Developmental stages of Sphaerospora ohlmacheri (Whinery, 1893) n.comb. (Myxozoa: Myxosporea) in the renal tubules of bullfrog tadpoles, Rana catesbeiana, from Lake of Two Rivers, Algonquin Park, Ontario

1986 ◽  
Vol 64 (10) ◽  
pp. 2213-2217 ◽  
Author(s):  
Sherwin S. Desser ◽  
Jǐrí Lom ◽  
Iva Dyková

Pseudoplasmodia and mature spores of Sphaerospora ohlmacheri (Whinery, 1893) n.comb. were found in the renal tubules and in the space of the Bowman's capsule of 2nd-year tadpoles of the bullfrog, Rana catesbeiana. Fresh spores and the sporogenic stages of S. ohlmacheri from tissue imprints and histological sections are described and illustrated. Dystrophic changes of renal tubule cells characterized by degeneration associated with hyaline droplets often accompanied the presence of the parasite. Features of the genera Leptotheca, Wardia, and Sphaerospora are discussed.

1992 ◽  
Vol 263 (5) ◽  
pp. R1086-R1092 ◽  
Author(s):  
D. A. Terreros ◽  
H. Kanli

Osmoregulatory Ca2+ signaling in hypotonic solutions was studied with videometric techniques in 158 proximal renal tubules isolated from the teleost Carassius auratus. Absence of extracellular Ca2+, hypoxia (23 mmHg), or NaCN (3 mM) did not alter regulatory volume decreases (RVD). Nevertheless, decrements of intracellular Ca2+ via the A23187 ionophore or after intracellular Ca2+ chelation with indo-1/AM (5 microM) inhibited RVD. In tubules depleted of Ca2+, RVD could only be fully elicited when intracellular Ca2+ pulses were given within 1 min after hypotonic stimulation. While inhibition of Ca2+ release from the endoplasmic reticulum (ER) with 8-(diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8, 50 microM) blunted RVD, some of its effects could be reversed with the anion carrier tributyltin (1 microM). Dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP, 0.5 and 1.0 mM) and forskolin (0.25 mM) also impeded RVD; however, their effects could be partially reversed with the K+ ionophore gramicidin (0.5 microM). In conclusion, in Carassius auratus proximal renal tubule cells, RVD is activated by an intracellular Ca2+ signal that likely emanates from the ER and not from the extracellular media or the mitochondrial Ca2+ pool. Ca2+ activation of a cAMP-modulated osmoregulatory K+ channel appears to play an important role.


1965 ◽  
Vol 32 (1) ◽  
pp. 44-50
Author(s):  
Antti Paalanen

This study comprises some observations about the structure of the connective tissue of the basement membrane and interstitium in some normal, post-natal human kidneys. The basis of the basement membrane is mainly a reticular, homogeneous membrane that belongs uniformly to both Bowman's capsule and the wall of the renal tubule. Outside it in the capsule is a durable collagenic membrane whose development must be considered and evincement of functional adaptation under the pressure conditions of the cavity. In renal tubules there is no such well-defined outer membrane, but in them the basement membrane has in addition collagenic traits to some extent and is thus reticular-collagenic when examined as a whole. The renal tubules are surrounded by a dense, spiraling reticular network of fibres which attaches to the connective tissue of the interstitium where fibrocytes are scarce. The network extends all the way around the renal corpuscle. There is no elastic tissue at all in the basement membranes.


1995 ◽  
Vol 6 (2) ◽  
pp. 269-272
Author(s):  
J W Foreman ◽  
L L Benson ◽  
M Wellons ◽  
E D Avner ◽  
W Sweeney ◽  
...  

The cause of Fanconi syndrome in cystinosis is enigmatic. It has previously been shown that renal tubules could be loaded with cystine by incubating them with cystine dimethylester (CDE), mimicking the biochemical hallmark of cystinosis. Such tubules have impaired transport, decreased whole-cell O2 consumption, and substrate utilization. In this study, the metabolic disturbances in cystine-loaded renal tubule cells were further characterized. Isolated rat renal tubules were loaded with cystine by incubating them with 2 mM CDE for 10 min. This had no significant effect on total ATPase, Na(+)-K(+)-ATPase, or the ouabain-insensitive ATPase activity of renal tissue homogenates from these cystine-loaded tubules. Intracellular K was significantly lower in the cystine-loaded tubules (37 +/- 2 versus 47 +/- 3 nEq/mg; P < 0.008). Intracellular ATP was reduced by 39% in the cystine-loaded tubules (23.7 +/- 2.4 versus 38.1 +/- 3.3 nmol/mg of protein; P < 0.0025). CDE (2 mM) reduced isolated mitochondrial O2 consumption with glutamate as the substrate by 66% (4.7 +/- 0.7 versus 13.9 +/- 0.8 nm/min per mg of protein, P < 0.001) but had no effect on mitochondrial O2 consumption with succinate as the substrate. It was speculated that the impaired transport from cystine loading with CDE is secondary to a decrease in energy generation.


1964 ◽  
Vol 207 (5) ◽  
pp. 983-988 ◽  
Author(s):  
Maurice B. Burg ◽  
Jack Orloff

In order to determine the capacity of renal cells to transport actively electrolytes at 0 C, separated rabbit renal tubules were incubated at this temperature and the effects of various inhibitors on Na, K, Cl, and water content and the fluxes of Na and K were measured. In contrast to previous studies with kidney slices, these observations indicate that cell K is completely exchangeable at 0 C and significant active transport persists. Thus, at 0 C as at higher temperatures, anoxia, strophanthidin, 2,4-DNP, and cyanide reduce the transcellular concentration gradients for Na, K, and Cl and cause the tubules to swell. In the presence of strophanthidin, both influx and efflux of K are slowed. It is concluded that at 0 C, as at higher temperatures, active cation transport by renal tubule cells accounts for the maintenance of transcellular electrolyte concentration gradients and limits colloid osmotic swelling.


