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Early-life perturbations in glucocorticoid activity impacts on the structure, function and molecular composition of the adult zebrafish (Danio rerio) heart.

Wilson KS, Baily J, Tucker CS, Matrone G, Vass S, Moran C, Chapman KE, Mullins JJ, Kenyon C, Hadoke PW, Denvir MA - Mol. Cell. Endocrinol. (2015)

Bottom Line: GR Mo embryos (120 hpf) had smaller hearts with fewer cardiomyocytes, less mature striation pattern, reduced cardiac function and reduced levels of vmhc and igf mRNA compared with controls.GR Mo adult hearts were smaller with diminished trabecular network pattern, reduced expression of vmhc and altered echocardiographic Doppler flow compared to controls.Perturbations in GR activity during embryonic development results in short and long-term alterations in the heart.

View Article: PubMed Central - PubMed

Affiliation: The British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh EH16 4TJ, UK.

No MeSH data available.


Related in: MedlinePlus

Effects of embryonic glucocorticoid manipulation on adult heart structure Long-term impact of embryonic glucocorticoid receptor (GR) manipulation with either GR agonist dexamethasone (Dex) [100 μM], or targeted translational GR knockdown using morpholino (GR Mo) was assessed in the heart of 120 day post fertilisation (dpf) adult zebrafish. Structural analyses of A) ventricle length, B) weight and C) cavity area were carried out. Data are n = 8 hearts per group, displayed as mean ± SEM analysed by one-way ANOVA with Dunnett's post hoc comparison (*p < 0.05, **p < 0.01, ***p < 0.001). D–F) Histology (haematoxylin and eosin staining) in adult fish hearts D) Controls (Vehicle only control shown here), E) Dex, F) GR Mo.
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fig5: Effects of embryonic glucocorticoid manipulation on adult heart structure Long-term impact of embryonic glucocorticoid receptor (GR) manipulation with either GR agonist dexamethasone (Dex) [100 μM], or targeted translational GR knockdown using morpholino (GR Mo) was assessed in the heart of 120 day post fertilisation (dpf) adult zebrafish. Structural analyses of A) ventricle length, B) weight and C) cavity area were carried out. Data are n = 8 hearts per group, displayed as mean ± SEM analysed by one-way ANOVA with Dunnett's post hoc comparison (*p < 0.05, **p < 0.01, ***p < 0.001). D–F) Histology (haematoxylin and eosin staining) in adult fish hearts D) Controls (Vehicle only control shown here), E) Dex, F) GR Mo.

Mentions: Adult zebrafish hearts (Fig. 5) derived from GR Mo embryos were shorter in length (normalised to total fish length (Fig. 5A) and weighed less (normalised to body weight (Fig. 5B) compared to controls. Histological examination highlighted these hearts had a more sparse trabecular network (Fig. 5F compared to controls Fig. 5D) which when quantified resulted in an increased ventricle cavity area (Fig. 5C). Adult hearts derived from Dex-treated embryos were heavier with similar length and trabecular pattern compared to controls (Figures A–C); histologically they were similar to controls (Fig. 5D and E).


Early-life perturbations in glucocorticoid activity impacts on the structure, function and molecular composition of the adult zebrafish (Danio rerio) heart.

Wilson KS, Baily J, Tucker CS, Matrone G, Vass S, Moran C, Chapman KE, Mullins JJ, Kenyon C, Hadoke PW, Denvir MA - Mol. Cell. Endocrinol. (2015)

Effects of embryonic glucocorticoid manipulation on adult heart structure Long-term impact of embryonic glucocorticoid receptor (GR) manipulation with either GR agonist dexamethasone (Dex) [100 μM], or targeted translational GR knockdown using morpholino (GR Mo) was assessed in the heart of 120 day post fertilisation (dpf) adult zebrafish. Structural analyses of A) ventricle length, B) weight and C) cavity area were carried out. Data are n = 8 hearts per group, displayed as mean ± SEM analysed by one-way ANOVA with Dunnett's post hoc comparison (*p < 0.05, **p < 0.01, ***p < 0.001). D–F) Histology (haematoxylin and eosin staining) in adult fish hearts D) Controls (Vehicle only control shown here), E) Dex, F) GR Mo.
© Copyright Policy - CC BY
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC4562295&req=5

fig5: Effects of embryonic glucocorticoid manipulation on adult heart structure Long-term impact of embryonic glucocorticoid receptor (GR) manipulation with either GR agonist dexamethasone (Dex) [100 μM], or targeted translational GR knockdown using morpholino (GR Mo) was assessed in the heart of 120 day post fertilisation (dpf) adult zebrafish. Structural analyses of A) ventricle length, B) weight and C) cavity area were carried out. Data are n = 8 hearts per group, displayed as mean ± SEM analysed by one-way ANOVA with Dunnett's post hoc comparison (*p < 0.05, **p < 0.01, ***p < 0.001). D–F) Histology (haematoxylin and eosin staining) in adult fish hearts D) Controls (Vehicle only control shown here), E) Dex, F) GR Mo.
Mentions: Adult zebrafish hearts (Fig. 5) derived from GR Mo embryos were shorter in length (normalised to total fish length (Fig. 5A) and weighed less (normalised to body weight (Fig. 5B) compared to controls. Histological examination highlighted these hearts had a more sparse trabecular network (Fig. 5F compared to controls Fig. 5D) which when quantified resulted in an increased ventricle cavity area (Fig. 5C). Adult hearts derived from Dex-treated embryos were heavier with similar length and trabecular pattern compared to controls (Figures A–C); histologically they were similar to controls (Fig. 5D and E).

Bottom Line: GR Mo embryos (120 hpf) had smaller hearts with fewer cardiomyocytes, less mature striation pattern, reduced cardiac function and reduced levels of vmhc and igf mRNA compared with controls.GR Mo adult hearts were smaller with diminished trabecular network pattern, reduced expression of vmhc and altered echocardiographic Doppler flow compared to controls.Perturbations in GR activity during embryonic development results in short and long-term alterations in the heart.

View Article: PubMed Central - PubMed

Affiliation: The British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh EH16 4TJ, UK.

No MeSH data available.


Related in: MedlinePlus