Ontogeny of Epidermal Growth Factor, Transforming Growth Factor-α, Epidermal Growth Factor Receptor, and Thyroid Hormone Receptor RNA Levels in Rat Kidney and Changes in Those Levels Induced by Early Thyroxine Treatment

North, Daniel L.; Lakshmanan, J.; Reviczky, A.; Kaser, Mathew; Fisher, Delbert A.

doi:10.1203/00006450-199204000-00005

Cited by 16 publications

(10 citation statements)

References 16 publications

(17 reference statements)

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“…PPAR activity may be released from suppression by TR due to decreased number of TR during fasting, resulting in the increased transcriptional levels of enzymes regulating fatty acid ␤-oxidation such as aox gene. Furthermore, TR expression is regulated by hormones (54) and strictly controlled during ontogeny and development (55)(56)(57)(58). TRs exert their effects on lipid metabolism through convergence of PPAR signaling pathways.…”

Section: Table I Protein Expression Of Tra1 and Its Dbd Mutant In Cosmentioning

confidence: 99%

Inhibition of Peroxisome Proliferator Signaling Pathways by Thyroid Hormone Receptor

Miyamoto¹,

Kaneko²,

Kakizawa

et al. 1997

Journal of Biological Chemistry

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Peroxisome proliferators (e.g. clofibric acid) and thyroid hormone play an important role in the metabolism of lipids. These effectors display their action through their own nuclear receptors, peroxisome proliferatoractivated receptor (PPAR) and thyroid hormone receptor (TR). PPAR and TR are ligand-dependent, DNA binding, trans-acting transcriptional factors belonging to the erbA-related nuclear receptor superfamily. The present study focused on the convergence of the effectors on the peroxisome proliferator response element (PPRE). Transcriptional activation induced by PPAR through a PPRE was significantly suppressed by cotransfection of TR in transient transfection assays. The inhibition, however, was not affected by adding 3,5,3-triiodo-L-thyronine (T3). Furthermore, the inhibition was not observed in cells cotransfected with retinoic acid receptor or vitamin D3 receptor. The inhibitory action by TR was lost by introducing a mutation in the DNA binding domain of TR, indicating that competition for DNA binding is involved in the molecular basis of this functional interaction. Gel shift assays revealed that TRs, expressed in insect cells, specifically bound to the 32 P-labeled PPRE as heterodimers with the retinoid X receptor (RXR). Both PPAR and TR bind to PPRE, although only PPAR mediates transcriptional activation via PPRE. TR⅐RXR heterodimers are potential competitors with PPAR•RXR for binding to PPREs. It is concluded that PPAR-mediated gene expression is negatively controlled by TR at the level of PPAR binding to PPRE. We report here the novel action of thyroid hormone receptor in controlling gene expression through PPREs.Peroxisomes are cytoplasmic organelles that are important in mammalian lipid homeostasis (1). The structurally diverse xenobiotic peroxisome proliferators (PPs), 1 such as clofibrate, nafenopin, and WY-14,643 stimulate the proliferation of peroxisomes (2-5) and cause tumorigenic transformation of hepatic cells in rodents (6, 7). Some of these compounds have been used in man as hypolipidemic agents. PPs have been shown to induce peroxisomal and microsomal enzymes involved in lipid metabolism through activation of the peroxisome proliferatoractivated receptor (PPAR) (8, 9). The PPAR is a member of the nuclear receptor superfamily of ligand-dependent transcriptional factors and is structurally related to the subfamily of receptors that includes the thyroid hormone receptor (TR), retinoic acid receptor (RAR), and vitamin D3 receptor (VDR) (10). To date, three subtypes of PPARs have been identified in amphibians, rodents, and humans, PPAR␣,9,[11][12][13][14]. Further investigation revealed that natural fatty acids are also potent activators of PPAR␣ (14, 15), although no direct interaction of PPAR␣ with either PPs or fatty acids has been described so far. Recently, ligands for PPAR␥ have been identified that are potent inducers of adipogenesis in vivo. These include thiazolidine diones, a class of anti-diabetic drugs, and the arachidonic acid derivative 15-deoxy-D12, 14-prostaglandin J2 (16 ...

