The correlation between sampling site and gene expression in the term human placenta

Wyatt, Solange; Kraus, Frederick T.; Roh, Cheong‐Rae; Elchalal, Uriel; Nelson, D. F.; Sadovsky, Yoel

doi:10.1016/j.placenta.2004.07.003

Cited by 135 publications

(102 citation statements)

References 43 publications

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Section: Discussionmentioning

confidence: 97%

“…Importantly, gene expression levels may vary with the sampling sites of the placenta. 20 We investigated this potential bias and demonstrated that there was no significant difference with respect to sampling variations.In summary, we presented a quantitative survey of 74 imprinted genes in normal and IUGR human placentas and explored their correlation with LOI using a functional and highly (paternally imprinted) genes, two (NNAT and PEG10) are paternally expressed. These results indicate that not all imprinted genes fit the "parental conflict" theory.…”

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confidence: 97%

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Differential expression of imprinted genes in normal and IUGR human placentas

Diplas¹,

Lambertini²,

Lee³

et al. 2009

Epigenetics

175

124

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Genomic imprinting refers to silencing of one parental allele in the zygotes of gametes depending upon the parent of origin. Loss of imprinting (LOI) is the gain of function from the silent allele that can have a maximum effect of doubling the gene dosage. LOI may play a significant role in the etiology of intrauterine growth restriction (IUGR). Using placental tissue from ten normal and seven IUGR pregnancies, we conducted a systematic survey of the expression of a panel of 74 "putatively" imprinted genes using quantitative RT-PCR. We found that 52/74 (~70%) of the genes were expressed in human placentas. Nine of the 52 (17%) expressed genes were significantly differentially expressed between normal and IUGR placentas; five were upregulated (PHLDA2, ILK2, NNAT, CCDC86, PEG10) and four downregulated (PLAGL1, DHCR24, ZNF331, CDKAL1). We also assessed LOI profile of 14 imprinted genes in 14 normal and 24 IUGR placentas using a functional and sensitive assay developed in our laboratory. Little LOI was observed in any placentas for five of the genes (PEG10, PHLDA2, MEG3, EPS15, CD44). With the 149 heterozygosities examined, 40 (26.8%) exhibited LOI >3%. Some genes exhibited frequent LOI in placentas regardless of the disease status (IGF2, TP73, MEST, SLC22A18, PEG3), while others exhibited LOI only in IUGR placentas (PLAGL1, DLK1, H19, SNRPN). Importantly, there was no correlation between gene expression and LOI profile. Our study suggests that genomic imprinting may play a role in IUGR pathogenesis, but mechanisms other than LOI may contribute to dysregulation of imprinted genes. IntroductionGenomic imprinting refers to silencing of one parental allele in the zygotes of gametes depending upon the parent of origin; this silencing occurs via epigenetic processes such as DNA methylation and/or histone modification. 1 It has been hypothesized in the "parental conflict" theory that paternally expressed genes favors the utilization of maternal resources for the benefit of the offspring while the maternally expressed genes act to preserve such resources. Thus, imprinted genes that are paternally expressed (maternally imprinted) are predicted to promote growth of the offspring, either in utero or in perinatal period, whilst maternally expressed (paternally imprinted) genes would act as growth suppressors to assure appropriate allocation of limited maternal resources to each conceptus. 2 Consequently, imprinted genes play critical roles in regulation of growth and development; disruption of this critical process, such as loss of imprinting (LOI), has been associated with a wide range of human diseases including birth defects neurodevelopmental disorders and cancer. [3][4][5][6][7] Compared to other mammalian genomes such as that of the mouse, the human genome is imprinted to a much lesser degree, possibly due to a lack of competition for maternal resources because human pregnancies are typically singletons. 8 The estimated number of imprinted genes is ~100-200 (<1% of the genome). This limited number of imprinted genes affo...

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 97%

Differential expression of imprinted genes in normal and IUGR human placentas

Diplas¹,

Lambertini²,

Lee³

et al. 2009

Epigenetics

175

124

View full text Add to dashboard Cite

show abstract

“…Each tree may show a varying degree of maturation or pathology, which may be reflected in localized differences in DNA methylation. Variation in maternal and fetal blood supplies may also contribute to spatial differences in gene expression and DNA methylation (Wyatt et al 2005). As the placenta is a dynamic structure, showing considerable ability to adapt to a variety pathological influences (Redline 2008), sampling strategy (in relation to organ anatomy) needs to be considered carefully in the planning and interpretation of placental DNA methylation studies (Burton et al 2014;Hogg et al 2014a).…”

Section: Influence Of Placental Architecture Villous Tree Structurementioning

confidence: 99%

The Human Placental Methylome

Robinson

Price

2015

Cold Spring Harbor Perspectives in Medicine

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This review provides an overview of the unique features of DNA methylation in the human placenta. We discuss the importance of understanding placental development, structure, and function in the interpretation of DNA methylation data. Examples are given of how DNA methylation is important in regulating placental-specific gene expression, including monoallelic expression and X-chromosome inactivation in the placenta. We also discuss studies of global DNA methylation changes in the context of placental pathology and environmental exposures.

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“…Among the most unique features of RGK proteins is their ability to be transcriptionally regulated [3,5,6,11,[20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] (Table 2). Indeed, Gem/Kir was discovered as a gene upregulated in human T cells after stimulation with mitogens [5] or in BCR-Abl-transformed B cells [11].…”

Section: Transcriptional Regulationmentioning

confidence: 99%

“…While the majority of Rad transcriptional regulation has been reported in muscle, other intriguing, but unexplored observations have emerged from other cell types. For instance, Rad is upregulated in human peripheral blood mononuclear cells after acute heat shock [34] and in human placenta post-hypoxia [22,31]. Rad expression is also correlated with the grade, size, and metastatic potential of breast cancer tumors [35].…”

Section: Transcriptional Regulationmentioning

confidence: 99%

The RGK family of GTP-binding proteins: Regulators of voltage-dependent calcium channels and cytoskeleton remodeling

Correll¹,

Pang²,

Niedowicz³

et al. 2008

Cellular Signalling

100

136

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RGK proteins constitute a novel subfamily of small Ras-related proteins that function as potent inhibitors of voltage-dependent (VDCC) Ca 2+ channels and regulators of actin cytoskeletal dynamics. Within the larger Ras superfamily, RGK proteins have distinct regulatory and structural characteristics, including nonconservative amino acid substitutions within regions known to participate in nucleotide binding and hydrolysis and a C-terminal extension that contains conserved regulatory sites which control both subcellular localization and function. RGK GTPases interact with the VDCC β-subunit (Ca V β) and inhibit Rho/Rho kinase signaling to regulate VDCC activity and the cytoskeleton respectively. Binding of both calmodulin and 14-3-3 to RGK proteins, and regulation by phosphorylation controls cellular trafficking and the downstream signaling of RGK proteins, suggesting that a complex interplay between interacting protein factors and trafficking contribute to their regulation.

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The correlation between sampling site and gene expression in the term human placenta

Cited by 135 publications

References 43 publications

Differential expression of imprinted genes in normal and IUGR human placentas

Differential expression of imprinted genes in normal and IUGR human placentas

The Human Placental Methylome

The RGK family of GTP-binding proteins: Regulators of voltage-dependent calcium channels and cytoskeleton remodeling

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