Figure 2.
(A) Fluorescence intensity of nephrin retained in the glomerulus, interstitial macrophage infiltration (defined by F4/F80-positive cells), and collagen IV deposition in the transgenic sickle and Hb AA mice. Representative images at 200× of hemosiderin deposition by Prussian blue stain (B) and interstitial fibrosis by Masson trichrome stain (C) in the transgenic sickle and Hb AA mice. (D) Representative images of ultrastructural changes by transmission electron microscopy. Yellow arrows represent foot process effacement, green arrows represent segmental basement membrane reduplication and subendothelial electron-lucent widening, and orange asterisks represent segmental mesangial interposition with new basement membrane formation. (E) Heat map of genes differentially expressed in isolated glomeruli and kidney cortices of GBT1118-treated sickle, control sickle, and Hb AA mice (false discovery rate <0.05). **P < .01 for differences between the GBT1118-treated vs control sickle mice.

(A) Fluorescence intensity of nephrin retained in the glomerulus, interstitial macrophage infiltration (defined by F4/F80-positive cells), and collagen IV deposition in the transgenic sickle and Hb AA mice. Representative images at 200× of hemosiderin deposition by Prussian blue stain (B) and interstitial fibrosis by Masson trichrome stain (C) in the transgenic sickle and Hb AA mice. (D) Representative images of ultrastructural changes by transmission electron microscopy. Yellow arrows represent foot process effacement, green arrows represent segmental basement membrane reduplication and subendothelial electron-lucent widening, and orange asterisks represent segmental mesangial interposition with new basement membrane formation. (E) Heat map of genes differentially expressed in isolated glomeruli and kidney cortices of GBT1118-treated sickle, control sickle, and Hb AA mice (false discovery rate <0.05). **P < .01 for differences between the GBT1118-treated vs control sickle mice.

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