Methylation of CpG islands: potential relevance for hypertension and kidney diseases

Methylation of DNA is an epigenetic process which modulates gene expression [1]. In the mammalian genome, methylation is almost exclusively observed at cytosines 50 to guanosines, i.e. in the CpG dinucleotides. Many of these CpG islands are associated with promoters [2,3]. Methylation of CpGs in the promoter region has the potential to silence gene expression. Mechanisms accounting for diminished or abrogated gene expression following CpG methylation comprise blocking of the binding of sequence-specific transactivating proteins or binding of proteins that interfere with transcription [3,4]. Prominent examples of gene silencing induced by CpG methylation comprise X-chromosome inactivation in females, developmental transcriptional regulation, genomic imprinting, carcinogenesis and tissue-specific expression of a gene [5–8].