD; *p < 0.05, **p < 0.01. WT, wild type; N.D., nondetectable; NE, neutrophil elastase; MPO, myeloperoxidase; HC, healthy controls; DM-NC, diabetes with no microvascular complications; NPDR, nonproliferative diabetic retinopathy