Research Paper Volume 13, Issue 11 pp 15307—15319

Constitutive activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway in mice with myocardial injury following acute myocardial infarction

NEAT1 aggravates myocardial injury in mice with CHD via upregulation of Ltb4rl by sponging miR-22-3p. MI mice were injected with sh-NEAT1 and/or AntagomiR-22-3p. (A) Quantification of LVEF, LVIDD, LVIDs, LVEF, LVFS, in myocardial tissues of MI mice. (B) Hemodynamic analysis of LV and dP/dt in myocardial tissues of MI mice. (C) The infarct size in myocardial tissues of MI mice detected using TTC staining upon treatment with sh-NEAT1, sh-NC, AntagoNC, or AntagomiR-22-3p. A-C * p vs. MI + sh-NC and # p vs. MI + sh-NEAT1 + AntagomiR NC. (D) ELISA of IL-1β, IL-6, and IL-18 in hypoxia-induced MI cardiomyocytes upon treatment with sh-NEAT1, sh-NC, AntagoNC, or AntagomiR-22-3p. (E), Apoptosis of hypoxia-induced MI cardiomyocytes detected using TUNEL staining (× 400). (F) Protein levels of Cleaved caspase-3, Bax, and Bcl-2 in hypoxia-induced MI cardiomyocytes determined using Western blot analysis, normalized to GAPDH. * p vs. MI mice injected with sh-NC or hypoxia-induced MI cardiomyocytes treated with sh-NC and # p vs. MI mice injected with sh-NEAT1 + AntagomiR NC or hypoxia-induced MI cardiomyocytes treated with sh-NEAT1 + NC inhibitor. Data among groups were analyzed by one-way ANOVA/Tukey’s test.

Figure 5. NEAT1 aggravates myocardial injury in mice with CHD via upregulation of Ltb4rl by sponging miR-22-3p. MI mice were injected with sh-NEAT1 and/or AntagomiR-22-3p. (A) Quantification of LVEF, LVIDD, LVIDs, LVEF, LVFS, in myocardial tissues of MI mice. (B) Hemodynamic analysis of LV and dP/dt in myocardial tissues of MI mice. (C) The infarct size in myocardial tissues of MI mice detected using TTC staining upon treatment with sh-NEAT1, sh-NC, AntagoNC, or AntagomiR-22-3p. A-C * p < 0.05 vs. MI + sh-NC and # p < 0.05 vs. MI + sh-NEAT1 + AntagomiR NC. (D) ELISA of IL-1β, IL-6, and IL-18 in hypoxia-induced MI cardiomyocytes upon treatment with sh-NEAT1, sh-NC, AntagoNC, or AntagomiR-22-3p. (E), Apoptosis of hypoxia-induced MI cardiomyocytes detected using TUNEL staining (× 400). (F) Protein levels of Cleaved caspase-3, Bax, and Bcl-2 in hypoxia-induced MI cardiomyocytes determined using Western blot analysis, normalized to GAPDH. * p < 0.05 vs. MI mice injected with sh-NC or hypoxia-induced MI cardiomyocytes treated with sh-NC and # p < 0.05 vs. MI mice injected with sh-NEAT1 + AntagomiR NC or hypoxia-induced MI cardiomyocytes treated with sh-NEAT1 + NC inhibitor. Data among groups were analyzed by one-way ANOVA/Tukey’s test.