scholarly journals Papillary Renal Adenoma of Distal Nephron Differentiation in a Horse

2007 ◽  
Vol 69 (7) ◽  
pp. 763-765 ◽  
Author(s):  
Kazuya MATSUDA ◽  
Yousuke KOUSAKA ◽  
Natsuko NAGAMINE ◽  
Nobuo TSUNODA ◽  
Hiroyuki TANIYAMA
Keyword(s):  
Distal Nephron ◽  
Nephron Differentiation

Low-grade myxoid renal epithelial neoplasms with distal nephron differentiation

2001 ◽  
Vol 32 (5) ◽  
pp. 506-512 ◽  
Author(s):  
Anil V. Parwani ◽  
Aliya N. Husain ◽  
Jonathan I. Epstein ◽  
J.Bruce Beckwith ◽  
Pedram Argani
Keyword(s):  
Low Grade ◽  
Distal Nephron ◽  
Nephron Differentiation ◽  
Epithelial Neoplasms

Activation of kininogen expression during distal nephron differentiation

1998 ◽  
Vol 275 (1) ◽  
pp. F173-F182 ◽  
Author(s):  
Samir S. El-Dahr ◽  
Susana Dipp ◽  
Igor V. Yosipiv ◽  
Luis A. Carbini
Keyword(s):  
Collecting Duct ◽  
Distal Nephron ◽  
Ureteric Bud ◽  
Adult Rats ◽  
Kinin System ◽  
Protein Levels ◽  
Mrna And Protein Expression ◽  
Nephron Differentiation ◽  
Developing Kidney ◽  
Kallikrein Kinin System

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.

scholarly journals Immunohistochemical localization of calbindin-D28k in the kidney and cerebellum of the porcupines (Hystrix cristata)

2012 ◽  
Vol 48 (No. 12) ◽  
pp. 369-372
Author(s):  
S. Timurkaan ◽  
A. Aydin ◽  
M. Kaban
Keyword(s):  
Purkinje Cells ◽  
Immunohistochemical Localization ◽  
Regulatory Mechanisms ◽  
Distal Nephron ◽  
Intracellular Protein ◽  
High Affinity ◽  
Hystrix Cristata ◽  
Calbindin D28k ◽  
Convoluted Tubules

The localization of calbindin in the kidney and cerebellum of Hystrix cristata was investigated immu&shy;nohistochemically using an antiserum against the 28k Da calbindin of chicken duodenum. Calbindin-D28k is an intracellular protein with a high affinity for calcium. This protein is exclusively localized in the distal convoluted tubules of the kidney and in Purkinje cells of the cerebellum. Functionaly, calbindin-D28k is supposed to be involved in the regulation of the reabsorption of calcium in the distal nephron, though the exact regulatory mechanisms are not yet known.

scholarly journals With-No-Lysine Kinase 1 (WNK1) Augments TRPV4 Function in the Aldosterone-Sensitive Distal Nephron

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1482
Author(s):  
Viktor N. Tomilin ◽  
Kyrylo Pyrshev ◽  
Naghmeh Hassanzadeh Khayyat ◽  
Oleg Zaika ◽  
Oleh Pochynyuk
Keyword(s):  
Collecting Duct ◽  
Chinese Hamster ◽  
Dominant Negative ◽  
K Channel ◽  
Apical Plasma Membrane ◽  
Dependent Manner ◽  
Distal Nephron ◽  
Potassium Homeostasis ◽  
Wnk Kinases ◽  
K Secretion

