Fig. 6 | Nature Communications

Fig. 6

From: Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis

Fig. 6

AngII-infused mouse serum reduces Snrk expression in cultured GnECs. a Western blot and densitometry analysis of Snrk levels in primary GnECs isolated from wild-type (WT) mice following treatment with different doses of AngII. b Quantification of miR-103a-3p levels by qRT-PCR in primary GnECs treated with different doses of AngII. c Western blot and densitometry analysis of Snrk levels in GnECs isolated from WT mice following different incubation times with 1 µM AngII. d Quantification of miR-103a-3p levels by qRT-PCR in primary GnECs treated with AngII for different durations. e–h Serum collected from WT mice infused with a vehicle control (Veh) or AngII (1 mg kg−1 d−1) for 4 weeks was used to treat GnECs. Snrk proteins levels (e) and miR-103a-3p abundance (f) were determined for GnECs treated for 8 h with different doses of AngII-treated mouse serum. n = 6; *p < 0.05 relative to untreated controls. GnECs pretreated with AAV-anti-miR-103a-3p or AAV-anti-miR-Control for 24 h and subsequently incubated with vehicle control- or AngII-treated mouse serum (10 µl) were subjected to the analysis of Snrk protein levels (g) and cytokine mRNA levels (h). n = 6 per group; *p < 0.05 relative to anti-miR-Control/AngII; #p < 0.05 relative to vehicle-treated mouse serum. Student’s two-tailed t-test was used for the statistical analysis. The corresponding source data are available in the Source Data file

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