Developmental and growth-related regulation of expression of serine dehydratase mRNA in rat liver

Noda, Chiseko; Ohguri, Miho; Ichihara, Akira

doi:10.1016/0006-291x(90)91713-3

Cited by 21 publications

(8 citation statements)

References 26 publications

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“…These observations mirrored our histological results, which showed a decrease in the proportion of hepatocytes at P1 followed by a large increase in hepatocytes between P5 and P10 (Table 1). Tryptophan 2,3-dioxygenase ( Tdo2 ) (Cai et al 2007; Nagao et al 1986) and serine hydratase ( Sds ) (Noda et al 1990) are markers of differentiated hepatocytes, and alpha-fetoprotein ( Afp , Figure 4) (Tanaka et al 2009) is a marker of hepatocyte precursors. Analysis of these markers revealed that hepatocyte differentiation began at P5 with the largest change occurring between P10 and P15 (Figure 4 and Figure S7).…”

Section: Resultsmentioning

confidence: 99%

Extensive Epigenetic Changes Accompany Terminal Differentiation of Mouse Hepatocytes After Birth

Cannon

Pilarowski

Liu

et al. 2016

G3 Genes|Genomes|Genetics

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DNA methylation is traditionally thought to be established during early development and to remain mostly unchanged thereafter in healthy tissues, although recent studies have shown that this epigenetic mark can be more dynamic. Epigenetic changes occur in the liver after birth, but the timing and underlying biological processes leading to DNA methylation changes are not well understood. We hypothesized that this epigenetic reprogramming was the result of terminal differentiation of hepatocyte precursors. Using genomic approaches, we characterized the DNA methylation patterns in mouse liver from E18.5 until adulthood to determine if the timing of the DNA methylation change overlaps with hepatocyte terminal differentiation, and to examine the genomic context of these changes and identify the regulatory elements involved. Out of 271,325 CpGs analyzed throughout the genome, 214,709 CpGs changed DNA methylation by more than 5% (e.g., from 5 to 10% methylation) between E18.5 and 9 wk of age, and 18,863 CpGs changed DNA methylation by more than 30%. Genome-scale data from six time points between E18.5 and P20 show that DNA methylation changes coincided with the terminal differentiation of hepatoblasts into hepatocytes. We also showed that epigenetic reprogramming occurred primarily in intergenic enhancer regions while gene promoters were less affected. Our data suggest that normal postnatal hepatic development and maturation involves extensive epigenetic remodeling of the genome, and that enhancers play a key role in controlling the transition from hepatoblasts to fully differentiated hepatocytes. Our study provides a solid foundation to support future research aimed at further revealing the role of epigenetics in stem cell biology.

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Section: Resultsmentioning

confidence: 99%

Extensive Epigenetic Changes Accompany Terminal Differentiation of Mouse Hepatocytes After Birth

Cannon

Pilarowski

Liu

et al. 2016

G3 Genes|Genomes|Genetics

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“…At a late gestation or perinatal stage, hepatocytes start producing a number of metabolic enzymes including glucose‐6‐phosphatase (G6Pase) and tyrosine aminotransferase (TAT) to prepare their metabolism for the change in the physiological role of the liver (Greengard, 1970; Haber et al ., 1995). Finally, several days after birth, serine dehydratase (SDH) and tryptophan oxygenase (TO) are induced in hepatocytes (Nagao et al ., 1986; Noda et al ., 1990, 1994). Interestingly, expression of these metabolic enzymes is often lost in hepatocytic carcinomas or malignant hepatomas and, conversely, AFP expression resumes in these tumors (Abelev, 1971).…”

Section: Introductionmentioning

confidence: 99%

Fetal liver development requires a paracrine action of oncostatin M through the gp130 signal transducer

et al. 1999

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Fetal liver, the major site of hematopoiesis during embryonic development, acquires additional various metabolic functions near birth. Although liver development has been characterized biologically as consisting of several distinct steps, the molecular events accompanying this process are just beginning to be characterized. In this study, we have established a novel culture system of fetal murine hepatocytes and investigated factors required for development of hepatocytes. We found that oncostatin M (OSM), an interleukin-6 family cytokine, in combination with glucocorticoid, induced maturation of hepatocytes as evidenced by morphological changes that closely resemble more differentiated hepatocytes, expression of hepatic differentiation markers and intracellular glycogen accumulation. Consistent with these in vitro observations, livers from mice deficient for gp130, an OSM receptor subunit, display defects in maturation of hepatocytes. Interestingly, OSM is expressed in CD45 ϩ hematopoietic cells in the developing liver, whereas the OSM receptor is expressed predominantly in hepatocytes. These results suggest a paracrine mechanism of hepatogenesis; blood cells, transiently expanding in the fetal liver, produce OSM to promote development of hepatocytes in vivo.

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“…On the other hand, two glyeolytic enzymes tested, lactate dehydrogenase and glyceraldehyde-3-phosphate dehydrogenase, which are expressed in many tissues, were increased in the liver ofjvs mice [3,6]. The pattern of these enzyme expressions resembles the one observed in undifferentiated and/or de-differentiated hepatocytes [7][8][9][10][11][12]. Therefore, jvs mice may be a useful animal model to study the regulation of gene expression in the liver during development and the possible effect of lipid accumulation on liver function.…”

Section: Introductionmentioning

confidence: 99%

Proto‐oncogene c‐jun and c‐fos messenger RNAs increase in the liver of carnitine‐deficient juvenile visceral steatosis (jvs) mice

1992

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We determined the mRNA levels ofc-jun and c-los in the liver of C3H-H-2* jvs mice. Both were higher injvs mice than in normal mice. The level of c-jun mRNA irxcreased gradually after birth, but in the control mice there was almost no change. In addition, ~-fetoprotein and aldolase A mRNA levels were also higher than in normal littermates. These results suggest that the pattern of the gene expression in jv~ mice partly resembles the one that occurs in undifferentiated hepatoeytes and/or hepatoccllular carcinoma.

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Developmental and growth-related regulation of expression of serine dehydratase mRNA in rat liver

Cited by 21 publications

References 26 publications

Extensive Epigenetic Changes Accompany Terminal Differentiation of Mouse Hepatocytes After Birth

Extensive Epigenetic Changes Accompany Terminal Differentiation of Mouse Hepatocytes After Birth

Fetal liver development requires a paracrine action of oncostatin M through the gp130 signal transducer

Proto‐oncogene c‐jun and c‐fos messenger RNAs increase in the liver of carnitine‐deficient juvenile visceral steatosis (jvs) mice

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