Fig 1: Western blotting assay of cTnT, cTnI, Bcl-2, Bax, and Caspase-3 expression. Results were shown as fold change compared with the expression of GAPDH. Data were shown as mean ± SD (n = 4). *P < 0.05, **P < 0.01, and ***P < 0.001 compared with the CON group; #P < 0.05, ##P < 0.01, and ###P < 0.001 compared with the EE group.
Fig 2: Effects on the activity of myocardial injury biomarkers (CK, CK-MB, LDH, and cTnI) in the rat serum (n = 7) after applying nicorandil. One-way ANOVA statistical analysis was conducted for multiple comparisons of group means. The same was used to analyze the results of each experimental group. *P < 0.05, **P < 0.01, and ***P < 0.001 compared with the CON group; #P < 0.05, ##P < 0.01, and ###P < 0.001 compared with the EE group.
Fig 3: DMSO induces iPS cells to differentiate into cardiomyocytes and express differentiation-related genes and proteins in iPS cells. (A) Experimental grouping. Reverse transcription-quantitative PCR assay for the expression of (B) ANP, (C) Nkx2.5, (D) cTnI, (E) a-MHC and (F) GATA4. (G) Western blotting assay for (H) ANP, (I) Nkx2.5, (J) cTnI, (K) a-MHC and (L) GATA4. n=3. *P<0.05, **P<0.01, ***P<0.005 and ****P<0.001. ns, not significant; iPS, induced pluripotent stem; DMSO, dimethyl sulfoxide; NC, negative control; circ, circular RNA; si, small interfering RNA; ANP, atrial natriuretic peptide; Nkx2.5, homobox transcription factor; cTnI, cardiac troponin I; a-MHC, a-myosin heavy chain; GATA4, GATA-binding protein 4.
Fig 4: cyclinD2 is a direct target of miR-17 and hsa_circ_105039-mediated regulation of cell viability and differentiation is reversed by the restoration of cyclinD2, ANP and cTnI levels in DMSO-induced iPS cardiomyocytes. (A) Experimental grouping. (B) Western blotting bands. The analysis histogram of (C and D) cyclinD2, (E and F) ANP and (G and H) cTnI. n=3. *P<0.05, **P<0.01, ***P<0.005 and ****P<0.001. ns, not significant; miR, microRNA; circ, circular RNA; ANP, atrial natriuretic peptide; cTnI, cardiac troponin I; iPS, induced pluripotent stem; NC, negative control; si, small interfering RNA.
Fig 5: CyclinD2 is a direct target of miR-17 and hsa_circ_105039-mediated regulation of cell viability and differentiation is reversed by the restoration of cyclinD2, ANP and cTnI levels in DMSO-induced iPS cardiomyocytes. (A) Experimental grouping. (B) Sequence alignment of cyclinD2 and the potential binding site in the 3'-UTR of miR-17. (C) Luciferase reporter assay was performed in iPS cells co-transfected with the cyclinD2-WT plasmid or cyclinD2 plasmid. (D and E) 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay of iPS cell viability. Reverse transcription-quantitative PCR assay of the expression of (F and G) cyclinD2, (H and I) ANP and (J and K) cTnI. n=3. *P<0.05, **P<0.01 and ***P<0.005. ns, not significant; miR, microRNA; circ, circular RNA; ANP, atrial natriuretic peptide; cTnI, cardiac troponin I; iPS, induced pluripotent stem; DMSO, dimethyl sulfoxide; WT, wild-type; MUT, mutated; NC, negative control; si, small interfering RNA.
Supplier Page from Abcam for Anti-Cardiac Troponin I antibody [EPR20307]