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Добірка наукової літератури з теми "Distal nephron differentiation"
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Статті в журналах з теми "Distal nephron differentiation"
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El-Dahr, Samir S., Susana Dipp, Igor V. Yosipiv, and Luis A. Carbini. "Activation of kininogen expression during distal nephron differentiation." American Journal of Physiology-Renal Physiology 275, no. 1 (July 1, 1998): F173—F182. http://dx.doi.org/10.1152/ajprenal.1998.275.1.f173.
Повний текст джерелаАнотація:
Previous studies have shown that the epithelial precursors of the connecting tubule and collecting duct express tissue kallikrein and bradykinin B2 receptors, respectively, suggesting the presence of a local kinin-producing/responsive system in the maturing distal nephron. However, evidence for the existence of kininogen in the developing nephron is still lacking. This study examined the spatiotemporal relationships between segmental nephron differentiation and the ontogeny of kininogen and kinins in the rat. Kininogen immunoreactivity is detectable in the metanephros as early as embryonic day 15. In the nephrogenic zone, the terminal ureteric bud branches are the main kinin-expressing segments. Kininogen is also observed in the stromal mesenchyme. In contrast, proximal ureteric bud branches, metanephrogenic mesenchyme, and pretubular aggregates express little or no kininogen. After completion of nephrogenesis, kininogen distribution assumes its classic “adult” pattern in the collecting ducts. Peak kininogen mRNA and protein expression occur perinatally, corresponding to the period of active nephrogenesis in the rat, and declines gradually thereafter. Estimations made by RT-PCR, Western blotting, and radioimmunoassays indicate that renal kininogen mRNA and protein levels are at least 20-fold higher in newborn than adult rats. Likewise, immunoreactive tissue kinin levels are 2.3-fold higher in newborn than adult kidneys ( P < 0.05). In summary, the present study demonstrates the activation of kininogen gene expression and kinin production in the developing kidney. The terminal ureteric bud branches and their epithelial derivatives are the principal kinin-producing segments in the maturing nephron. The results suggest an autocrine/paracrine role for the kallikrein-kinin system in distal nephron maturation.
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Chambers, Brooke E., Eleanor G. Clark, Allison E. Gatz, and Rebecca A. Wingert. "Kctd15 regulates nephron segment development by repressing Tfap2a activity." Development 147, no. 23 (October 7, 2020): dev191973. http://dx.doi.org/10.1242/dev.191973.
Повний текст джерелаАнотація:
ABSTRACTA functional vertebrate kidney relies on structural units called nephrons, which are epithelial tubules with a sequence of segments each expressing a distinct repertoire of solute transporters. The transcriptiona`l codes driving regional specification, solute transporter program activation and terminal differentiation of segment populations remain poorly understood. Here, we demonstrate that the KCTD15 paralogs kctd15a and kctd15b function in concert to restrict distal early (DE)/thick ascending limb (TAL) segment lineage assignment in the developing zebrafish pronephros by repressing Tfap2a activity. During renal ontogeny, expression of these factors colocalized with tfap2a in distal tubule precursors. kctd15a/b loss primed nephron cells to adopt distal fates by driving slc12a1, kcnj1a.1 and stc1 expression. These phenotypes were the result of Tfap2a hyperactivity, where kctd15a/b-deficient embryos exhibited increased abundance of this transcription factor. Interestingly, tfap2a reciprocally promoted kctd15a and kctd15b transcription, unveiling a circuit of autoregulation operating in nephron progenitors. Concomitant kctd15b knockdown with tfap2a overexpression further expanded the DE population. Our study reveals that a transcription factor-repressor feedback module employs tight regulation of Tfap2a and Kctd15 kinetics to control nephron segment fate choice and differentiation during kidney development.
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Parwani, Anil V., Aliya N. Husain, Jonathan I. Epstein, J. Bruce Beckwith, and Pedram Argani. "Low-grade myxoid renal epithelial neoplasms with distal nephron differentiation." Human Pathology 32, no. 5 (May 2001): 506–12. http://dx.doi.org/10.1053/hupa.2001.24320.
Повний текст джерела
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MATSUDA, Kazuya, Yousuke KOUSAKA, Natsuko NAGAMINE, Nobuo TSUNODA, and Hiroyuki TANIYAMA. "Papillary Renal Adenoma of Distal Nephron Differentiation in a Horse." Journal of Veterinary Medical Science 69, no. 7 (2007): 763–65. http://dx.doi.org/10.1292/jvms.69.763.
