Phosphatidylethanolamine metabolism in rat liver after partial hepatectomy. Control of biosynthesis of phosphatidylethanolamine by the availability of ethanolamine

Houweling, Martin; Tijburg, Lilian B.M.; Vaartjes, W.J.; Golde, L.M.G. Van

doi:10.1042/bj2830055

Cited by 51 publications

(34 citation statements)

References 53 publications

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“…In this pathway, both the availability of Etn and 1,2-diacylglycerol and the activity of enzymes, choline (ethanolamine) kinase and CTP:phosphoethanolamine cytidylyltransferase, are required (11). Among these, the supply of Etn seems to primarily inf luence PtdEtn synthesis in hepatocytes (12). PtdEtn can also be synthesized by the decarboxylation of phosphatidylserine (13) and by a base-exchange reaction (14).…”

Section: Discussionmentioning

confidence: 99%

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Ethanolamine modulates the rate of rat hepatocyte proliferationin vitroandin vivo

Sasaki

Kume

Nemoto

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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A low molecular weight, heat-resistant hepatotrophic factor in an extract from the bovine intestinal mucosa was purified and identified as ethanolamine by structural analyses. The mode of action of ethanolamine in vitro and in vivo coincided with that of the crude extract of the tissue, indicating that ethanolamine is the active component. Ethanolamine synergistically elevated the stimulation of DNA synthesis in hepatocytes in primary culture when added together with a growth factor, such as epidermal growth factor, with the ED 50 being 20 M, although it showed little stimulatory effect by itself. Contrary to these in vitro results, the intraperitoneal administration of ethanolamine hydrochloride (24 mg of ethanolamine per kg of body weight) enhanced hepatocyte proliferation in regenerating rat livers after two-thirds hepatectomy without the administration of any growth factors. In the regenerating liver, hepatocyte proliferation may be initiated by an endogenous growth factor, but the supply of ethanolamine in circulation may not be sufficient for optimal hepatocyte proliferation; thus, the exogenous administration of ethanolamine may further enhance hepatocyte proliferation. Ethanolamine in circulation may be a humoral hepatotrophic factor.Previously we reported that the proliferation of hepatocytes in primary culture was synergistically stimulated by a low molecular weight (LMW, Ͻ1,000) and a high molecular weight (HMW, Ͼ10,000) factor that were derived from the bovine small intestine mucosa, separated by their solubility in methanol (1). The LMW factor synergistically enhanced the basal level of stimulation by the HMW factor, while it had little effect when added alone. Since the LMW factor could enhance the level of DNA synthesis in hepatocytes that were stimulated by epidermal growth factor (EGF) or hepatocyte growth factor (HGF), it acts by amplifying the effects of a growth factor. Contrary to the in vitro result, the LMW factor could stimulate hepatocyte proliferation in regenerating livers even when added alone. We speculate that an endogenous growth factor(s) is probably produced in the animals with the regenerating liver, but the supply of the LMW factor is below the optimal level, thus the exogenous supply of the LMW factor can further stimulate hepatocyte proliferation. The LMW factor may function as a humoral hepatotrophic factor for liver regeneration.We purified the LMW factor from the bovine small intestinal mucosa, and we identified it as ethanolamine (Etn). The commercially available Etn had effects identical to those of the LMW factor before purification; i.e., Etn synergistically stimulated the proliferation of hepatocytes in primary culture when added with the HMW factor, and it stimulated hepatocyte proliferation in the regenerating liver when administered alone. Etn can synergistically enhance DNA synthesis in hepatocytes when added with EGF, suggesting that it enhances the actions of hepatotrophic growth factors. Etn in circulation may function as a humoral hepatotrophic factor ...

