Expression of the imprinted genesMEST/Mest in human and murine placenta suggests a role in angiogenesis

Mayer, Wolfgang; Hemberger, Myriam; Frank, Hans-Georg; Grümmer, Ruth; Winterhager, Elke; Kaufmann, Peter; Fundele, Reinald

doi:10.1002/(sici)1097-0177(200001)217:1<1::aid-dvdy1>3.0.co;2-4

Cited by 89 publications

(43 citation statements)

References 26 publications

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“…The second imprinted domain on mouse chromosome 6 contains the paternally expressed Mest. Mest is not expressed in trophoblast lineages, with expression restricted to fetal endothelial cells of the labyrinth (Mayer et al 2000). Loss of function results in a placental weight deficit and late gestation embryonic growth restriction, although placental morphology appears otherwise normal (Lefebvre et al 1998).…”

Section: R126 S J Tunster and Othersmentioning

confidence: 99%

Imprinted genes in mouse placental development and the regulation of fetal energy stores

2013

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Imprinted genes, which are preferentially expressed from one or other parental chromosome as a consequence of epigenetic events in the germline, are known to functionally converge on biological processes that enable in utero development in mammals. Over 100 imprinted genes have been identified in the mouse, the majority of which are both expressed and imprinted in the placenta. The purpose of this review is to provide a summary of the current knowledge regarding imprinted gene function in the mouse placenta. Few imprinted genes have been assessed with respect to their dosage-related action in the placenta. Nonetheless, current data indicate that imprinted genes converge on two key functions of the placenta, nutrient transport and placental signalling. Murine studies may provide a greater understanding of certain human pathologies, including low birth weight and the programming of metabolic diseases in the adult, and complications of pregnancy, such as pre-eclampsia and gestational diabetes, resulting from fetuses carrying abnormal imprints.Reproduction (2013) 145 R117-R137

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Section: R126 S J Tunster and Othersmentioning

confidence: 99%

Imprinted genes in mouse placental development and the regulation of fetal energy stores

2013

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“…Sections (10 to 12 m thick) were cut, allowed to dry, and either refrozen (at Ϫ80°C) or immediately processed for RNA in situ hybridization (16). RNA probes were generated as previously described: Cited1 (17), 4311 (Tpbp) (14), Mest (Peg1) (38), proliferin (PLF) (33), and mouse placental lactogen II (mPLII) (58). The sections were counterstained with eosin.…”

Section: Targeting Vectors and Generation Of The Cited1mentioning

confidence: 99%

Cited1 Is Required in Trophoblasts for Placental Development and for Embryo Growth and Survival

Rodríguez¹,

Sparrow²,

Scott³

et al. 2004

Molecular and Cellular Biology

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Cited1 is a transcriptional cofactor that interacts with Smad4, estrogen receptors ␣ and ␤, TFAP2, and CBP/p300. It is expressed in a restricted manner in the embryo as well as in extraembryonic tissues during embryonic development. In this study we report the engineering of a loss-of-function Cited1 mutation in the mouse. Cited1 null mutants show growth restriction at 18.5 days postcoitum, and most of them die shortly after birth. Half the heterozygous females, i.e., those that carry a paternally inherited wild-type Cited1 allele, are similarly affected. Cited1 is normally expressed in trophectoderm-derived cells of the placenta; however, in these heterozygous females, Cited1 is not expressed in these cells. This occurs because Cited1 is located on the X chromosome, and thus the wild-type Cited1 allele is not expressed because the paternal X chromosome is preferentially inactivated. Loss of Cited1 resulted in abnormal placental development. In mutants, the spongiotrophoblast layer is irregular in shape and enlarged while the labyrinthine layer is reduced in size. In addition, the blood spaces within the labyrinthine layer are disrupted; the maternal sinusoids are considerably larger in mutants, leading to a reduction in the surface area available for nutrient exchange. We conclude that Cited1 is required in trophoblasts for normal placental development and subsequently for embryo viability.

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“…This hypothesis is supported by evidence suggesting that MEST/Mest is a potential angiogenesis factor in humans and mice. 21,22) Although increased levels of Mest mRNA have only been found in adipocytes of obese mice, [16][17][18] the expression level of Mest in non-adipocyte cells in the stromal vascular fraction is higher than that of adipocytes from non-obese mice. It has been speculated that a genetic system exists to increase the number of adipocytes after the expansion of adipose tissue in order to control the adipose tissue mass and that then mature adipocytes symmetrically or asymmetrically divide into adipocytes or fibroblastic non-adipocytes.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Mesoderm-specific Transcript in Cell Growth of 3T3-L1 Preadipocytes

Kadota

Kawakami

Suzuki

et al. 2009

JOURNAL OF HEALTH SCIENCE

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Mesoderm-specific transcript (Mest) is an imprinted gene that is predominantly expressed in the embryonic and extraembryonic mesoderm, and its gene expression is the marker of the size of adipocytes. To characterize the expression effect of Mest gene products, we transfected mouse Mest into the 3T3-L1 cell line, which is a mouse preadipocyte cell line. The proliferation of the transfected 3T3-L1 cells was assessed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) colorimetry, and cell growth was assessed by counting the nuclei stained by Hoechst 33258. The 3T3-L1 cells transfected with recombinant Mest cDNA acquired the increased cell growth ability. Therefore, the gene products of Mest could be related to not only adipocyte expansion and adiposity but also mesoderm formation by enhancing the cell proliferation.Key words --mesoderm-specific transcript, preadipocyte, 3T3-L1, cell growth INTRODUTIONWhite adipose tissue is the organ that not only stores energy in the form of fat but also secretes endocrine hormones, adipokines, to maintain the homeostasis of an organism. 1, 2) Obesity is a growing and serious public health problem in developed countries. Obesity harms the homeostatic balance of adipose tissues; eventually, obesity can harm the whole body through the development of * To whom correspondence should be addressed: Faculty of Pharmaceutical Sciences, Tokushima Bunri University, 180 Yamashiro-cho, Tokushima 770-8514, Japan. Tel.: +81-88-602-8458; Fax: +81-88-655-3051; E-mail: ykadota@ph.bunriu.ac.jp type 2 diabetes mellitus, atherosclerosis, hypertension, and hyperlipidemia. 3,4) Adipocytes that ingest large quantities of lipids secrete adipokines, such as TNF-α and resistin, which cause insulin resistance. 5) Various factors such as sterol regulatory element-binding protein-1 (SREBP-1) and peroxisome proliferative activated receptor γ (PPARγ) enhance the proliferation, differentiation, and enlargement of adipocytes in obesity. 4,6)

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Expression of the imprinted genesMEST/Mest in human and murine placenta suggests a role in angiogenesis

Cited by 89 publications

References 26 publications

Imprinted genes in mouse placental development and the regulation of fetal energy stores

Imprinted genes in mouse placental development and the regulation of fetal energy stores

Cited1 Is Required in Trophoblasts for Placental Development and for Embryo Growth and Survival

Involvement of Mesoderm-specific Transcript in Cell Growth of 3T3-L1 Preadipocytes

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