Profiling of genes differentially expressed between fetal liver and postnatal liver using high-density oligonucleotide DNA array

Nagata, Toshihito; Takahashi, Yasuo; Ishii, Yoshinori; Asai, Satoshi; Sugahara, Megumi; Nishida, Yusuke; Murata, Akiko; Chin, Motoaki; Schichino, Hiroyuki; Koshinaga, Tsugumichi; Fukuzawa, Masahiro; Mugishima, Hideo

doi:10.3892/ijmm.11.6.713

Cited by 19 publications

(19 citation statements)

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“…A major limiting factor in comparing the two studies is that the report by Treluyer et al (1997) was limited to an aggregate CYP2C expression pattern. The current data are consistent with a more recent study by Nagata et al (2003) in which expression profiling was used to examine differential gene expression between the human fetal and adult liver. CYP2C9 mRNA levels were detected in 17-to 37-week fetal liver samples (n ϭ 7) and were elevated 13-fold in postnatal samples (ages 5-65 years, n ϭ 14).…”

Section: Discussionsupporting

confidence: 79%

Developmental Expression of Human Hepatic CYP2C9 and CYP2C19

Koukouritaki¹,

Manro²,

Marsh³

et al. 2003

J Pharmacol Exp Ther

286

200

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The CYP2C subfamily is responsible for metabolizing many important drugs and accounts for about 20% of the cytochrome P450 in adult liver. To determine developmental expression patterns, liver microsomal CYP2C9 and -2C19 were measured (n ϭ 237; ages, 8 weeks gestation-18 years) by Western blotting and with diclofenac or mephenytoin, respectively, as probe substrates. CYP2C9-specific content and catalytic activity were consistent with expression at 1 to 2% of mature values (i.e., specific content, 18.3 pmol/mg protein and n ϭ 79; specific activity, 549.5 pmol/mg/min and n ϭ 72) during the first trimester, with progressive increases during the second and third trimesters to levels approximately 30% of mature values. From birth to 5 months, CYP2C9 protein values varied 35-fold and were significantly higher than those observed during the late fetal period, with 51% of samples exhibiting values commensurate with mature levels. Less variable CYP2C9 protein and activity values were observed between 5 months and 18 years. CYP2C19 protein and catalytic activities that were 12 to 15% of mature values (i.e., specific content, 14.6 pmol/mg and n ϭ 20; specific activity, 18.5 pmol/mg/min and n ϭ 19) were observed as early as 8 weeks of gestation and were similar throughout the prenatal period. CYP2C19 expression did not change at birth, increased linearly over the first 5 postnatal months, and varied 21-fold from 5 months to 10 years. Adult CYP2C19 protein and activity values were observed in samples older than 10 years. The ontogeny of CYP2C9 and -2C19 were dissimilar among both fetal and 0-to 5-months postnatal samples, implying different developmental regulatory mechanisms.

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Section: Discussionsupporting

confidence: 79%

Developmental Expression of Human Hepatic CYP2C9 and CYP2C19

Koukouritaki¹,

Manro²,

Marsh³

et al. 2003

J Pharmacol Exp Ther

286

200

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“…Indeed, the placenta does not pose a metabolic barrier to nicotine transfer from the mother (Pastrakuljic et al, 1998), and therefore nicotine can readily cross through the placenta and accumulate in utero (Luck et al, 1985). In addition, the expression of nicotine-metabolizing enzymes appears either near birth (CYP2B) or 2 week postpartum (CYP2A) (Nagata et al, 2003;Rich and Boobies, 1997). Together, in agreement with a phenomenon referred to as the 'fetal basis of adult disease' (Barker, 1998), this provides a basis for pathological shifts in the developmental patterns of nicotine-exposed embryos leading to postpartum health consequences.…”

