Literature DB >> 30520682

Anti-Remodeling and Anti-Fibrotic Effects of the Neuregulin-1β Glial Growth Factor 2 in a Large Animal Model of Heart Failure.

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Abstract

Entities:  

Year:  2015        PMID: 30520682      PMCID: PMC4330042          DOI: 10.1161/JAHA.114.000528

Source DB:  PubMed          Journal:  J Am Heart Assoc        ISSN: 2047-9980            Impact factor:   5.501


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In the article by Galindo et al, “Anti‐Remodeling and Anti‐Fibrotic Effects of the Neuregulin‐1β Glial Growth Factor 2 in a Large Animal Model of Heart Failure,” which published online October 23, 2014, and appeared in the October 2014 issue of the journal (J Am Heart Assoc. 2014;3:e000773 doi: 10.1161/JAHA.113.000773), incorrect versions of Figures 5 and 8 were published.
Figure 5.

Results of transcription factor analysis using Ingenuity Pathway Analysis software program for NRG‐1β treatment‐induced gene expression changes observed in post‐MI swine. Based on this analysis of observed gene expression alterations, AHR (aryl hydrocarbon receptor) activity was predicted to be activated (center, orange square). Conversely, TGFbeta (TGFbeta shown in blue) was predicted to be inhibited. Genes regulated by AHR and/or TGFbeta that were altered in expression based on microarrays are shown on the periphery and colored according to level of alteration. Up‐regulated genes are colored in various shades of pink to red, with darker indicating higher magnification of change. Similarly, down‐regulated genes are shown in light to dark green, the latter indicating a greater magnitude of inhibition compared to lighter shades. Figure produced using Ingenuity Pathway Analysis program (Qiagen). MI indicates myocardial infarction; NRG‐1β, neuregulin‐1β.

Figure 8.

Representative immunohistochemistry of swine LV tissues from untreated (A) and GGF2‐treated (B) post‐MI pigs. Tissues were stained with DAPI (blue), phalloidin (red), and anti‐αSMA (green). C, Representative cytofluorographic dot plots showing the percentage of αSMA+ fibroblasts incubated in the absence (vehicle, upper panel) or presence of 30 ng/mL NRG‐1β (lower panel) for 48 hours; (D) Graphic representation of data from flow cytometric analysis of αSMA expression in cardiac fibroblasts incubated in the absence (vehicle, open bar) or presence of 30 ng/mL NRG‐1β (closed bar) for 48 hours. Number of αSMA+ cells was calculated from percentage of αSMA‐expressing and total number of cells; E, Mean fluorescence intensity of αSMA expression in cardiac fibroblasts as assessed by flow cytometry. Data represent mean±SEM from 3 independent experiments. P‐values indicate significance level calculated by t test. GGF2 indicates glial growth factor 2; LV, left ventricular; MI, myocardial infarction; NRG‐1β, neuregulin‐1β; αSMA, α smooth muscle.

Results of transcription factor analysis using Ingenuity Pathway Analysis software program for NRG‐1β treatment‐induced gene expression changes observed in post‐MI swine. Based on this analysis of observed gene expression alterations, AHR (aryl hydrocarbon receptor) activity was predicted to be activated (center, orange square). Conversely, TGFbeta (TGFbeta shown in blue) was predicted to be inhibited. Genes regulated by AHR and/or TGFbeta that were altered in expression based on microarrays are shown on the periphery and colored according to level of alteration. Up‐regulated genes are colored in various shades of pink to red, with darker indicating higher magnification of change. Similarly, down‐regulated genes are shown in light to dark green, the latter indicating a greater magnitude of inhibition compared to lighter shades. Figure produced using Ingenuity Pathway Analysis program (Qiagen). MI indicates myocardial infarction; NRG‐1β, neuregulin‐1β. Representative immunohistochemistry of swine LV tissues from untreated (A) and GGF2‐treated (B) post‐MI pigs. Tissues were stained with DAPI (blue), phalloidin (red), and anti‐αSMA (green). C, Representative cytofluorographic dot plots showing the percentage of αSMA+ fibroblasts incubated in the absence (vehicle, upper panel) or presence of 30 ng/mL NRG‐1β (lower panel) for 48 hours; (D) Graphic representation of data from flow cytometric analysis of αSMA expression in cardiac fibroblasts incubated in the absence (vehicle, open bar) or presence of 30 ng/mL NRG‐1β (closed bar) for 48 hours. Number of αSMA+ cells was calculated from percentage of αSMA‐expressing and total number of cells; E, Mean fluorescence intensity of αSMA expression in cardiac fibroblasts as assessed by flow cytometry. Data represent mean±SEM from 3 independent experiments. P‐values indicate significance level calculated by t test. GGF2 indicates glial growth factor 2; LV, left ventricular; MI, myocardial infarction; NRG‐1β, neuregulin‐1β; αSMA, α smooth muscle. The publisher regrets this error. The online version of the article has been updated and is available at http://jaha.ahajournals.org/content/3/5/e000773.
  2 in total

1.  Effects of endogenous serum neuregulin-1β on morbidity and mortality in patients with heart failure and left ventricular systolic dysfunction.

Authors:  Jennifer Miao; Shi Huang; Yan Ru Su; Carrie A Lenneman; Meera Wright; Frank E Harrell; Douglas B Sawyer; Daniel J Lenihan
Journal:  Biomarkers       Date:  2018-08-17       Impact factor: 2.658

Review 2.  Neuregulin‑1: An underlying protective force of cardiac dysfunction in sepsis (Review).

Authors:  Wen Kang; Yue Cheng; Xi Wang; Fang Zhou; Chenliang Zhou; Long Wang; Liang Zhong
Journal:  Mol Med Rep       Date:  2020-03-20       Impact factor: 2.952

  2 in total

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