Повний текст джерела
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Schmitt, Roland, David H. Ellison, Nicolette Farman, Bernard C. Rossier, Robert F. Reilly, W. Brian Reeves, Ilse Oberbäumer, Rosemarie Tapp, and Sebastian Bachmann. "Developmental expression of sodium entry pathways in rat nephron." American Journal of Physiology-Renal Physiology 276, no. 3 (March 1, 1999): F367—F381. http://dx.doi.org/10.1152/ajprenal.1999.276.3.f367.
Повний текст джерелаАнотація:
During the past several years, sites of expression of ion transport proteins in tubules from adult kidneys have been described and correlated with functional properties. Less information is available concerning sites of expression during tubule morphogenesis, although such expression patterns may be crucial to renal development. In the current studies, patterns of renal axial differentiation were defined by mapping the expression of sodium transport pathways during nephrogenesis in the rat. Combined in situ hybridization and immunohistochemistry were used to localize the Na-Pi cotransporter type 2 (NaPi2), the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), the thiazide-sensitive Na-Cl cotransporter (NCC), the Na/Ca exchanger (NaCa), the epithelial sodium channel (rENaC), and 11β-hydroxysteroid dehydrogenase (11HSD). The onset of expression of these proteins began in post-S-shape stages. NKCC2 was initially expressed at the macula densa region and later extended into the nascent ascending limb of the loop of Henle (TAL), whereas differentiation of the proximal tubular part of the loop of Henle showed a comparatively retarded onset when probed for NaPi2. The NCC was initially found at the distal end of the nascent distal convoluted tubule (DCT) and later extended toward the junction with the TAL. After a period of changing proportions, subsegmentation of the DCT into a proximal part expressing NCC alone and a distal part expressing NCC together with NaCa was evident. Strong coexpression of rENaC and 11HSD was observed in early nascent connecting tubule (CNT) and collecting ducts and later also in the distal portion of the DCT. Ontogeny of the expression of NCC, NaCa, 11HSD, and rENaC in the late distal convolutions indicates a heterogenous origin of the CNT. These data present a detailed analysis of the relations between the anatomic differentiation of the developing renal tubule and the expression of tubular transport proteins.
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Davis, I. D., T. W. LeBien, B. J. Lindman, and J. L. Platt. "Biochemical and histochemical characterization of a murine tubular antigen." Journal of the American Society of Nephrology 1, no. 10 (April 1991): 1153–61. http://dx.doi.org/10.1681/asn.v1101153.
Повний текст джерелаАнотація:
Cellular components of the developing fetal nephron express certain cell surface antigens at discrete stages of nephron development. To further evaluate the expression of antigens by tubular epithelium, a rat monoclonal antibody (BL26) was developed against murine fetal kidney. BL26 identified a differentiation antigen expressed by epithelial cells of the ureteric bud and late S-body in developing nephrons and by endothelium, mesangium, and distal tubular epithelium in mature nephrons. The polypeptide identified by BL26 was shown to be synthesized by fetal kidney and renal adenocarcinoma cells. The polypeptide contained no detectable carbohydrate modifications but was found in two isoforms, an acylated (26,000-Da) form and a nonacylated (24,000-Da) form. The murine antigen recognized by BL26 and the human CD9 moiety, an acylated polypeptide with a tissue distribution similar to that of the BL26 antigen, comigrated in polyacrylamide gels. We speculate that expression of the BL26 antigen and CD9 reflects processes relating to the activation of epithelial cells.
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Marneros, Alexander G. "AP-2β/KCTD1 Control Distal Nephron Differentiation and Protect against Renal Fibrosis". Developmental Cell 54, № 3 (серпень 2020): 348–66. http://dx.doi.org/10.1016/j.devcel.2020.05.026.
Повний текст джерела
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Wesselman, Hannah M., Allison E. Gatz, Mairead R. Pfaff, Liana Arceri, and Rebecca A. Wingert. "Estrogen Signaling Influences Nephron Segmentation of the Zebrafish Embryonic Kidney." Cells 12, no. 4 (February 20, 2023): 666. http://dx.doi.org/10.3390/cells12040666.