Kidneys play a central role in regulation of potassium homeostasis and maintenance of plasma K+ levels within a narrow physiological range. With-no-lysine (WNK) kinases, specifically WNK1 and WNK4, have been recognized to regulate K+ balance, in part, by orchestrating maxi K+ channel (BK)-dependent K+ secretion in the aldosterone-sensitive distal nephron (ASDN), which includes the connecting tubule and collecting duct. We recently demonstrated that the Ca2+-permeable TRPV4 channel is essential for BK activation in the ASDN. Furthermore, high K+ diet increases TRPV4 activity and expression largely in an aldosterone-dependent manner. In the current study, we aimed to test whether WNK kinases contribute to regulation of TRPV4 activity and its stimulation by aldosterone. Systemic inhibition of WNK with WNK463 (1 mg/kgBW for 3 days) markedly decreased TRPV4-dependent Ca2+ influx in freshly isolated split-opened collecting ducts. Aldosterone greatly increased TRPV4 activity and expression in cultured mpkCCDc14 cells and this effect was abolished in the presence of WNK463. Selective inhibition of WNK1 with WNK-in-11 (400 nM, 24 h) recapitulated the effects of WNK463 on TRPV4-dependent Ca2+ influx. Interestingly, WNK-in-11 did not interfere with up-regulation of TRPV4 expression by aldosterone, but prevented translocation of the channel to the apical plasma membrane. Furthermore, co-expression of TRPV4 and WNK1 into Chinese hamster ovary (CHO) cells increased the macroscopic TRPV4-dependent cation currents. In contrast, over-expression of TRPV4 with a dominant negative WNK1 variant (K233M) decreased the whole-cell currents, suggesting both stimulatory and permissive roles of WNK1 in regulation of TRPV4 activity. Overall, we show that WNK1 is essential for setting functional TRPV4 expression in the ASDN at the baseline and in response to aldosterone. We propose that this new mechanism contributes to regulation of K+ secretion and, by extension, urinary K+ levels to maintain systemic potassium homeostasis.

scholarly journals Short-term nonpressor angiotensin II infusion stimulates sodium transporters in proximal tubule and distal nephron

2015 ◽  
Vol 3 (9) ◽  
pp. e12496 ◽  
Author(s):  
Mien T. X. Nguyen ◽  
Jiyang Han ◽  
Donna L. Ralph ◽  
Luciana C. Veiras ◽  
Alicia A. McDonough
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Distal Nephron ◽  
Short Term ◽  
Sodium Transporters

scholarly journals The ClC-K2 Chloride Channel Is Critical for Salt Handling in the Distal Nephron

2016 ◽  
Vol 28 (1) ◽  
pp. 209-217 ◽  
Author(s):  
J. Christopher Hennings ◽  
Olga Andrini ◽  
Nicolas Picard ◽  
Marc Paulais ◽  
Antje K. Huebner ◽  
...  
Keyword(s):  
Chloride Channel ◽  
Distal Nephron

Sulphated proteoglycan is required for collecting duct growth and branching but not nephron formation during kidney development

Development ◽  
1995 ◽  
Vol 121 (5) ◽  
pp. 1507-1517 ◽  
Author(s):  
J. Davies ◽  
M. Lyon ◽  
J. Gallagher ◽  
D. Garrod
Keyword(s):  
Kidney Development ◽  
Collecting Duct ◽  
Sodium Chlorate ◽  
Ureteric Bud ◽  
Nephron Differentiation ◽  
Bud Growth ◽  
Nephron Development ◽  
Sulphated Glycosaminoglycans ◽  
Sulphated Proteoglycan ◽  
Hepatocyte Growth

Kidney epithelia have separate origins; collecting ducts develop by ureteric bud growth and arborisation, nephrons by induced mesenchyme-epithelium transition. Both express sulphated glycosaminoglycans (GAGs) which are strikingly upregulated during nephron differentiation. However, sodium chlorate, an inhibitor of GAG sulphation, and the GAG-degrading enzymes heparitinase plus chondroitinase, did not prevent nephron development. In contrast, ureteric bud growth and branching were reversibly inhibited by the above reagents, the inhibition correlating quantitatively with sulphated GAG deprivation caused by a range of chlorate concentrations. Growth and branching could be independently restored during GAG deprivation by hepatocyte growth factor and phorbol-12-myristate acetate (PMA) respectively. Together these signalling effectors stimulated both branch initiation and growth. Thus growth and morphogenesis of ureteric bud involve distinct signalling pathways both regulated by GAGs.

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