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. 2017 Jan 13;2(1):18–26. doi: 10.1016/j.ncrna.2016.12.002

Fig. 3.

Fig. 3

Pharmacological inhibition of miR-199b attenuates cardiac dysfunction following MI. (a) Real-time PCR analysis of miR-199b expression levels in the LV of antagomir-control or antagomir-199b-treated animals after subjection to either 4 weeks of sham or MI. Rnu6-2 was used as a reference gene for normalization. (b,c) Quantification of (b) fractional shortening (FS) and (c) LV internal diameter at systole (LVIDs) by echocardiography in antagomir-control or antagomir-199b-treated mice after subjection to 4 weeks of either sham or MI. (d) Representative images of WGA-labeled cardiac histological sections from mice subjected to sham or MI, and treated either with antagomir-control or antagomir-199b. (e) Quantification of cardiomyocyte surface area in histological sections from mice subjected to sham or MI, and treated either with antagomir-control or antagomir-199b. (f) Gravimetric analysis of corrected hearts weights of animals that underwent sham or MI surgery and after treatment with antagomir-control or antagomir-199b. (g) Real-time PCR analysis of transcript abundance of the fetal gene markers: natriuretic peptide atrial natriuretic factor (nppa), β−myosin heavy chain (myh7) and the sarcomeric proteins α-skeletal actin (acta1) in antagomir-control or antagomir-199b treated mice after subjection to 4 weeks of sham or MI. (h) Real-time PCR analysis of transcript abundance of fibrosis related genes: collagen type I alpha 2 chain (col1a2), collagen type 3 alpha 1 chain (col3a1) and fibronectin-1 (fn1) in antagomir-control or antagomir-199b treated mice after subjection to 4 weeks of sham or MI. n = 8–13 *P < 0.05 (mean ± s.e.m.).