Alterations of protein expression in serum of infants with intrauterine growth restriction and different gestational ages

Ruis-González, María D.; Cañete, María Dolores; Gomez-Chaparro, Jose Luis; Abril, Nieves; Cañete, Ramón; López-Barea, Juán

doi:10.1016/j.jprot.2015.02.003

Cited by 22 publications

(15 citation statements)

References 53 publications

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“…Regarding MBOAT7, one study reported its upregulation in the serum proteome of infants with IUGR. This, however, could only be an adaptive response to protect the brain from an adverse environment . Therefore, we decided to focus our analysis on ZNF331 , a maternally imprinted gene encoding a zinc‐finger protein specifically imprinted in the placenta, which appears to be a strong candidate gene to explain the observed IUGR .…”

Section: Discussionmentioning

confidence: 63%

“…This, however, could only be an adaptive response to protect the brain from an adverse environment. 11 Therefore, we decided to focus our analysis on ZNF331, a maternally imprinted gene encoding a zinc-finger protein specifically imprinted in the placenta, which appears to be a strong candidate gene to explain the observed IUGR. 12 Analysis of the methylation status of the ZNF331 promoter by MS-MLPA in fetal and paternal samples revealed that the duplicated allele is methylated in the father but not in the fetus, suggesting that both copies of the ZNF331 gene are expressed in the fetus, probably generating an abnormal double dose of this factor.…”

Section: Discussionmentioning

confidence: 99%

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Genomic duplication in the 19q13.42 imprinted region identified as a new genetic cause of intrauterine growth restriction

Pètre

Lorès

Sartelet³

et al. 2018

Clinical Genetics

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We report findings from a male fetus of 26 weeks' gestational age with severe isolated intrauterine growth restriction (IUGR). Chromosomal microarray analysis (CMA) on amniotic fluid cells revealed a 1.06-Mb duplication in 19q13.42 inherited from the healthy father. This duplication contains 34 genes including ZNF331, a gene encoding a zinc-finger protein specifically imprinted (paternally expressed) in the placenta. Study of the ZNF331 promoter by methylation-specific-multiplex ligation-dependent probe amplification showed that the duplicated allele was not methylated in the fetus unlike in the father's genome, suggesting both copies of the ZNF331 gene are expressed in the fetus. The anti-ZNF331 immunohistochemical analysis confirmed that ZNF331 was expressed at higher levels in renal and placental tissues from this fetus compared to controls. Interestingly, ZNF331 expression levels in the placenta have previously been reported to inversely correlate with fetal growth parameters. The original observation presented in this report showed that duplication of ZNF331 could be a novel genetic cause of isolated IUGR and underlines the usefulness of CMA to investigate the genetic causes of isolated severe IUGR.

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Genomic duplication in the 19q13.42 imprinted region identified as a new genetic cause of intrauterine growth restriction

Pètre

Lorès

Sartelet³

et al. 2018

Clinical Genetics

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“…APOL1 levels, APOL1-derived peptides, and APOL1 autoantibodies in mothers are linked to both preeclampsia and intrauterine growth retardation. [52][53][54] The pregnancy-associated phenotypes observed in our transgenic mice suggest an important role for Nephrin and APOL1 in placental function. Data from the Nephrotic Syndrome Study Network cohort, 55 confirmed in the Chronic Kidney Disease in Children cohort, 56 found preterm birth was more common in black children with glomerular disease and two APOL1 risk alleles.…”

Section: Discussionmentioning

confidence: 84%

APOL1-G0 or APOL1-G2 Transgenic Models Develop Preeclampsia but Not Kidney Disease

Bruggeman

Luo

et al. 2016

JASN

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APOL1 risk variants are associated with kidney disease in blacks, but the mechanisms of renal injury associated with APOL1 risk variants are unknown. Because APOL1 is unique to humans and some primates, we created transgenic (Tg) mice using the promoter of nephrin-encoding Nphs1 to express the APOL1 reference sequence (G0) or the G2 risk variant in podocytes, establishing Tg lines with a spectrum of APOL1 expression levels. Podocytes from Tg-G0 and Tg-G2 mice did not undergo necrosis, apoptosis, or autophagic cell death in vivo, even in lines with highly expressed transgenes. Further, Tg-G0 and Tg-G2 mice did not develop kidney pathology, proteinuria, or azotemia as of 300 days of age. However, by 200 days of age, Tg-G2 mice had significantly lower podocyte density than age-matched WT and Tg-G0 mice had, a difference that was not evident at weaning. Notably, a pregnancy-associated phenotype that encompassed eclampsia, preeclampsia, fetal/neonatal deaths, and small litter sizes occurred in some Tg-G0 mice and more severely in Tg-G2 mice. Similar to human placenta, placentas of Tg mice expressed APOL1. Overall, these results suggest podocyte depletion could predispose individuals with APOL1 risk genotypes to kidney disease in response to a second stressor, and add to other published evidence associating APOL1 expression with preeclampsia.

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“…(7,10) In this regard, up-regulation of MBOAT7 in response to an insult (e.g., viral hepatitis infection) might be a compensatory or adaptive mechanism to overcome pathogen-induced liver damage, similar to that observed in contexts such as intrauterine growth restriction and shock. (34) Further studies are required to understand the mechanisms of MBOAT7 function and to explore the role of MBOAT7 in the regulation of inflammatory cell activity.…”

Section: Discussionmentioning

confidence: 99%

The membrane‐bound O‐acyltransferase domain‐containing 7 variant rs641738 increases inflammation and fibrosis in chronic hepatitis B

et al. 2017

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Alterations of protein expression in serum of infants with intrauterine growth restriction and different gestational ages

Cited by 22 publications

References 53 publications

Genomic duplication in the 19q13.42 imprinted region identified as a new genetic cause of intrauterine growth restriction

Genomic duplication in the 19q13.42 imprinted region identified as a new genetic cause of intrauterine growth restriction

APOL1-G0 or APOL1-G2 Transgenic Models Develop Preeclampsia but Not Kidney Disease

The membrane‐bound O‐acyltransferase domain‐containing 7 variant rs641738 increases inflammation and fibrosis in chronic hepatitis B

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