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Section: Discussionmentioning

confidence: 99%

“…PtdEtn can also be synthesized by the decarboxylation of phosphatidylserine (13) and by a base-exchange reaction (14). These pathways, however, are not the major routes of PtdEtn synthesis in hepatocytes (9,12,14).…”

Section: Discussionmentioning

confidence: 99%

Ethanolamine modulates the rate of rat hepatocyte proliferationin vitroandin vivo

Sasaki

Kume

Nemoto

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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“…Pulse-label studies demonstrated that exposure of freshly isolated hepatocytes to increasing concentrations of ethanolamine resulted in an enhanced incorporation of labelled glycerol and ethanolamine into PtdEtn. The enhanced PtdEtn synthesis was accompanied by a considerable increase in the pool size of phosphoethanolamine, whereas the amount of CDPethanolamine remained constant [13,14]. Furthermore, exposure of hepatocytes to phorbol ester has been shown to stimulate PtdEtn synthesis, to enhance the activity of ECT and to reduce phosphoethanolamine and CDPethanolamine pool sizes [37].…”

Section: Discussionmentioning

confidence: 99%

“…The ratecontrolling role of ECT is partially determined on the basis of experiments with freshly isolated hepatocytes. Sundler and Åkesson [13] and Houweling et al [14] reported that, at physiological extracellular ethanolamine concentrations, phosphoethanolamine starts to accumulate with the level of CDPethanolamine remaining constant, implicating that ECT has become rate-limiting.…”

Section: Introductionmentioning

confidence: 99%

“…Our results strongly suggest that, at physiological ethanolamine concentrations, the supply of CDPethanolamine, via the expression level of ECT, together with the amount of cellular DAG (diacylglycerol) available to EPT are major factors regulating the flux through the CDPethanolamine pathway. [1,[2][3][4][5][6][7][8][9][10][11][12][13][14] C]ethanolamine with partially purified ethanolamine kinase as described previously [22]. sn-1,2-DAG kinase was from Calbiochem (La Jolla, CA, U.S.A.).…”

Section: Introductionmentioning

confidence: 99%

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Control of the CDPethanolamine pathway in mammalian cells: effect of CTP:phosphoethanolamine cytidylyltransferase overexpression and the amount of intracellular diacylglycerol

Bleijerveld

Klein

Vaandrager

et al. 2004

Biochemical Journal

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For an insight regarding the control of PtdEtn (phosphatidylethanolamine) synthesis via the CDPethanolamine pathway, rat liver cDNA encoding ECT (CTP:phosphoethanolamine cytidylyltransferase) was transiently or stably transfected in Chinesehamster ovary cells and a rat liver-derived cell line (McA-RH7777), resulting in a maximum of 26-and 4-fold increase in specific activity of ECT respectively. However, no effect of ECT overexpression on the rate of [ 3 H]ethanolamine incorporation into PtdEtn was detected in both cell lines. This was explored further in cells overexpressing four times ECT activity (McA-ECT1). The rate of PtdEtn breakdown and PtdEtn mass were not changed in McA-ECT1 cells in comparison with controltransfected cells. Instead, an accumulation of CDPethanolamine (label and mass) was observed, suggesting that in McA-ECT1 cells the ethanolaminephosphotransferase-catalysed reaction became rate-limiting. However, overexpression of the human choline/ethanolaminephosphotransferase in McA-ECT1 and control-transfected cells had no effect on PtdEtn synthesis. To investigate whether the availability of DAG (diacylglycerol) limited PtdEtn synthesis in these cells, intracellular DAG levels were increased using PMA or phospholipase C. Exposure of cells to PMA or phospholipase C stimulated PtdEtn synthesis and this effect was much more pronounced in McA-ECT1 than in controltransfected cells. In line with this, the DAG produced after PMA exposure was consumed more rapidly in McA-ECT1 cells and the CDPethanolamine level decreased accordingly. In conclusion, our results suggest that the supply of CDPethanolamine, via the expression level of ECT, is an important factor governing the rate of PtdEtn biosynthesis in mammalian cells, under the condition that the amount of DAG is not limiting.

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Tumour phospholipid metabolism

1999

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Phosphatidylethanolamine metabolism in rat liver after partial hepatectomy. Control of biosynthesis of phosphatidylethanolamine by the availability of ethanolamine

Cited by 51 publications

References 53 publications

Ethanolamine modulates the rate of rat hepatocyte proliferationin vitroandin vivo

Ethanolamine modulates the rate of rat hepatocyte proliferationin vitroandin vivo

Control of the CDPethanolamine pathway in mammalian cells: effect of CTP:phosphoethanolamine cytidylyltransferase overexpression and the amount of intracellular diacylglycerol

Tumour phospholipid metabolism

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