Повний текст джерелаАнотація:
Despite significant advances in understanding nephron segment patterning, many questions remain about the underlying genes and signaling pathways that orchestrate renal progenitor cell fate choices and regulate differentiation. In an effort to identify elusive regulators of nephron segmentation, our lab conducted a high-throughput drug screen using a bioactive chemical library and developing zebrafish, which are a conserved vertebrate model and particularly conducive to large-scale screening approaches. 17β-estradiol (E2), which is the dominant form of estrogen in vertebrates, was a particularly interesting hit from this screen. E2 has been extensively studied in the context of gonad development, but roles for E2 in nephron development were unknown. Here, we report that exogenous estrogen treatments affect distal tubule composition, namely, causing an increase in the distal early segment and a decrease in the neighboring distal late. These changes were noted early in development but were not due to changes in cell dynamics. Interestingly, exposure to the xenoestrogens ethinylestradiol and genistein yielded the same changes in distal segments. Further, upon treatment with an estrogen receptor 2 (Esr2) antagonist, PHTPP, we observed the opposite phenotypes. Similarly, genetic deficiency of the Esr2 analog, esr2b, revealed phenotypes consistent with that of PHTPP treatment. Inhibition of E2 signaling also resulted in decreased expression of essential distal transcription factors, irx3b and its target irx1a. These data suggest that estrogenic compounds are essential for distal segment fate during nephrogenesis in the zebrafish pronephros and expand our fundamental understanding of hormone function during kidney organogenesis.
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Wolf, D. C., H. E. Whiteley, and J. I. Everitt. "Preneoplastic and Neoplastic Lesions of Rat Hereditary Renal Cell Tumors Express Markers of Proximal and Distal Nephron." Veterinary Pathology 32, no. 4 (July 1995): 379–86. http://dx.doi.org/10.1177/030098589503200406.
Повний текст джерелаАнотація:
Long-Evans (Eker) rats carry a mutation that predisposes them to develop spontaneous renal cell tumors of two morphologic patterns: solid chromophilic masses or cystic lesions lined by eosinophilic cells. Previous studies have suggested that these tumors arise from the proximal tubules. In the present study, lectin-binding characteristics and cytokeratin expression of various stages of hereditary rat renal epithelial neoplasia were examined to localize the portion of the nephron from which tumors arise. Lectin-binding histochemistry has been used as a marker of cell surface glycoprotein expression, thought to be important in the differentiation of benign from malignant epithelial lesions and in the determination of their cell of origin. The presence or absence of keratin intermediate filaments in the rat nephron has been used to identify nephron segments. The polyclonal antibody to high- and low-molecular-weight cytokeratin stained the cells of the collecting ducts but not the proximal or distal tubules. Binding to the proximal tubules by the lectins Conavalia ensiformis (Con A), Dolichas biflorus, Ricinus communis (RCA-1), and Triticum vulgare and to the distal tubules by Con A, RCA-1, Arachis hypogaea (PNA) with and without neuraminidase, and the antibody for cytokeratins was demonstrated. The lectin binding and cytokeratin staining patterns of rat hereditary renal cell carcinoma, adenoma and the preneoplastic lesions of atypical tubules and hyperplasias suggest that cystic adenomas arise from the distal nephron, principally the collecting duct, whereas the solid atypical tubules, hyperplasias, and adenomas arise from the proximal nephron, principally the proximal tubule.
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Li, Jun, Jinshu Xu, Huihui Jiang, Ting Zhang, Aarthi Ramakrishnan, Li Shen, and Pin-Xian Xu. "Chromatin Remodelers Interact with Eya1 and Six2 to Target Enhancers to Control Nephron Progenitor Cell Maintenance." Journal of the American Society of Nephrology 32, no. 11 (October 29, 2021): 2815–33. http://dx.doi.org/10.1681/asn.2021040525.
Повний текст джерелаАнотація:
BackgroundEya1 is a critical regulator of nephron progenitor cell specification and interacts with Six2 to promote NPC self-renewal. Haploinsufficiency of these genes causes kidney hypoplasia. However, how the Eya1-centered network operates remains unknown.MethodsWe engineered a 2×HA-3×Flag-Eya1 knock-in mouse line and performed coimmunoprecipitation with anti-HA or -Flag to precipitate the multitagged-Eya1 and its associated proteins. Loss-of-function, transcriptome profiling, and genome-wide binding analyses for Eya1's interacting chromatin-remodeling ATPase Brg1 were carried out. We assayed the activity of the cis-regulatory elements co-occupied by Brg1/Six2 in vivo.ResultsEya1 and Six2 interact with the Brg1-based SWI/SNF complex during kidney development. Knockout of Brg1 results in failure of metanephric mesenchyme formation and depletion of nephron progenitors, which has been linked to loss of Eya1 expression. Transcriptional profiling shows conspicuous downregulation of important regulators for nephrogenesis in Brg1-deficient cells, including Lin28, Pbx1, and Dchs1-Fat4 signaling, but upregulation of podocyte lineage, oncogenic, and cell death–inducing genes, many of which Brg1 targets. Genome-wide binding analysis identifies Brg1 occupancy to a distal enhancer of Eya1 that drives nephron progenitor–specific expression. We demonstrate that Brg1 enrichment to two distal intronic enhancers of Pbx1 and a proximal promoter region of Mycn requires Six2 activity and that these Brg1/Six2-bound enhancers govern nephron progenitor–specific expression in response to Six2 activity.ConclusionsOur results reveal an essential role for Brg1, its downstream pathways, and its interaction with Eya1-Six2 in mediating the fine balance among the self-renewal, differentiation, and survival of nephron progenitors.
