Chen and colleagues,35 then again, reported the presence of PTEN hypermethylation in three of 21 regular placentas ex amined. These information are in contrast to ours.We further carried out bisulfite sequencing and failed to find evidence of PTEN hypermethylation during the 5 to start with and third trimester placentas studied.Despite the fact that the main difference in sample dimension may make clear the discrepancy in information, it is noteworthy that the earlier study35 was according to the usage of methylation delicate restriction enzyme digestion followed by nested PCR. Whilst a positive control to the methylated se quence plus a blank control were incorporated during the analysis, the usage of a control for that restriction digestion of your un methylated sequence was not reported. 35 Genomic imprinting is a further probable article source motive for cer tain genes for being partially methylated while in the placenta.
For genomic imprinting, monoallelic methylation contributing to 50% of your sequenced clones to be methylated can be anticipated. 36 Usually, the methylated web page frequencies from the placental tissues had been much higher than 0. 500 for RASSF1A. Therefore, RASSF1A read more here hypermethylation in placental tissues is unlikely to be attributable to imprinting. Formal exclusion of imprinting management would entail the demonstra tion of biallelic expression of RASSF1A. We think that the study findings may perhaps be of relevance to investigators learning the biology of RASSF1A and postu late that RASSF1A hypermethylation during the human placenta may perform a substantial biological part determined by the following lines of evidence. RASSF1A hypermethylation was consis tently observed in all studied placental tissues from all three trimesters of pregnancy. We have demonstrated a relation ship among its expression and promoter methylation.
The potential biological significance of this phenomenon in pri mate placentation could possibly be inferred by its conservation from the placenta of the rhesus macaque but not from the murine placenta. Not long ago, a examine on nasopharyngeal carcinoma reported that RASSF1A expression modulates the expres sion of inhibitor of DNA binding two.37 Incidentally, ID2 continues to be reported to be an essential helix loop helix protein that regulates cytotrophoblast differentiation and function. 38 Therefore, there exists a likelihood that RASSF1A could possibly without a doubt play a significant biological part in cytotrophoblast produce ment by way of its effects on ID2. More studies ought to thus be directed to tackle if ID2 expression in pla cental tissues is similarly modulated by RASSF1A, as while in the case for nasopharyngeal carcinoma cells. On the other hand, if RASSF1A plays a significant role in placental development, its methylation standing may well be altered in sure placental pathologies and is obviously a different course of investigation worth pursuing. We have carried out a preliminary research investigating RASSF1A hypermethylation in placental tissues collected from pre eclamptic pregnancies.