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CDK9 and its repressor LARP7 modulate cardiomyocyte proliferation and response to injury in the zebrafish heart.

Matrone G, Wilson KS, Maqsood S, Mullins JJ, Tucker CS, Denvir MA - J. Cell. Sci. (2015)

Bottom Line: Cdk9 expression and activity were inhibited in the zebrafish (Danio rerio) embryo.We show that dephosphorylation of residue Ser2 on the C-terminal domain of RNA polymerase II is associated with impaired cardiac structure and function, and cardiomyocyte proliferation and also results in impaired functional recovery following cardiac laser injury.Larp7 knockdown rescued the structural and functional phenotype associated with knockdown of Cdk9.

View Article: PubMed Central - PubMed

Affiliation: British Heart Foundation Centre for Cardiovascular Science, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK Center for Cardiovascular Regeneration, Department of Cardiovascular Sciences, Methodist Hospital Research Institute, Houston, TX 77030, USA.

No MeSH data available.


Related in: MedlinePlus

Effects of Cdk9 modulation on the response of the ventricle to laser injury. Cdk9 activity was modulated pharmacologically and genetically by incubation in 3 μmol/l flavopiridol and injection of Cdk9- and Larp7-targeting morpholinos (appropriate mismatch controls, grey bars; Cdk9-Mo-SB or Larp7-Mo-SB, dark bars) prior to injury. Laser injury (single pulse to the mid-ventricular cavity) was performed at 72 hpf. Ejection fraction and cardiomyocyte number were assessed pre-laser, and 2 and 24 h post-laser injury (n=3 experiments, n>10 embryos per experiment, two-way ANOVA test followed by Bonferroni's post-hoc test; *P<0.05, **P<0.01, ***P<0.001). Means±s.e.m. are shown in each figure.
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JCS175018F7: Effects of Cdk9 modulation on the response of the ventricle to laser injury. Cdk9 activity was modulated pharmacologically and genetically by incubation in 3 μmol/l flavopiridol and injection of Cdk9- and Larp7-targeting morpholinos (appropriate mismatch controls, grey bars; Cdk9-Mo-SB or Larp7-Mo-SB, dark bars) prior to injury. Laser injury (single pulse to the mid-ventricular cavity) was performed at 72 hpf. Ejection fraction and cardiomyocyte number were assessed pre-laser, and 2 and 24 h post-laser injury (n=3 experiments, n>10 embryos per experiment, two-way ANOVA test followed by Bonferroni's post-hoc test; *P<0.05, **P<0.01, ***P<0.001). Means±s.e.m. are shown in each figure.

Mentions: In control larvae, laser injury of the ventricle at 72 hpf resulted in a significant reduction in the ejection fraction and VCt at 2 h post laser treatment (Fig. 7). By 24 h post laser treatment, both parameters recovered to baseline levels that were comparable to those before laser injury.Fig. 7.


CDK9 and its repressor LARP7 modulate cardiomyocyte proliferation and response to injury in the zebrafish heart.

Matrone G, Wilson KS, Maqsood S, Mullins JJ, Tucker CS, Denvir MA - J. Cell. Sci. (2015)

Effects of Cdk9 modulation on the response of the ventricle to laser injury. Cdk9 activity was modulated pharmacologically and genetically by incubation in 3 μmol/l flavopiridol and injection of Cdk9- and Larp7-targeting morpholinos (appropriate mismatch controls, grey bars; Cdk9-Mo-SB or Larp7-Mo-SB, dark bars) prior to injury. Laser injury (single pulse to the mid-ventricular cavity) was performed at 72 hpf. Ejection fraction and cardiomyocyte number were assessed pre-laser, and 2 and 24 h post-laser injury (n=3 experiments, n>10 embryos per experiment, two-way ANOVA test followed by Bonferroni's post-hoc test; *P<0.05, **P<0.01, ***P<0.001). Means±s.e.m. are shown in each figure.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4696495&req=5

JCS175018F7: Effects of Cdk9 modulation on the response of the ventricle to laser injury. Cdk9 activity was modulated pharmacologically and genetically by incubation in 3 μmol/l flavopiridol and injection of Cdk9- and Larp7-targeting morpholinos (appropriate mismatch controls, grey bars; Cdk9-Mo-SB or Larp7-Mo-SB, dark bars) prior to injury. Laser injury (single pulse to the mid-ventricular cavity) was performed at 72 hpf. Ejection fraction and cardiomyocyte number were assessed pre-laser, and 2 and 24 h post-laser injury (n=3 experiments, n>10 embryos per experiment, two-way ANOVA test followed by Bonferroni's post-hoc test; *P<0.05, **P<0.01, ***P<0.001). Means±s.e.m. are shown in each figure.
Mentions: In control larvae, laser injury of the ventricle at 72 hpf resulted in a significant reduction in the ejection fraction and VCt at 2 h post laser treatment (Fig. 7). By 24 h post laser treatment, both parameters recovered to baseline levels that were comparable to those before laser injury.Fig. 7.

Bottom Line: Cdk9 expression and activity were inhibited in the zebrafish (Danio rerio) embryo.We show that dephosphorylation of residue Ser2 on the C-terminal domain of RNA polymerase II is associated with impaired cardiac structure and function, and cardiomyocyte proliferation and also results in impaired functional recovery following cardiac laser injury.Larp7 knockdown rescued the structural and functional phenotype associated with knockdown of Cdk9.

View Article: PubMed Central - PubMed

Affiliation: British Heart Foundation Centre for Cardiovascular Science, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK Center for Cardiovascular Regeneration, Department of Cardiovascular Sciences, Methodist Hospital Research Institute, Houston, TX 77030, USA.

No MeSH data available.


Related in: MedlinePlus