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. 2020 Jun 19;117(27):15862–15873. doi: 10.1073/pnas.2004651117

Fig. 2.

Fig. 2.

Glomerular NPY expression is significantly down-regulated in human renal disease. (A) NPY expression (log2 mRNA intensity) in Pima early diabetic nephropathy (DN, n = 69) vs. healthy living donors (n = 18). *P < 0.05. (B) Data from Nephroseq: NPY expression (log2 median-centered intensity) in the Ju CKD Glom dataset: healthy living donor (n = 21) and DN (n = 12); under-expression gene rank 3,211 (in top 19%). *P < 0.05. (C) Correlation between glomerular NPY expression (log2 median-centered intensity) and eGFR in the Ju CKD Glom dataset: healthy living donors and diabetic nephropathy, n = 33. (D) NPY expression (log2 median-centered mRNA intensity) in Ju CKD Glom, showing a significant regulation in glomerular NPY in FSGS (n = 46), vasculitis (n = 44), lupus nephritis (n = 53), arterial hypertension (n = 36), and thin basement membrane disease (n = 24) vs. healthy living donors. (E) qPCR results showing relative levels of NPY expression in human glomerular cell lines (Pod, podocytes; Endo, glomerular endothelial cells; Mes, mesangial cells); n = 3 to 5; *P < 0.05. (F) RT-PCR for NPY and β-Actin in human glomerular cell lines under conditions of active (33 °C) and inactive (37 °C) SV40 expression (Endo, glomerular endothelial cells; Pod1 and Pod2, two independent human podocyte cell lines; Mes, mesangial cells) and isolated human glomeruli.