Literature DB >> 32391143

Correction to: Angiotensin II receptor blocker LCZ696 attenuates cardiac remodeling through the inhibition of the ERK signaling pathway in mice with pregnancy‑associated cardiomyopathy.

Yi Wang1, Zhiheng Guo1, Yongmei Gao1, Ping Liang1, Yanhong Shan1, Jin He1.   

Abstract

[This corrects the article DOI: 10.1186/s13578-019-0348-1.].
© The Author(s) 2020.

Entities:  

Year:  2020        PMID: 32391143      PMCID: PMC7199318          DOI: 10.1186/s13578-020-00419-x

Source DB:  PubMed          Journal:  Cell Biosci        ISSN: 2045-3701            Impact factor:   7.133


Correction to: Cell BioSci (2019) 9:86 10.1186/s13578-019-0348-1

Following publication of the original article [1], the authors identified an error in Figs. 1b, 5b. The corrected figures are given below.
Fig. 1

LCZ696 alleviates cardiac injury in PAH mice and represses the Ang II receptor pathway. PAH mice were either treated with or without LCZ696. a Effect of LCZ696 on survival rate of PAH mice detected by Kaplan–Meier method (N = 7). b Heart size (scale bar = 100 mm) and ratio of heart weight/body weight of mice. c HE staining analysis of cardiac tissues (upper panels: scale bar = 50 mm; lower panels: bar = 25 μm). d Cardiac fibrosis observed by Masson’s trichrome staining (scale bar = 25 μm). e Apoptosis of cardiomyocytes detected by TUNEL staining (scale bar = 25 μm). f Western blot analysis of ACE2 protein. N = 7. *p < 0.05 vs. normal mice; #p < 0.05 vs. PAH mice. Measurement data (mean ± S.D.) among multiple groups were analyzed by one-way ANOVA, followed by Tukey post hoc test. Survival rate was calculated by the Kaplan–Meier method, and compared by a log-rank test

Fig. 5

LCZ696 reduces cardiac remodeling through inhibiting the ERK signaling pathway. PAH mice were treated with sh-ERK with sh-NC as the control, or sh-ERK in the presence of LCZ696 with sh-NC in the presence of LCZ696 or control. a Heart size (scale bar = 100 mm) and ratio of heart weight/body weight in PAH mice. b HE staining of ventricular transection of heart (upper panels: scale bar = 50 mm; lower panels: scale bar = 25 μm). c Cardiomyocyte fibrosis observed by Masson’s trichrome staining (scale bar = 25 μm). d mRNA expression of collagen I, collagen III and TGF-β detected by RT-qPCR. e Isolectin B4 immunofluorescence of the capillary in ventricular tissues (blood vessel: yellow; cell membrane: red; nucleus: blue). f mRNA expression of ANP, βMHC and TIMP2 in cardiomyocytes detected by RT-qPCR. g Apoptosis of cardiomyocytes treated with LCZ696 detected by TUNEL staining (scale bar = 25 μm). h Western blot analysis of ERK protein and extent of ERK phosphorylation. *p < 0.05 vs. PAH mice treated with sh-NC; #p < 0.05 vs. PAH mice treated with sh-ERK; &p < 0.05 vs. PAH mice treated with sh-NC + LCZ696. N = 7. Measurement data (mean ± S.D.) among multiple groups was analyzed by one-way ANOVA, followed by Tukey post hoc test

LCZ696 alleviates cardiac injury in PAH mice and represses the Ang II receptor pathway. PAH mice were either treated with or without LCZ696. a Effect of LCZ696 on survival rate of PAH mice detected by Kaplan–Meier method (N = 7). b Heart size (scale bar = 100 mm) and ratio of heart weight/body weight of mice. c HE staining analysis of cardiac tissues (upper panels: scale bar = 50 mm; lower panels: bar = 25 μm). d Cardiac fibrosis observed by Masson’s trichrome staining (scale bar = 25 μm). e Apoptosis of cardiomyocytes detected by TUNEL staining (scale bar = 25 μm). f Western blot analysis of ACE2 protein. N = 7. *p < 0.05 vs. normal mice; #p < 0.05 vs. PAH mice. Measurement data (mean ± S.D.) among multiple groups were analyzed by one-way ANOVA, followed by Tukey post hoc test. Survival rate was calculated by the Kaplan–Meier method, and compared by a log-rank test LCZ696 reduces cardiac remodeling through inhibiting the ERK signaling pathway. PAH mice were treated with sh-ERK with sh-NC as the control, or sh-ERK in the presence of LCZ696 with sh-NC in the presence of LCZ696 or control. a Heart size (scale bar = 100 mm) and ratio of heart weight/body weight in PAH mice. b HE staining of ventricular transection of heart (upper panels: scale bar = 50 mm; lower panels: scale bar = 25 μm). c Cardiomyocyte fibrosis observed by Masson’s trichrome staining (scale bar = 25 μm). d mRNA expression of collagen I, collagen III and TGF-β detected by RT-qPCR. e Isolectin B4 immunofluorescence of the capillary in ventricular tissues (blood vessel: yellow; cell membrane: red; nucleus: blue). f mRNA expression of ANP, βMHC and TIMP2 in cardiomyocytes detected by RT-qPCR. g Apoptosis of cardiomyocytes treated with LCZ696 detected by TUNEL staining (scale bar = 25 μm). h Western blot analysis of ERK protein and extent of ERK phosphorylation. *p < 0.05 vs. PAH mice treated with sh-NC; #p < 0.05 vs. PAH mice treated with sh-ERK; &p < 0.05 vs. PAH mice treated with sh-NC + LCZ696. N = 7. Measurement data (mean ± S.D.) among multiple groups was analyzed by one-way ANOVA, followed by Tukey post hoc test
  1 in total

1.  Sequencing Analysis of mRNA Profile in Endothelial Cells in Response to ox-LDL.

Authors:  Dongmei Su; Li Yi; Lina Guan; Qian Li; Cuige Shi; Xu Ma
Journal:  Biochem Genet       Date:  2021-02-02       Impact factor: 1.890

  1 in total

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