Fig. 1: Kidney damage and autophagolysosome accumulation in Sidt2−/− mice. | Cell Death & Disease

Fig. 1: Kidney damage and autophagolysosome accumulation in Sidt2−/− mice.

From: Sidt2 is a key protein in the autophagy-lysosomal degradation pathway and is essential for the maintenance of kidney structure and filtration function

Fig. 1

A Cre-LoxP system gene targeting schematic; B above is the exported sequence diagram of Sidt2 gene knockout mouse tail DNA; below is the sequencing map, the arrow indicating the location of the missing gene. Compared with WT mice, a 199 bp gene loss occurs in exon 2; C DNA level verification of Sidt2 (extracted from tail tissue). The primer-amplified product contains the base knockout region, shown as Sidt2+ /+(WT), Sidt2+/−, or Sidt2−/−; D protein level verification to detect Sidt2 protein expression levels by western blot; E kidney 24 h urine protein in WT and Sidt2−/− mice; F ultra-micro-morphological structure of the kidneys of WT mice (a, f) and Sidt2−/− mice (g–n). Compared with the WT mouse, the Sidt2−/− mouse kidney displays foot process fusion, basement membrane thickening (g, h), renal tubular epithelial cell edema, microvilli damage (i, j), mitochondrial destruction (k, l), and autophagolysosome accumulation (m, n); G total number of renal autophagolysosomes in WT and Sidt2−/− mice. *P < 0.05, **P < 0.01.

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