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Section: Table I Protein Expression Of Tra1 and Its Dbd Mutant In Cosmentioning

confidence: 99%

Inhibition of Peroxisome Proliferator Signaling Pathways by Thyroid Hormone Receptor

Miyamoto¹,

Kaneko²,

Kakizawa

et al. 1997

Journal of Biological Chemistry

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“…The strong hybridization signal observed in day-20 and neonatal rat kidneys does not completely agree with the low amount of TGFα mRNA found in neonatal rat kidney extracts by other authors [15]: they defined their observation as unexpected and suggested that the reason for the low TGFα mRNA level they found might be ascribed to the mRNA instability.…”

Section: Discussionmentioning

confidence: 43%

“…More recent studies demonstrated that organ cultures of gestational day-13 rat metanephros produce TGFα in vitro, thus suggesting the organogenetic role of the metanephric-derived TGFα [7]. Further experiments carried out in vivo by North et al [15]reported that only small amounts of TGFα mRNA could be extracted from neonatal rat kidneys. In conclusion the presence of this growth factor, necessary for metanephric development, and particularly its related mRNA is still not well documented throughout the sequential stages of renal organogenesis and, although fragmentary results on this matter have been published for rodent embryos, no detailed data are available for the in situ localization of TGFα transcripts in human renal primordia.…”

Section: Discussionmentioning

confidence: 99%

TGF-Alpha mRNA Expression in Renal Organogenesis: A Study in Rat and Human Embryos

Bernardini

Mattii²,

Bianchi³

et al. 2001

Nephron Exp Nephrol

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The peptides belonging to the epidermal growth factor (EGF) family play a significant role in kidney development by binding the EGF receptor. Transforming growth factor-α (TGFα), a member of this family, is thought to be the fetal ligand of the EGF receptor. The present study aims to localize the TGFα transcripts in rat and human embryonic kidneys using a nonradioactive in situ hybridization method on paraffin-embedded embryonic samples. The results obtained in this study, beside demonstrating the usefulness of the nonradioactive technique for the detection of TGFα mRNA in paraffin sections, allowed TGFα-producing cells to be seen in developing kidneys. TGFα mRNA and its respective peptide were found in the primitive mesonephric structures and within metanephric blastema and ureteric bud cells. The presence of the TGFα gene transcript in the developing rat and human kidney suggests that the TGFα peptide is of embryonic origin and that it may contribute to renal organogenetic processes together with other growth factors.

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“…T 4 has been shown to augment the levels of EGF mRNA as well as EGF immunoreactivity in neonatal rodent kidneys [7, 17]. Thyroid hormone was also found to upregulate gene expression, synthesis, and release of pro-EGF in adult rat kidneys [18].…”

Section: Discussionmentioning

confidence: 99%

“…Several studies [3, 4, 5, 6] showed evidence of renal origin of urinary EGF in human neonates, developmental patterns of urinary EGF in premature infants, and decreased urinary EGF excretions in neonates with intrauterine growth retardation. In animal experiments, thyroid hormone can enhance renal EGF synthesis and thus increase urinary EGF excretion [7, 8, 9]. The urinary EGF level is high in neonates with hyperthyroidism, whereas it is low in those with hypothyroidism [10].…”

Section: Introductionmentioning

confidence: 99%

Correlation between Urinary Epidermal Growth Factor Excretion and Serum Thyroid Hormone in Premature and Term Neonates

Tsau¹,

Teng²,

Chen³

1998

Nephron

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Eighty neonates, including 14 full-term, 31 premature, 27 twin or triplet, 6 small-for-gestational-age, and 2 infants with hyperthyroidism, were evaluated. The urinary epidermal growth factor/creatinine ratio (EGF/Cr) on the 1st postnatal day was not statistically different among full-term, premature, multiple-pregnancy, and small-for-gestational-age infants (F = 1.06, p = 0.6). There was no difference in urinary EGF/Cr between the 1st postnatal day and the 7th day (p = 0.4 by paired t test). The urinary EGF/Cr was not correlated with the serum thyroid-stimulating hormone level (r = –0.162, n = 60, p = 0.21), but showed a positive correlation with serum total T₃ (r = 0.526, n = 60, p < 0.001) and with serum total T₄ (r = 0.460, n = 60, p < 0.001). The correlation between urinary EGF/Cr and serum free T₄ was even much better (r = 0.727, n = 25, p < 0.001). These results implicate that thyroid hormone may play a role in regulating urinary EGF excretion.

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Ontogeny of Epidermal Growth Factor, Transforming Growth Factor-α, Epidermal Growth Factor Receptor, and Thyroid Hormone Receptor RNA Levels in Rat Kidney and Changes in Those Levels Induced by Early Thyroxine Treatment

Cited by 16 publications

References 16 publications

Inhibition of Peroxisome Proliferator Signaling Pathways by Thyroid Hormone Receptor

Inhibition of Peroxisome Proliferator Signaling Pathways by Thyroid Hormone Receptor

TGF-Alpha mRNA Expression in Renal Organogenesis: A Study in Rat and Human Embryos

Correlation between Urinary Epidermal Growth Factor Excretion and Serum Thyroid Hormone in Premature and Term Neonates

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