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. 2024 Nov 28;36(1):102408. doi: 10.1016/j.omtn.2024.102408

Figure 1.

Figure 1

Hypertension, proteinuria, renal pathology, and reduced fetal weight in pregnant Axl knockout mice

(A) Repeated tail-cuff systolic blood pressure (SBP) measurements of Axl+/+(n = 6) and Axl−/− (n = 7) mice before and during pregnancy. (B) Urine albumin/creatinine ratios of Axl+/+ and Axl−/− mice. Urine samples were collected (from E14.5 to E17.5) in metabolic cages (n = 3). (C) H&E and PAS staining of renal tissues from pregnant Axl+/+ and Axl−/− mice. The H&E staining reveals glomerular enlargement in Axl−/− mice. The PAS staining shows increased extracellular matrixes and collapsed glomerular capillaries in the Axl−/− mice. The findings were observed in at least three individual samples. (D) Transmission electron microscopy (TEM) imaging of the narrow glomerular capillary lumen (L), thick glomerular basement membranes (GBM), and the shortened secondary processes of podocytes indicate endothelial hyperplasia and extracellular matrix (EC) expansion in Axl−/− glomeruli (indicated by red lines) (n = 3). X-magnification 15,000× and Y-magnification 6,000×. (E) Uterine artery blood flow velocity waveforms in Axl+/+ and Axl−/− mice, assessed using pulse Doppler ultrasonography starting from E14.5 (n = 3). (F and G) Uterine artery waveforms from Axl+/+ and Axl−/− were analyzed to obtain resistance and pulsatility indexes. Values are means ± SEMs. Data are from 4 to 5 independent litters. (H) Representative photographs of placentas and fetuses of E14.5 Axl+/+ and Axl−/− mice. (I and J) Placental and fetal weights (E14.5) were reduced in Axl−/− females compared to Axl+/+ females. All data are expressed as means ± SDs. Scale bar, 20 μm. np, not pregnant. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001.