Early innervation of the metanephric kidney

Development ◽  
1988 ◽  
Vol 104 (4) ◽  
pp. 589-599 ◽  
Author(s):  
H. Sariola ◽  
K. Holm ◽  
S. Henke-Fahle
Keyword(s):  
Primary Cultures ◽  
Neuronal Cell ◽  
Similar Distribution ◽  
Renal Tubules ◽  
Experimental Conditions ◽  
Tissue Sections ◽  
Neuronal Cell Bodies ◽  
Metanephric Kidney ◽  
Kidney Morphogenesis

During kidney differentiation, the nephrogenic mesenchyme converts into renal tubules and the ureter bud branches to form the collecting system. Here we show that in the early undifferentiated kidney rudiment there is a third cell type present. In whole-mount preparations of cultured undifferentiated metanephric kidneys, neurones can be detected by immunohistochemical means with antibodies against the neurofilament triplet, 13AA8, and against neuronal cell surface gangliosides, Q211. Clusters of neuronal cell bodies can be seen in the mesenchyme close to the ureter bud. The terminal endings of neurites are found around the mesenchymal condensates that later become kidney tubules. A similar distribution of neurites can be revealed in tissue sections of kidney grafts growing in the chicken chorioallantoic membranes. In primary cultures of the ureter bud cells, neurones are constantly present. In another report, we have shown that, in experimental conditions, neurones are involved in regulation of kidney morphogenesis. The present results raise the possibility that neurones of the metanephric kidney may have this function in vivo as well.

scholarly journals Sevoflurane protects against renal ischemia and reperfusion injury in mice via the transforming growth factor-β1 pathway

2008 ◽  
Vol 295 (1) ◽  
pp. F128-F136 ◽  
Author(s):  
H. Thomas Lee ◽  
Sean W. C. Chen ◽  
Thomas C. Doetschman ◽  
Chuxia Deng ◽  
Vivette D. D'Agati ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Nuclear Translocation ◽  
Primary Cultures ◽  
Volatile Anesthetics ◽  
Proximal Tubules ◽  
Renal Ischemia ◽  
Renal Tubules ◽  
Renal Protection

We previously demonstrated that several clinically utilized volatile anesthetics including sevoflurane protected against renal ischemia-reperfusion (IR) injury by reducing necrosis and inflammation in vivo. We also demonstrated that volatile anesthetics produced direct anti-necrotic and anti-inflammatory effects in cultured renal tubules via mechanisms involving the externalization of phosphatidylserine and subsequent release of transforming growth factor (TGF)-β1. In this study, we tested the hypothesis that volatile anesthetic-mediated renal protection requires TGF-β1 and SMAD3 signaling in vivo. We subjected TGF-β1+/+, TGF-β1+/−, SMAD3+/+, or SMAD3−/− mice to renal IR under anesthesia with pentobarbital sodium or with sevoflurane. Although TGF-β1+/+ and SMAD3+/+ mice were significantly protected against renal IR injury under sevoflurane anesthesia with reduced necrosis and inflammation, TGF-β1+/− mice and SMAD3−/− mice were not protected against renal IR with sevoflurane. Furthermore, a neutralizing TGF-β1 antibody blocked renal protection with sevoflurane in TGF-β1+/+ mice. Sevoflurane caused nuclear translocation of SMAD3 and reduced the TNF-α-induced nuclear translocation of NF-κB in primary cultures of proximal tubules from TGF-β1+/+ but not in TGF-β1+/− mice. Finally, sevoflurane protected against necrosis induced with hydrogen peroxide in primary cultures of proximal tubules from TGF-β1+/+ mice or SMAD3+/+ mice but not in proximal tubules from TGF-β1+/− or SMAD3−/− mice. Therefore, we demonstrate in this study that sevoflurane-mediated renal protection in vivo requires the TGF-β1→SMAD3 signaling pathway.

