Fig. 9: LncDACH1 affected NIH in the context of AVF by regulating VSMC phenotype switching. | Nature Communications

Fig. 9: LncDACH1 affected NIH in the context of AVF by regulating VSMC phenotype switching.

From: LncRNA-LncDACH1 mediated phenotypic switching of smooth muscle cells during neointimal hyperplasia in male arteriovenous fistulas

Fig. 9

a The expression level of Ki67, CD68, CD31, α-SMA, Vimentin and FSP-1 in mouse before AVF (n = 10) versus 14 days after AVF (n = 9) were detected by immunohistochemistry assay. b The expression level of Ki67, CD68, CD31, α-SMA, Vimentin and FSP-1 in mouse without established AVF in AAV-Vector (n = 9) and AAV-LncDACH1 (n = 9) were detected by immunohistochemistry assay. c The expression level of Ki67, CD68, CD31, α-SMA, Vimentin and FSP-1 in mouse without established AVF in CTRL (n = 9) and CKO-LncDACH1 (n = 9) were detected by immunohistochemistry assay. d The expression level of Ki67, CD68, CD31, α-SMA, Vimentin and FSP-1 in mouse with established AVF in AAV-Vector (n = 9) and AAV-LncDACH1 (n = 8) were detected by immunohistochemistry assay. e The expression level of Ki67, CD68, CD31, α-SMA, Vimentin and FSP-1 in mouse with established AVF in CTRL (n = 8) and CKO-LncDACH1 (n = 8) were detected by immunohistochemistry assay. f The expression levels of Tunel in the above groups by immunofluorescence assay. Arteriovenous fistula (AVF), conditional knockout (CKO), adeno-associated virus (AAV), control (CTRL). The statistical analysis is shown in Supplementary Fig. 10. The n numbers represent biologically independent samples. Scale bar, 20 μm.Source data are provided as a Source Data file.

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