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. 2022 Jun 22;7(12):e158754. doi: 10.1172/jci.insight.158754

Figure 2. Blocking CDK4/6 reduces tubular injury, fibrosis, and senescence after UniNx/AngII.

Figure 2

(A and B) Diagram of cell cycle progression at G1/S and injury schematic for UniNx/AngII. (C and D) UniNx/AngII-treated kidney lysates were blotted for retinoblastoma protein (Rb) phosphorylated at serine807/811, the target of CDK4/6. (E and F) H&E of kidneys injured by UniNx/AngII and treated with either gavage or palbociclib, a CDK4/6 inhibitor (E) and quantification of tubular injury (F). (G and H) Gene expression of KIM-1 from injured kidney cortices measured by qPCR and BUN from plasma at the time of sacrifice. (I–L and N–Q) Staining and quantification of Picrosirius red (I and J), collagen I (K and L), F4/80 (N and O), and TUNEL (P and Q). (M) Collagen I gene expression (Col1a1) measured from renal cortices using qPCR. (R–T) Senescence assessed by β-galactosidase staining on frozen sections (R and S) and gene expression of p21 (Cdkn1a) on injured renal tissue (T). The percentage of β-galactosidase+ area was quantified on 400× fields (S). *P < 0.05,**P < 0.01, and ***P < 0.001 calculated by 2-tailed Student’s t test. Scale bar: 50 μm for 400× and 100 μm for 200×.