scholarly journals SURFACE STRUCTURE OF ISOLATED NEURONS

1970 ◽  
Vol 47 (2) ◽  
pp. 319-331 ◽  
Author(s):  
Anders Hamberger ◽  
Hans-Arne Hansson ◽  
Johan Sjöstrand
Keyword(s):  
Electron Microscopy ◽  
Hypoglossal Nerve ◽  
Light And Electron Microscopy ◽  
Neuronal Cell ◽  
Spherical Particles ◽  
Hypoglossal Nucleus ◽  
Isolated Neurons ◽  
Tissue Sections ◽  
Neuronal Cell Bodies ◽  
Transmission Electron

Freehand, isolated neuronal perikarya from the hypoglossal nucleus of the rabbit have been examined with light-and electron-microscopy (transmission and scanning). The surface of the cell bodies was largely covered with spherical particles which were 0.5–2 µ in diameter. Transmission electron microscopy proved that the spherical particles were synaptic nerve terminals. Crush of the hypoglossal nerve which leads to chromatolysis and swelling of the neuronal cell bodies results in a conspicuous reduction in the number of terminals attached to the surface of hypoglossal neurons. This effect was observed both for isolated neurons and in tissue sections. The effect is considered in relation to earlier reported variations in the adherence of neuropil to isolated neuronal perikarya. The functional importance of nerve ending detachment in connection with nerve injury is discussed.

scholarly journals Antenatal betamethasone attenuates the angiotensin-(1–7)-Mas receptor-nitric oxide axis in isolated proximal tubule cells

2017 ◽  
Vol 312 (6) ◽  
pp. F1056-F1062 ◽  
Author(s):  
Yixin Su ◽  
Jianli Bi ◽  
Victor M. Pulgar ◽  
Mark C. Chappell ◽  
James C. Rose
Keyword(s):  
Nitric Oxide ◽  
Proximal Tubule ◽  
Cell Model ◽  
Primary Cultures ◽  
Specific Effect ◽  
Renal Tubules ◽  
Proximal Tubule Cells ◽  
Mas Receptor ◽  
Tubule Cells

We previously reported a sex-specific effect of antenatal treatment with betamethasone (Beta) on sodium (Na+) excretion in adult sheep whereby treated males but not females had an attenuated natriuretic response to angiotensin-(1–7) [Ang-(1–7)]. The present study determined the Na+ uptake and nitric oxide (NO) response to low-dose Ang-(1–7) (1 pM) in renal proximal tubule cells (RPTC) from adult male and female sheep antenatally exposed to Beta or vehicle. Data were expressed as percentage of basal uptake or area under the curve for Na+ or percentage of control for NO. Male Beta RPTC exhibited greater Na+ uptake than male vehicle cells (433 ± 28 vs. 330 ± 26%; P < 0.05); however, Beta exposure had no effect on Na+ uptake in the female cells (255 ± 16 vs. 255 ± 14%; P > 0.05). Ang-(1–7) significantly inhibited Na+ uptake in RPTC from vehicle male (214 ± 11%) and from both vehicle (190 ± 14%) and Beta (209 ± 11%) females but failed to attenuate Na+ uptake in Beta male cells. Beta exposure also abolished stimulation of NO by Ang-(1–7) in male but not female RPTC. Both the Na+ and NO responses to Ang-(1–7) were blocked by Mas receptor antagonist d-Ala7-Ang-(1–7). We conclude that the tubular Ang-(1–7)-Mas-NO pathway is attenuated in males and not females by antenatal Beta exposure. Moreover, since primary cultures of RPTC retain both the sex and Beta-induced phenotype of the adult kidney in vivo they appear to be an appropriate cell model to examine the effects of fetal programming on Na+ handling by the renal tubules.

scholarly journals Fate of tetanus toxin bound to the surface of primary neurons in culture: evidence for rapid internalization.