Section: Discussionmentioning

confidence: 99%

The cholinergic system is involved in regulation of the development of the hematopoietic system

et al. 2007

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Gene expression profiling demonstrated that components of the cholinergic system, including choline acetyltransferase, acetylcholinesterase and nicotinic acetylcholine receptors (nAChRs), are expressed in embryonic stem cells and differentiating embryoid bodies (EBs). Triggering of nAChRs expressed in EBs by nicotine resulted in activation of MAPK and shifts of spontaneous differentiation toward hemangioblast. In vivo, non-neural nAChRs are detected early during development in fetal sites of hematopoiesis. Similarly, in vivo exposure of the developing embryo to nicotine resulted in higher numbers of hematopoietic progenitors in fetal liver. However postpartum, the number of hematopoietic stem/progenitor cells (HSPC) was decreased, suggesting an impaired colonization of the fetal bone marrow with HSPCs. This correlated with increased number of circulating HSPC and decreased expression of CXCR4 that mediates migration of circulating cells into the bone marrow regulatory niche. In addition, protein microarrays demonstrated that nicotine changed the profile of cytokines produced in the niche. While the levels of IL1α, IL1β, IL2, IL9 and IL10 were not changed, the production of hematopoiesis-supportive cytokines including G-CSF, GM-CSF, IL3, IL6 and IGFBP-3 was decreased. This correlated with the decreased repopulating ability of HSPC in vivo and diminished hematopoietic activity in bone marrow cultures treated with nicotine. Interestingly, nicotine stimulated the production of IL4 and IL5, implying a possible role of the cholinergic system in pathogenesis of allergic diseases. Our data provide evidence that the nicotine-induced imbalance of the cholinergic system during gestation interferes with normal development and provides the basis for negative health outcomes postpartum in active and passive smokers.

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“…Moreover, its overexpression inhibits cell growth and proliferation in vitro and in vivo, thus suggesting a possible role as a tumor suppressor . The differential expression of HtrA1 in human tissues and the observation that the transcription of this gene is highly regulated between fetal liver and postnatal liver (Nagata et al 2003) strongly suggest that HtrA1 exerts its function of control on cell growth not only in neoplastic cells but also under physiological conditions.…”

mentioning

confidence: 99%

The Serine Protease HtrA1 Is Upregulated in the Human Placenta during Pregnancy

Luca

Falco

Fedele

et al. 2004

J Histochem Cytochem.

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(AB) S U M M A R Y The placenta has a dynamic and continuous capacity for self-renewal. The molecular mechanisms responsible for controlling trophoblast proliferation are still unclear. It is generally accepted that the simultaneous activity of proteins involved in cell proliferation, apoptosis, and extracellular matrix degradation plays an important role in correct placental development. We investigated in depth the expression of the serine protease HtrA1 during pregnancy in human placenta by in situ hybridization and immunohistochemistry, we demonstrated that HtrA1 displayed a low level of expression in the first trimester of gestation and a strong increase of HtrA1 expression in the third trimester. Finally, by electron microscopy, we demonstrated that HtrA1 was localized either in the cytoplasm of placental cells, especially close to microvilli that characterized the plasma membrane of syncytiotrophoblast cells, or in the extracytoplasmic space of the stroma of placental villi, particularly in the spaces between collagen fibers and on collagen fibers themselves. The expression pattern of HtrA1 in human placentas strongly suggests a role for this protein in placental development and function. Moreover, on the basis of its subcellular distribution it can be postulated that HtrA1 acts on different targets, such as intracellular growth factors or extracellular matrix proteins, to favor the correct formation/function of the placenta.

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Profiling of genes differentially expressed between fetal liver and postnatal liver using high-density oligonucleotide DNA array

Cited by 19 publications

References 0 publications

Developmental Expression of Human Hepatic CYP2C9 and CYP2C19

Developmental Expression of Human Hepatic CYP2C9 and CYP2C19

The cholinergic system is involved in regulation of the development of the hematopoietic system

The Serine Protease HtrA1 Is Upregulated in the Human Placenta during Pregnancy

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