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. 2016 Dec 5;28(5):1475–1490. doi: 10.1681/ASN.2016070709

Figure 2.

Figure 2.

Figure 2.

Periostin KO mice are protected from the development of NTS-induced GN. (A and B) Periostin mRNA (A) and protein (B) are increased in NTS-induced GN. (C and D) Periostin KO mice are highly protected from the increase in weight (C) and proteinuria (D) caused by NTS. (E) Masson trichrome staining showing reduced fibrosis and tissue damage in periostin KO mice (upper panels, ×200; lower panels, ×400). (F) Quantification of glomerular lesions. (G–I) mRNA expression of the fibrotic molecules COL1 (G), COL3 (H), and TGF-β1 (I) is highly decreased in periostin KO mice after NTS. (J–L) mRNA expression of the inflammatory mediators MCP-1 (J), RANTES (K), and VCAM-1 (L) is diminished in periostin KO mice after NTS. (M and N) F4/80 (M) and CD3 (N) staining showing markedly decreased accumulation of macrophages and lymphocytes, respectively, in periostin KO mice after NTS. Quantification of the staining is shown in the graphs below. mRNA and protein results from the whole kidney are shown (A, B, G–L). Animals were euthanized after 14 days of NTS administration. Scale bars, 100 μm (E, M, and N). n=6–7 per group. *P<0.05; **P<0.01 versus WT PBS or WT NTS; #P<0.05 versus WT NTS. WT, wild type.