Poster Presentation Epigenetics 2013

Quantification of global DNA methylation in the kidneys of spontaneously hypertensive mice (#127)

Christine L Chiu 1 , Joanne M Lind 1
  1. School of Medicine, University of Western Sydney, Sydney, NSW, Australia

Background

Hypertension is caused by a combination of environmental and genetic factors. Growing evidence suggests that epigenetic factors, such as DNA methylation, may have a role in the development of hypertension. This study aimed to determine whether global DNA methylation status differed between hypertensive and normotensive mice.

Methods

Spontaneously hypertensive Schlager mice (BPH/2J) and their normotensive controls (BPN/3J) were used in this study. Genomic DNA was extracted from kidney tissue of 12 week old male hypertensive and normotensive mice (n=10/group). DNA methylation was measured using the Epigentek MethyFlash™ Methylated DNA quantification kit (Colourmetric). General linear models were used to compare DNA methylation between the two groups. P<0.05 was considered significant.

Results

The global methylation status of kidney genomic DNA was calculated in both hypertensive and normotensive mice. The level of methylation was 2.75% and 2.07% in the hypertensive and normotensive kidneys respectively. Comparison between the two groups found no significant difference in the level of DNA methylation in the kidneys of male hypertensive and normotensive mice (p=0.09).

Conclusion

Global DNA methylation status in the kidney did not significantly differ between hypertensive and normotensive mice. Despite this we cannot rule out the involvement of epigenetics in disease development as this assay is unable to distinguish methylation differences at a chromosome or gene level. Further research comparing methylation profiles in kidneys and other tissue is needed.