1998 ◽  
Vol 54 (4) ◽  
pp. 1139-1149 ◽  
Author(s):  
Ingeborg A. Hauser ◽  
Michael Koziolek ◽  
Ulrich Hopfer ◽  
Frank Thévenod

Development ◽  
1962 ◽  
Vol 10 (4) ◽  
pp. 465-470
Author(s):  
Charles L. Foote ◽  
Florence M. Foote

Earlier reports (Foote & Foote, 1958a, b, 1959) describe growth and maintenance in vitro of larval organs, particularly gonads, of Rana catesbeiana and Xenopus laevis. Immature germ cells of both testes and ovaries are well maintained in vitro, especially if the culture medium is supplemented with watersoluble sex-hormonal substances, although germ cells in process of maturation become necrotic. Recently some urogenital organs from the salamander, Pleurodeles waltlii, have been grown in vitro. Tissues and organs from this amphibian might prove to be more suitable for tissue and organ culture investigations than those of Anurans. Animals at three different ages were used in this study: recently hatched larvae, metamorphosing animals, and adults. To determine whether sex differentiation would occur in vitro, trunk portions of young larvae of Pleurodeles waltlii of developmental stages 37–38 (Gallien & Durocher, 1957) were placed in organ cultures.


1991 ◽  
Vol 260 (3) ◽  
pp. F420-F430 ◽  
Author(s):  
P. D. Wilson ◽  
A. C. Sherwood ◽  
K. Palla ◽  
J. Du ◽  
R. Watson ◽  
...  

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder in which renal tubules become enormously enlarged due to fluid accumulation. Na(+) -K(+) -ATPase was compared in normal and cystic regions of whole kidneys and in confluent primary cultures of microdissected renal tubule and cyst-lining epithelia. Immunostaining with antibodies directed against the Na(+) -K(+) -ATPase catalytic alpha-subunit was confined to apical, luminal plasma membranes of ADPKD epithelia, which was a complete reversal of the normal renal tubule polarized location in basolateral membranes. Mislocated Na(+) -K(+) -ATPase was shown to be functionally active, because identical intense apical staining was observed by use of a cytochemical assay. In addition, biochemical assays showed a significant increase in these ouabain-inhibitable Na(+) -K(+) -ATPase specific activity levels in ADPKD kidneys compared with age-matched normal kidneys. Specific binding of [3H] ouabain was not only increased but also confined to the apical membrane vesicles prepared from cystic regions of ADPKD kidneys compared with normal age-matched controls, in which binding was confined to basolateral membrane vesicles. Although steady-state levels of Na(+) -K(+) -ATPase alpha- and beta-subunit in mRNAs were increased somewhat in ADPKD kidneys, this alone was not sufficient to account for the observed activation. Confluent ADPKD epithelia grown on dual-chamber, permeable membrane supports also showed reversed polarity of 22NaCl vectorial transport, because this was from basal to apical media compartments. Because this transport could also be blocked by ouabain, this suggested apical Na(+) -K(+) -ATPase was responsible and implicated altered polarity of Na(+) -K(+) -ATPase and resultant Na+ secretion as a mechanism for cyst formation in ADPKD. Because no reversal of polarity of other basolateral or apical membrane proteins was detected, an intracellular sorting defect specific for Na(+) -K(+) -ATPase is proposed.


2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Shoujun Bai ◽  
Xiaoyan Xiong ◽  
Bo Tang ◽  
Tingting Ji ◽  
Xiaoying Li ◽  
...  

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. The association between epithelial-mesenchymal transition (EMT) and fibrosis is quite ascertained, but its link to eventual tubule dysfunction is missing. Here, we show that human microRNA- (hsa-miR-) 199b-3p protects renal tubules from diabetic-induced injury by repressing KDM6A, a histone lysine demethylase regulating E-cadherin expression. Lower E-cadherin expression is related to a higher level of KDM6A, while E-cadherin is promoted upon treatment with the KDM6A inhibitor GSK-J4 in both high glucose- (HG-) induced HK2 cells and the kidneys from streptozotocin- (STZ-) induced type 1 diabetic mice. However, overexpression or RNA silencing of E-cadherin fails to alter KDM6A expression. We also show that the upregulation of KDM6A is associated with the increased methylation level of the E-cadherin promoter. Then, the target prediction results and a dual-luciferase assay show that hsa-miR-199b-3p is a new miRNA that targets KDM6A. Overexpression of hsa-miR-199b-3p increases E-cadherin expression and prevents EMT through repressing KDM6A expression in HG-induced HK2 cells. In contrast, inhibitor-induced hsa-miR-199b-3p knockdown has opposite effects, as it decreases E-cadherin level and worsens EMT, accompanied by increased levels of KDM6A. Besides, Mir199b-knockout mice without mmu-miR-119b-3p expression exhibit more renal tubule dysfunction and more serious kidney tissue damage upon treatment with STZ. These results demonstrate that hsa-miR-199b-3p improves E-cadherin expression and prevents the progression of DN through targeting KDM6A. miR-199b-3p could be a future biomarker or target for the diagnosis or treatment of DN.


1989 ◽  
Vol 2 (7) ◽  
pp. 563-566 ◽  
Author(s):  
Maria-Luisa Melzi ◽  
Alejandro Bertorello ◽  
Yutaka Fukuda ◽  
Ingrid Muldin ◽  
Fabio Sereni ◽  
...  

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