1985 ◽  
Vol 100 (5) ◽  
pp. 1499-1507 ◽  
Author(s):  
D R Critchley ◽  
P G Nelson ◽  
W H Habig ◽  
P H Fishman
Keyword(s):  
Cell Surface ◽  
Tetanus Toxin ◽  
Polyacrylamide Gel Electrophoresis ◽  
Primary Cultures ◽  
Protein A ◽  
Sodium Dodecyl ◽  
Neuronal Cell ◽  
Subcellular Compartment ◽  
Membrane Components

We examined the nature of the tetanus toxin receptor in primary cultures of mouse spinal cord by ligand blotting techniques. Membrane components were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transferred to nitrocellulose sheets, which were overlaid with 125I-labeled tetanus toxin. The toxin bound only to material at or near the dye front, which was lost when the cells were delipidated before electrophoresis. Gangliosides purified from the lipid extract were separated by thin-layer chromatography and the chromatogram was overlaid with 125I-toxin. The toxin bound to gangliosides corresponding to GD1b and GT1b. Similar results were obtained with brain membranes; thus, gangliosides rather than glycoproteins appear to be the toxin receptors both in vivo and in neuronal cell cultures. To follow the fate of tetanus toxin bound to cultured neurons, we developed an assay to measure cell-surface and internalized toxin. Cells were incubated with tetanus toxin at 0 degree C, washed, and sequentially exposed to antitoxin and 125I-labeled protein A. Using this assay, we found that much of the toxin initially bound to cell surface disappeared rapidly when the temperature was raised to 37 degrees C but not when the cells were kept at 0 degree C. Some of the toxin was internalized and could only be detected by our treating the cells with Triton X-100 before adding anti-toxin. Experiments with 125I-tetanus toxin showed that a substantial amount of the toxin bound at 0 degree C dissociated into the medium upon warming of the cells. Using immunofluorescence, we confirmed that some of the bound toxin was internalized within 15 min and accumulated in discrete structures. These structures did not appear to be lysosomes, as the cell-associated toxin had a long half-life and 90% of the radioactivity released into the medium was precipitated by trichloroacetic acid. The rapid internalization of tetanus toxin into a subcellular compartment where it escapes degradation may be important for its mechanism of action.

scholarly journals CYTOCHEMICAL LOCALIZATION OF BRAIN NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE (OXIDIZED)-DEPENDENT DEHYDROGENASES QUALITATIVE AND QUANTITATIVE DISTRIBUTIONS

1974 ◽  
Vol 22 (1) ◽  
pp. 7-19 ◽  
Author(s):  
K. L. SIMS ◽  
F. C. KAUFFMAN ◽  
E. C. JOHNSON ◽  
V. M. PICKEL
Keyword(s):  
Nervous System ◽  
Nicotinamide Adenine Dinucleotide ◽  
Molecular Layer ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Neuronal Cell ◽  
Nicotinamide Adenine ◽  
Experimental Conditions ◽  
Cytochemical Localization ◽  
Neuronal Cell Bodies ◽  
Neuronal Processes

This study compares the histochemical and microchemical localizations of nicotinamide adenine dinucleotide phosphate (reduced) and nicotinamide adenine dinucleotide (reduced) diaphorases and four nicotinamide adenine dinucleotide phosphate (oxidized)-dependent enzymes (glucose 6-phosphate, 6-phosphogluconate, malate and isocitrate dehydrogenases) in areas of rat metencephalon and spinal cord. For the four nicotinamide adenine dinucleotide phosphate (NADP) enzymes, the pattern of localization following use of a modified tetrazolium procedure was compared with quantitative data obtained by microdissection from the same areas in adjacent sections. Optimal experimental conditions for reaction pH, temperature, substrate, cofactor and divalent cation concentrations were used for both the quantitative analysis following microdissection and the histochemical tetrazolium procedure. Consecutive sections were also examined for isocitrate dehydrogenase (nicotinamide adenine dinucleotide (oxidized)) and nicotinamide adenine dinucleotide (reduced) diaphorase activities in addition to seriatim thionine reference sections. Our results indicate that, within the central nervous system, certain characteristic qualitative differences exist in the distribution of the nicotinamide adenine dinucleotide phosphate (oxidized)- and nicotinamide adenine dinucleotide (oxidized)-dependent dehydrogenase enzymes. Nicotinamide adenine, dinucleotide enzymes are visualized predominantly in neuronal cell bodies or neuropil consisting primarily of neuronal processes; in adjacent sections, NADP enzyme activities are visualized almost exclusively in glial elements with two important exceptions. The first is the cerebellar molecular layer where the results from both micro- and histochemical techniques indicate high levels of the NADP enzymes relative to other dehydrogenases and high activity relative to the levels of these NADP enzymes in other nervous system areas. The second exception occurs in those neuronal groups known to contain high levels of catecholamines; these data are the subject of a companion report.

