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. 2019 May 15;14(5):e0216987. doi: 10.1371/journal.pone.0216987

Fig 2. Ninjurin1 expression increases in the left ventricle of mice with pathological left ventricular hypertrophy.

Fig 2

(A) Quantitative RT-PCR analysis of atrial (Nppa) and B-type natriuretic peptide (Nppb) on RNA from left ventricular tissue of 9- to 10-wk-old male mice subjected to two weeks of transverse aortic constriction (TAC) (n = 5) or sham surgery (n = 5). Glyceraldehyde-3 phosphate dehydrogenase (GAPDH) expression was used as reference. Data are presented as mean ± SD. * P < 0.05. (B) Immunoblots of proteins isolated from left ventricles of mice subjected to sham (n = 5) or TAC (n = 5) surgery using anti-Ninjurin1 antibody. GAPDH was used as loading control. The Ninjurin1 isoforms at 16kDa (Ninjurin1-16) and 24kDa (Ninjurin1-24) are differentially expressed, therefore the membranes underwent short (short exp.) and long exposure (long exp.), respectively. (C) Densitometric analysis of (B); data are presented as mean ± SEM. * P < 0.05. (D) Quantitative RT-PCR analysis of Nppa and Nppb on RNA from left ventricular tissue of 12-wk-old male mice subjected to chronic Angiotensin II (Ang II, n = 8) or vehicle (n = 4) infusion, respectively, via osmotic mini-pumps for two weeks. GAPDH expression was used as reference. Data are presented as mean ± SD. *** P < 0.001. (E) Immunoblots of proteins isolated from left ventricles of mice subjected to vehicle (n = 4) or Ang II (n = 8) treatment using anti-Ninjurin1 antibody. GAPDH was used as loading control. (F) Densitometric analysis of (E); data are presented as mean ± SEM. ** P < 0.01. A two-tailed, unpaired Student’s t-test was used to calculate the P values.