scholarly journals Tissue- and developmental-stage-specific methylation in the two kidney promoters of the rat γ-glutamyl transpeptidase gene

1992 ◽  
Vol 287 (3) ◽  
pp. 691-694 ◽  
Author(s):  
J H Baik ◽  
S Siegrist ◽  
G Giuili ◽  
O Lahuna ◽  
F Bulle ◽  
...  

We have investigated, using DNA methylation patterning, the site-specific methylation of promoters I and II of the rat gamma-glutamyl transpeptidase gene. This analysis was done in fetal, newborn and adult rat kidney, in which promoters I and II are progressively active during development, as well as in rat liver, which never expresses mRNAs from these two promoters. During kidney development, a progressive demethylation occurs in the promoter I and II region, specially at the level of the most proximal MspI site of promoter II. A progressive reorganization of the methylated sites within the 5′ end of the gene also occurs during liver development.

1984 ◽  
Vol 22 (1) ◽  
pp. 31-39 ◽  
Author(s):  
C. Lafarge-Frayssinet ◽  
S. Estrade ◽  
B. Rosa-Loridon ◽  
C. Frayssinet ◽  
R. Cassingena

1986 ◽  
Vol 238 (3) ◽  
pp. 913-917 ◽  
Author(s):  
J A Green ◽  
N D Cook ◽  
M M Manson

Monoclonal antibodies have been raised against rat kidney gamma-glutamyl transpeptidase (GGT). All five antibodies immunoprecipitate enzyme activity from solubilized kidney brush-border membranes, but not from hepatocellular carcinoma membranes. Three of the antibodies react immunohistochemically with brush-border membranes in sections of adult rat kidney, but none of the antibodies cross-react with sections of guinea-pig, mouse or marmoset kidney or with untreated or carcinogen-treated rat liver. The antibodies do not recognize GGT in foetal-rat kidney and react poorly with kidney from 2-year-old rat. They do react with tubules trapped within mesenchymal kidney tumours induced by dimethylnitrosamine, but epithelial tumours, which are GGT-positive (although much less so than normal kidney), are not immunoreactive.


1997 ◽  
Vol 273 (3) ◽  
pp. F386-F395 ◽  
Author(s):  
M. E. Choi ◽  
A. Liu ◽  
B. J. Ballermann

Transforming growth factor-beta 1 (TGF-beta 1) is strongly expressed during embryogenesis and in sites undergoing intense development and morphogenesis. Two receptor serine/threonine kinases (types I and II) have been identified as signal-transducing TGF-beta receptors. This study was undertaken to further explore the role of the distinct TGF-beta receptors during kidney development. The species-specific sequence information for the two T beta R-I, namely, activin receptor-like kinase-5 (ALK-5) and Tsk7L, in the rat was sought. Two full-length T beta R-I cDNAs were cloned from a neonatal rat kidney and lung libraries, and sequencing revealed that they were the rat homologs of human ALK-5 and murine Tsk7L. Both types I and II TGF-beta receptors are expressed in the kidney as determined by Northern blot analysis. T beta R-II mRNA abundance was significantly greater in the neonatal rat kidney compared with the adult rat kidney. Similarly, ALK-5 mRNA was more highly expressed in the fetal and neonatal rat kidney than the adult rat kidney. In contrast, there was no significant difference in Tsk7L mRNA abundance among the fetal, neonatal, and adult rat kidney. Thus, based on these findings, both T beta R-II and ALK-5 are developmentally regulated in the kidney. Increased expression of T beta R-II and ALK-5 proteins in the developing kidney was confirmed by immunohistochemistry. Interestingly, the two TGF-beta receptors did not entirely colocalize, raising the intriguing possibility that other TGF-beta signaling receptors may be involved.


1999 ◽  
Vol 260 (3) ◽  
pp. 844-854 ◽  
Author(s):  
Evgenia Bluvshtein ◽  
George A. Glass ◽  
Gloria Volohonsky ◽  
Margalit Yaakubowitz ◽  
Ella Harness ◽  
...  

1998 ◽  
Vol 46 (9) ◽  
pp. 1025-1032 ◽  
Author(s):  
Pangala V. Bhat ◽  
Mieczyslaw Marcinkiewicz ◽  
Yuan Li ◽  
Sylvie Mader

We have recently characterized a cytosolic aldehyde dehydrogenase from rat kidney that functions as a retinal dehydrogenase (RALDH) and have cloned the corresponding gene. RALDH catalyzes the oxidation of retinal to retinoic acid, which regulates cell growth and differentiation by activating retinoic acid receptors. In situ hybridization demonstrates that RALDH mRNA expression is prominent in kidney in 2-day-old rats, is detected in lung and in epithelia of several tissues, but is not found in liver tissue. Retinal dehydrogenase activity peaks in kidney at Day 2 after birth and decreases gradually until adulthood, correlating well with RALDH expression. Weaker activity is also detectable in lungs but not in liver. Notably, distribution patterns of RALDH in kidney tissues are dramatically altered during postnatal development (P). From P0 to P6, hybridization is essentially concentrated within the marginal nephrogenic zone of the cortex. Expression progresses to deeper cortical layers from P12 to P16 and is intense in the medulla at P42, and focal expression is still detectable in the cortex. Immunocytochemical localization of RALDH in neonatal kidney shows staining mostly in cortical zone convoluted tubules and in adult rat shows staining in segments of distal and proximal tubules. These data suggest an important role for RALDH in modulating retinoic acid levels in different cell types during rat kidney development. The changing patterns of RALDH expression mirror stages of nephron formation in the developing rat kidney, strongly suggesting a central role for RALDH and thus for retinoids in controlling kidney development.


Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2819
Author(s):  
Nesrine Ebrahim ◽  
Omnia Badr ◽  
Mohamed Yousef ◽  
Amira Hassouna ◽  
Dina Sabry ◽  
...  

Background. Liver transplantation remains the only viable therapy for liver failure but has a severely restricted utility. Here, we aimed to decellularize rat livers to form acellular 3D bio-scaffolds suitable for seeding with induced pluripotent cells (iPSCs) as a tool to investigate the role of Wnt/β-catenin signaling in liver development and generation. Methods. Dissected rat livers were randomly divided into three groups: I (control); II (decellularized scaffolds) and III (recellularized scaffolds). Liver decellularization was established via an adapted perfusion procedure and assessed through the measurement of extracellular matrix (ECM) proteins and DNA content. Liver recellularization was assessed through histological examination and measurement of transcript levels of Wnt/β-catenin pathway, hepatogenesis, liver-specific microRNAs and growth factors essential for liver development. Adult rat liver decellularization was confirmed by the maintenance of ECM proteins and persistence of growth factors essential for liver regeneration. Results. iPSCs seeded rat decellularized livers displayed upregulated transcript expression of Wnt/β-catenin pathway-related, growth factors, and liver specification genes. Further, recellularized livers displayed restored liver-specific functions including albumin secretion and urea synthesis. Conclusion. This establishes proof-of-principle for the generation of three-dimensional liver organ scaffolds as grafts and functional re-establishment.


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