On the Application of Cultured Neuronal Cell Lines in Neurotoxicological Studies: Implications of Acrylamide-induced Neurite Disintegration

1983 ◽  
Vol 11 (4) ◽  
pp. 194-203
Author(s):  
Elisabet Nyberg ◽  
Erik Walum
Keyword(s):  
Cell Line ◽  
Neuroblastoma Cell ◽  
Membrane Integrity ◽  
Neuronal Cell ◽  
Specific Effect ◽  
Glycolytic Enzyme ◽  
Neuroblastoma Cell Line ◽  
Experimental Conditions ◽  
Neuronal Cell Lines

Summary Cultures of the mouse neuroblastoma cell line C1300, clone N1E115 were exposed to acrylamide at 3.5 x 10-4M for 14 days (subacute situation) or at 2.8 x 10-3 M for 24 hr (acute situation). In the subacute situation the total uptake of 2-deoxy-D-glucose was stimulated. This could be explained by an increase in both the non-specific diffusion and the specific transport. The activity of the glycolytic enzyme, enolase (EC4.2.1.11), was unaffected by exposure to acrylamide, whereas the activity of glyceraldehyde-3-phosphate-dehydrogenase (EC1.2.1.12) was inhibited. Acrylamide had a marked stimulating effect on the respiratory activity of the cells, whereas the incorporation of tritiated leucine remained unchanged. Furthermore, membrane integrity was maintained throughout the acrylamide exposure as judged by an unchanged rate of 2-deoxy-D-glucose-6-phosphate efflux. Corresponding results were obtained in the acute situation. In N1E115 cultures and under the experimental conditions used in this work acrylamide caused neurite degeneration resembling distal axonopathy in vivo. It is suggested that these degenerative changes are not due to a general intoxication of the cells, but rather to a specific effect. Consequently, the N1E115 cell line might be useful in studies of chemically-induced axonopathies.

scholarly journals New oligodendrocytes exhibit more abundant and accurate myelin regeneration than those that survive demyelination

2020 ◽  
Author(s):  
Sarah A Neely ◽  
Jill M Williamson ◽  
Anna Klingseisen ◽  
Lida Zoupi ◽  
Jason J Early ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Neuronal Cell ◽  
Live Imaging ◽  
Therapeutic Strategies ◽  
Demyelinating Diseases ◽  
Neuronal Cell Bodies ◽  
The Central Nervous System

Regeneration of myelin (remyelination) in the central nervous system (CNS) has long been thought to be principally mediated by newly generated oligodendrocytes, a premise underpinning therapeutic strategies for demyelinating diseases, including multiple sclerosis (MS). Recent studies have indicated that oligodendrocytes that survive demyelination can also contribute to remyelination, including in MS, but it is unclear how remyelination by surviving oligodendrocytes compares to that of newly generated oligodendrocytes. Here we studied oligodendrocytes in MS, and also imaged remyelination in vivo by surviving and new oligodendrocytes using zebrafish. We define a previously unappreciated pathology in MS, myelination of neuronal cell bodies, which is recapitulated during remyelination by surviving oligodendrocytes in zebrafish. Live imaging also revealed that surviving oligodendrocytes make very few new sheaths, but can support sheath growth along axons. In comparison, newly made oligodendrocytes make abundant new sheaths, properly targeted to axons, and exhibit a much greater capacity for regeneration.

