Thyroid Hormone Modulates the Expression of Rat Liver Gammaglutamyl transpeptidase Activity

Voci, Adriana; Marchis, M. de; Massajoli, M.; Fugassa, E; Gallo, Gabriella

doi:10.1055/s-2007-1000793

Cited by 4 publications

(4 citation statements)

References 10 publications

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“…Recently, a net increase in GGT activity in liver of methimazole-treated hypothyroid rats, which was completely prevented by T3-replacement therapy has been reported (Voci et at. 1994).…”

Section: Discussionmentioning

confidence: 97%

“…Recently, we have demonstrated that thyroid hormone, which influences growth and development of almost all mammalian tissues, regulates GGT expression in adult rat liver (Voci, de Marchis, Massajoli, Fugassa and Gallo 1994). It has been observed that the expression of GGT is increased in the liver of hypothyroid rat, whereas thyroid hormone replacement therapy decreases the enzyme expression suggesting a crucial role for thyroid function in maintaining the phenotype of adult rat liver.…”

Section: Introductionmentioning

confidence: 98%

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Triiodothyronine Decreases Gammaglutamyltranspeptidase Expression in Cultured Rat Hepatocytes

Demori¹,

Bottazzi²,

Fugassa³

1995

Horm Metab Res

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Recently, an increase in gammaglutamyltranspeptidase (GGT) activity and mRNA in liver of hypothyroid rats has been reported. The aim of this study was to verify if triiodothyronine (T3) can directly affect GGT expression in primary cultures of rat hepatocytes. Results obtained from adult rat hepatocytes cultured in serum-free medium demonstrate: 1) a rise in GGT mRNA level magnified by dexamethasone during the maintenance of hepatocytes in culture which parallels the stimulation of GGT activity; 2) a negative effect of T3 on GGT activity of cultured hepatocytes which reflects a specific inhibition of GGT gene expression. The T3 effect on GGT expression in cultured hepatocytes is in line with previous observations on hypothyroid rat liver suggesting an important role for thyroid hormone in maintaining the differentiated adult liver phenotype in the rat.

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“…Recently, a net increase in GGT activity in liver of methimazole-treated hypothyroid rats, which was completely prevented by T3-replacement therapy has been reported (Voci et at. 1994).…”

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

Triiodothyronine Decreases Gammaglutamyltranspeptidase Expression in Cultured Rat Hepatocytes

Demori¹,

Bottazzi²,

Fugassa³

1995

Horm Metab Res

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“…In a recent study, Ruedig and Dringen (2004) reported that the cytokine TNFα elevates the specific activity of γGT in astrocyte cultures, an effect that is considered to be significant under pathological conditions. In cultures of hepatocytes (Voci et al, 1994; Demori et al, 1995), however, TH exerted a negative regulation of γGT. The molecular mechanism involved for the differential effect of the hormone on γGT: the positive effect of TH in astrocytes and the negative effect of the hormone in hepatocytes (Demori et al, 1995), is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…As a first step to elucidate the molecular basis of thyroidal regulation of GSH in the developing brain, we investigated thyroidal effects on γGT expression. Several earlier reports (Fernandez et al, 1991; Voci et al, 1994; Demori et al, 1995) describing the sensitivity of γGT to TH in liver were contradictory. Hemmings and Storey (1999) reported that congenital hypothyroidism had no effect on γGT in plasma membrane from neuronal or glial cells but reduced the activity of the enzyme by 33% in microvessels.…”

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confidence: 93%

Thyroid hormone stimulates γ‐glutamyl transpeptidase in the developing rat cerebra and in astroglial cultures

Dasgupta¹,

Das²,

Sarkar³

2005

J of Neuroscience Research

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Hypothyroidism in the developing rat brain is associated with enhanced oxidative stress, one of the earliest manifestations of which is a decline in the level of glutathione (GSH). To investigate the role of thyroid hormone (TH) on GSH homeostasis, the effect of TH on gamma-glutamyl transpeptidase (gammaGT), the key enzyme involved in the catalysis of GSH, was studied. Hypothyroidism declined the specific activity of cerebral gammaGT at all postnatal ages examined (postnatal day 1-20) with a maximum inhibition of 42% at postnatal day 10. Intraperitoneal injection of TH to 15-day-old rat pups increased the specific activity of gammaGT by 25-30% within 4-6 hr. Treatment of primary cultures of astrocytes by TH also enhanced the specific activity of gammaGT by 30-40% within 4-6 hr. The induction of gammaGT by TH was blocked by actinomycin D or cycloheximide. gammaGT is an ectoenzyme that is normally involved in the catabolism of GSH released by astrocytes. In the presence of the gammaGT-inhibitor, acivicin, GSH released in the culture medium of astrocytes increased linearly for at least 6 hr and TH had no effect on this accumulation pattern. In the absence of acivicin, GSH content of the medium from TH-treated cells was significantly lower than that of untreated controls due to activation of gammaGT by TH and a faster processing of GSH. Because the products of gammaGT reaction are putative precursors for neuronal GSH, the activation of gammaGT by TH may be conducive to GSH synthesis in neurons and their protection from oxidative stress.

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Identification of a Sixth Promoter That Directs the Transcription of γ-Glutamyl Transpeptidase Type III RNA in Mouse

Habib

Carter

Sepulveda

et al. 1995

Journal of Biological Chemistry

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We have previously identified five promoters in the 5'-flanking region of the mouse gamma-glutamyl transpeptidase (gamma GT) gene. We now report the localization of a sixth promoter that supports the transcription of type III RNA, the major gamma GT RNA in fetal liver. We made a fetal liver cDNA library enriched for gamma GT RNA and obtained 12 gamma GT type III-specific clones. The longest clone is consistent with a transcription start site for type III RNA at a position 5' to the type IV promoter and about 5 kilobase(s) (kb) 5' to the first coding exon. We estimated by ribonuclease protection assay that about 80% of the gamma GT mRNA in fetal liver was type III. Primer extension and nuclease protection analyses mapped the 5' end of type III mRNA in fetal liver and kidney to a single cluster of potential major and minor transcription start sites. Deletion analysis using transient expression of chloramphenicol acetyltransferase constructs of the type III promoter region revealed the greatest activity with a 1-kb 5'-flanking fragment in mouse kidney proximal tubular cells and no detectable activity in NIH-3T3 fibroblasts. These studies demonstrate that the type III 5' region of the mouse gamma GT gene is organized into two distinct exons (IIIa and IIIb) and that type III RNA is expressed under the control of its own promoter.

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Thyroid Hormone Modulates the Expression of Rat Liver Gammaglutamyl transpeptidase Activity

Cited by 4 publications

References 10 publications

Triiodothyronine Decreases Gammaglutamyltranspeptidase Expression in Cultured Rat Hepatocytes

Triiodothyronine Decreases Gammaglutamyltranspeptidase Expression in Cultured Rat Hepatocytes

Thyroid hormone stimulates γ‐glutamyl transpeptidase in the developing rat cerebra and in astroglial cultures

Identification of a Sixth Promoter That Directs the Transcription of γ-Glutamyl Transpeptidase Type III RNA in Mouse

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