ArticlePloS one2019
Abundances of placental imprinted genes CDKN1C, PHLDA2 and IGF-2 are related to low birth weight and early catch-up growth in full-term infants born small for gestational age.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- Adiponectin and leptin levels in mothers, fetuses, and neonates with intrauterine growth restriction compared to those with appropriate gestational age.Frontiers in endocrinology · 2026Article
- Genomic profiling of selective sweeps through haplotype differentiation unravelled genes associated with production and reproduction traits in Indian goat breeds.Tropical animal health and production · 2024Article
- Downregulation of miR-637 promotes vascular smooth muscle cell proliferation and migration via regulation of insulin-like growth factor-2.Cellular & molecular biology letters · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Children born small for gestational age (SGA) generally have a catch-up growth and rapid weight gain in the first years of life, which is a high risk of insulin resistance and cardiovascular diseases later in life. It was reported that the level of imprinted genes IGF-2, CDKN1C and PHLDA2 regulates placental growth. We assessed these imprinted genes expression levels in placental tissue and their influences on catch-up growth of full-term SGA infants. The protein and mRNA levels of placental CDKN1C, PHLDA2 and IGF-2 were analyzed in 29 full-term SGA and 29 full-term infants born appropriate for gestational age (AGA) using quantitative RT-PCR and Western blot assay, respectively. Catch-up growth was indicated by increased standard deviation score (ΔSDS) of weight at 1, 3 and 6 months relative to birth weight (BW). Correlations between indicated variables were evaluated using Pearson correlation coefficient analysis. Compared to AGA infants, CDKN1C and PHLDA2 levels were significantly increased, whereas IGF-2 was significantly reduced in SGA infants. The value of ΔSDS was significantly higher in SGA than that in AGA infants. For SGA status, Pearson analysis shows i) a negative correlation of CDKN1C and PHLDA2 abundances with BW, and a positive correlation of IGF-2 with BW, ii) no correlation between the three imprinted gene abundances and placental weight (PW), and between PW and BW, iii) a positive correlation of PHLDA2 abundance with CDKN1C, and iv) a positive correlation of CDKN1C and PHLDA2 abundances with ΔSDS, and a negative correlation of IGF-2 with ΔSDS at 1, 3 and 6 months. Taken together, increased CDKN1C and PHLDA2 and reduced IGF-2 abundances in placental tissue were related to BW and early period catch-up growth in full-term SGA infants. Placental CDKN1C, PHLDA2 and IGF-2 level monitoring may be useful for predicting and preventing the development of SGA.
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