PCO2 in renal cortex

1990 ◽  
Vol 259 (2) ◽  
pp. F357-F365 ◽  
Author(s):  
M. De Mello Aires ◽  
M. J. Lopes ◽  
G. Malnic
Keyword(s):  
Renal Vein ◽  
Respiratory Acidosis ◽  
Renal Tubules ◽  
Buffer Solution ◽  
Systemic Blood ◽  
Experimental Conditions ◽  
High Pump ◽  
Ph Electrodes

In a number of recent investigations a renal cortical PCO2 higher than that of systemic blood was reported. We have studied this problem with the use of micro-Severinghaus electrodes based on antimony, H+ liquid ion exchange, and glass pH electrodes with an inner buffer solution containing 0.5 mg/ml carbonic anhydrase (CA). Measurements in renal cortical structures (renal tubules, star vessels, capillaries, and glomeruli in Munich-Wistar rats) were compared with determinations in renal vein or artery performed with the same electrode in sequence. No significant differences in PCO2 were found between cortical structures and renal vein in control rats, in metabolic alkalosis, respiratory acidosis and alkalosis, and after CA inhibition. Nevertheless, absolute PCO2 levels, which followed the PCO2 of systemic blood, were markedly different in these groups. Measurements of pH and PCO2 at the same tubule site were compatible with HCO3- determinations in tubule fluid in vitro (made with use of the Henderson-Hasselbalch equation) in control rats. When proximal tubules were pump-perfused in vivo with a solution containing 30 mM NaHCO3, measured PCO2 approached that of the perfusing solution at high pump rates, and approached the free-flow value as rates were reduced to zero, indicating that the CO2 generated in the lumen equilibrated rapidly across the epithelium. Reducing renal blood flow by aortic clamping reduced renal cortical PCO2. In conclusion, in a large number of experimental conditions renal cortical PCO2 was never higher than that measured in systemic blood.

scholarly journals APAF1 is a key transcriptional target for p53 in the regulation of neuronal cell death

2001 ◽  
Vol 155 (2) ◽  
pp. 207-216 ◽  
Author(s):  
Andre Fortin ◽  
Sean P. Cregan ◽  
Jason G. MacLaurin ◽  
Neena Kushwaha ◽  
Emma S. Hickman ◽  
...  
Keyword(s):  
Cell Death ◽  
Binding Sites ◽  
Primary Cultures ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Acute Injury ◽  
Mobility Shift ◽  
Transcriptional Target

p53 is a transcriptional activator which has been implicated as a key regulator of neuronal cell death after acute injury. We have shown previously that p53-mediated neuronal cell death involves a Bax-dependent activation of caspase 3; however, the transcriptional targets involved in the regulation of this process have not been identified. In the present study, we demonstrate that p53 directly upregulates Apaf1 transcription as a critical step in the induction of neuronal cell death. Using DNA microarray analysis of total RNA isolated from neurons undergoing p53-induced apoptosis a 5–6-fold upregulation of Apaf1 mRNA was detected. Induction of neuronal cell death by camptothecin, a DNA-damaging agent that functions through a p53-dependent mechanism, resulted in increased Apaf1 mRNA in p53-positive, but not p53-deficient neurons. In both in vitro and in vivo neuronal cell death processes of p53-induced cell death, Apaf1 protein levels were increased. We addressed whether p53 directly regulates Apaf1 transcription via the two p53 consensus binding sites in the Apaf1 promoter. Electrophoretic mobility shift assays demonstrated p53–DNA binding activity at both p53 consensus binding sequences in extracts obtained from neurons undergoing p53-induced cell death, but not in healthy control cultures or when p53 or the p53 binding sites were inactivated by mutation. In transient transfections in a neuronal cell line with p53 and Apaf1 promoter–luciferase constructs, p53 directly activated the Apaf1 promoter via both p53 sites. The importance of Apaf1 as a p53 target gene in neuronal cell death was evaluated by examining p53-induced apoptotic pathways in primary cultures of Apaf1-deficient neurons. Neurons treated with camptothecin were significantly protected in the absence of Apaf1 relative to those derived from wild-type littermates. Together, these results demonstrate that Apaf1 is a key transcriptional target for p53 that plays a pivotal role in the regulation of apoptosis after neuronal injury.

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