Дисертації з теми "Distal nephron differentiation"
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BRUNELLI, Matteo. "Combining interphase and metaphase analyses in the differential diagnosis among renal cell neoplasms with distal nephron differentiation." Doctoral thesis, 2008. http://hdl.handle.net/11562/337610.
Повний текст джерелаАнотація:
non disponibileCytogenetic analysis usually reveals low number of chromosomes 1, 2, 6, 10 and 17 in chromophobe renal cell carcinoma and a normal numerical complement of chromosomes in renal oncocytoma. However, different chromosomal patterns have been rarely reported in both renal cell neoplasms. We investigated 23 renal cell neoplasms (11 chromophobe renal cell carcinomas, 12 renal oncocytomas) by metaphase karyotyping and interphase FISH for chromosomes 1, 2, 6, 10 and 17 and flow cytometric analyses on tissue sections. FISH showed losses of two or more chromosomes in 10 chromophobe renal cell carcinomas (91%) and gains of multiple chromosomes in one (9%). Six (50%) renal oncocytomas were totally disomic, five (42%) showed one chromosomal loss (chromosome 1 in 3 cases), one case (8%) two losses. Among 9 chromophobe renal cell carcinomas with available istograms 6 (67%) showed aneuploid stemlines whereas the three remaining and 8/9 (89%) renal oncocytomas were diploid. Karyotypically, 3 chromophobe renal cell carcinomas (33%) were hypodiploid, 3 (33%) were polydiploid, one (11%) was diploid and 4 (36%) failed to grow. Nine out of 12 (75%) renal oncocytomas were diploid, one showed -Y (8%), one 47,XX,+7 (8%), one multiple different clones (9%). All chromophobe renal carcinomas which failed to grow and 2/3 (75%) showing gains by metaphase analyses displayed multiple chromosomal losses by FISH. Eight renal oncocytomas with normal DNA content and those three with additional chromosomal abnormalities (91%) by karyotyping showed normal complement of chromosomes by FISH. Conclusion: 1) chromophobe renal carcinomas usually display multiple chromosomal losses by FISH analysis in spite of a different spectrum found by karyotyping and flow cytometric analyses; 2) chromophobe renal carcinomas that fail to grow in culture are characterized by chromosomal losses in FISH; 3) renal oncocytomas usually show a normal numerical complement of chromosomes by both interphase and metaphase analyses.
Книги з теми "Distal nephron differentiation"
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Winyard, Paul. Human kidney development. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0343.
Повний текст джерелаАнотація:
The kidneys perform diverse functions including excretion of nitrogenous waste products, homeostasis of water, electrolytes and acid–base balance, and hormone secretion. The simplest functional unit within the kidneys is the nephron, which consists of specialized segments from glomerulus, through proximal tubule, loop of Henle, and distal tubule. Human nephrogenesis starts with two stages of transient kidneys, termed the pronephros and mesonephros, and ends with development of a permanent organ from the metanephros on each side. The latter consists of just a few hundred cells when it is formed in the fifth week of pregnancy but progresses to a nephron endowment of between 0.6 to 1.3 million by the time nephrogenesis is completed at 32–36 weeks of gestation. Key events during this process include outgrowth of the epithelial ureteric bud from the mesonephric duct, interactions between the bud and the metanephric blastema (a specific region of mesenchyme) that cause the bud to branch and mesenchyme to condense, epithelialization of the mesenchyme to form proximal parts of the nephron, and differentiation of segment specific cells. Molecular control of these events is being unpicked with data from human genetic syndromes and animal models, and this chapter highlights several of the most important factors/systems involved. Increased understanding of development is not just relevant to congenital kidney malformations, but may also be important in designing rational therapies for diseases of the mature kidney where recapitulation of developmental pathways is common.