Abstract:Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) is an orphan nuclear hormone receptor of unknown ligands. This molecule has two interesting features: (1) it is a developmental gene, and (2) it is a potential hormone receptor. Here, we describe the possible roles of COUP-TFII in the organogenesis of the kidneys and protection from adult renal diseases, primarily in mouse models. COUP-TFII is highly expressed in embryos, including primordial kidneys, and is essential for the formation of … Show more
Altered epigenetic mechanisms have been previously reported in growth restricted offspring whose mothers experienced environmental insults during pregnancy in both human and rodent studies. We previously reported changes in the expression of the DNA methyltransferase
Dnmt3a
and the imprinted genes
Cdkn1c
(Cyclin-dependent kinase inhibitor 1C) and
Kcnq1
(Potassium voltage-gated channel subfamily Q member 1) in the kidney tissue of growth restricted rats whose mothers had uteroplacental insufficiency induced on day 18 of gestation, at both embryonic day 20 (E20) and postnatal day 1 (PN1). To determine the mechanisms responsible for changes in the expression of these imprinted genes, we investigated DNA methylation of KvDMR1, an imprinting control region (ICR) that includes the promoter of the antisense long non-coding RNA
Kcnq1ot1
(
Kcnq1
opposite strand/antisense transcript 1).
Kcnq1ot1
expression decreased by 51% in growth restricted offspring compared to sham at PN1. Interestingly, there was a negative correlation between
Kcnq1ot1
and
Kcnq1
in the E20 growth restricted group (Spearman’s
ρ =
0.014). No correlation was observed between
Kcnq1ot1
and
Cdkn1c
expression in either group at any time point. Additionally, there was a 11.25% decrease in the methylation level at one CpG site within KvDMR1 ICR. This study, together with others in the literature, supports that long non-coding RNAs may mediate changes seen in tissues of growth restricted offspring.
Altered epigenetic mechanisms have been previously reported in growth restricted offspring whose mothers experienced environmental insults during pregnancy in both human and rodent studies. We previously reported changes in the expression of the DNA methyltransferase
Dnmt3a
and the imprinted genes
Cdkn1c
(Cyclin-dependent kinase inhibitor 1C) and
Kcnq1
(Potassium voltage-gated channel subfamily Q member 1) in the kidney tissue of growth restricted rats whose mothers had uteroplacental insufficiency induced on day 18 of gestation, at both embryonic day 20 (E20) and postnatal day 1 (PN1). To determine the mechanisms responsible for changes in the expression of these imprinted genes, we investigated DNA methylation of KvDMR1, an imprinting control region (ICR) that includes the promoter of the antisense long non-coding RNA
Kcnq1ot1
(
Kcnq1
opposite strand/antisense transcript 1).
Kcnq1ot1
expression decreased by 51% in growth restricted offspring compared to sham at PN1. Interestingly, there was a negative correlation between
Kcnq1ot1
and
Kcnq1
in the E20 growth restricted group (Spearman’s
ρ =
0.014). No correlation was observed between
Kcnq1ot1
and
Cdkn1c
expression in either group at any time point. Additionally, there was a 11.25% decrease in the methylation level at one CpG site within KvDMR1 ICR. This study, together with others in the literature, supports that long non-coding RNAs may mediate changes seen in tissues of growth restricted offspring.
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