Localization, synthetic regulation, and biology of renal atriopeptin-like prohormone

1992 ◽  
Vol 263 (3) ◽  
pp. F503-F509 ◽  
Author(s):  
D. Ritter ◽  
J. Chao ◽  
P. Needleman ◽  
E. Tetens ◽  
J. E. Greenwald
Keyword(s):  
Cell Cultures ◽  
Rat Kidney ◽  
Cortical Cell ◽  
Mouse Cell ◽  
Sprague Dawley ◽  
Adult Rat ◽  
Camp Generation ◽  
Synthetic Cell ◽  
Cortical Cell Cultures ◽  
Immunohistochemical Techniques

We recently demonstrated the synthesis and secretion of an atriopeptin (AP)-like prohormone in rat neonatal and adult cortical kidney cell cultures. However, these cultures contained proximal as well as distal tubular epithelial cells; thus characterization of the peptide synthetic cell was not possible. Also, by immunohistochemical techniques, we localized this AP-like prohormone to the distal cortical nephron in adult rat kidney. In this study, we examined further details of the kidney cortical cell type that expresses and secretes this AP-like peptide in adult renal cortical cell cultures, its regulation by adenylate cyclase via adenosine 3',5'-cyclic monophosphate (cAMP) generation, and its ability to stimulate guanylate cyclase. Tubular fragments were derived from cortical tissue of adult Sprague-Dawley rats and separated into four fractions on Percoll density gradient. Cell cultures generated from fraction 3 secreted 5- to 10-fold the amount of this renal peptide compared with fractions 2 and 4. Further cell culture characterization was performed by agonist-stimulated cAMP formation, kallikrein localization, and prostaglandin E2 formation. From these analyses, it was determined that tissue band 3 was enriched for distal cortical connecting tubules. To further evaluate whether mammalian distal nephron synthesizes an AP-like protein, we determined that two immortalized mouse cell lines, derived from either the distal convoluted tubule or cortical collecting tubule, synthesized a radiolabeled AP after being pulsed with [35S]-methionine.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals NMDA Receptor-Mediated Neuroprotective Effect of theScutellaria baicalensisGeorgi Extract on the Excitotoxic Neuronal Cell Death in Primary Rat Cortical Cell Cultures

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Jinsong Yang ◽  
Xiaohong Wu ◽  
Haogang Yu ◽  
Xinbiao Liao ◽  
Lisong Teng
Keyword(s):  
Cell Death ◽  
Nmda Receptor ◽  
Cell Cultures ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Cortical Cell ◽  
Neuronal Cell ◽  
Ethanol Extract ◽  
Phytochemical Analysis ◽  
Cortical Cell Cultures

The objective of the current research work was to evaluate the neuroprotective effect of the ethanol extract ofScutellaria baicalensis(S.B.) on the excitotoxic neuronal cell death in primary rat cortical cell cultures. The inhibitory effects of the extract were qualitatively and quantitatively estimated by phase-contrast microscopy and lactate dehydrogenase (LDH) assays. The extract exhibited a potent and dose-dependent inhibition of the glutamate-induced excitotoxicity in the culture media. Further, using radioligand binding assays, it was observed that the inhibitory effect of the extract was more potent and selective for the N-methyl-D-aspartate (NMDA) receptor-mediated toxicity. The S.B. ethanol extract competed with [3H] MDL 105,519 for the specific binding to the NMDA receptor glycine site with 50% inhibition occurring at 35.1 μg/mL. Further, NMDA receptor inactivation by the S.B. ethanol extract was concluded from the decreasing binding capability of [3H]MK-801 in the presence of the extract. Thus, S.B. extract exhibited neuroprotection against excitotoxic cell death, and this neuroprotection was mediated through the inhibition of NMDA receptor function by interacting with the glycine binding site of the NMDA receptor. Phytochemical analysis of the bioactive extract revealed the presence of six phytochemical constituents including baicalein, baicalin, wogonin, wogonoside, scutellarin, and Oroxylin A.

scholarly journals Ca2+-Mediated Activation of c-Jun N-Terminal Kinase and Nuclear Factor κB by NMDA in Cortical Cell Cultures

2002 ◽  
Vol 71 (4) ◽  
pp. 1390-1395 ◽  
Author(s):  
Hyuk Wan Ko ◽  
Kye-Yoon Park ◽  
Hansin Kim ◽  
Pyung-Lim Han ◽  
Youn Uck Kim ◽  
...  
Keyword(s):  
Cell Cultures ◽  
Cortical Cell ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Cortical Cell Cultures

Ontogeny of glycine transport in isolated rat renal tubules

1977 ◽  
Vol 233 (3) ◽  
pp. F241-F246
Author(s):  
K. S. Roth ◽  
S. M. Hwang ◽  
J. W. London ◽  
S. Segal
Keyword(s):  
Rat Kidney ◽  
Renal Tubules ◽  
Sprague Dawley ◽  
Entry Rate ◽  
Glycine Uptake ◽  
Adult Rat ◽  
High Affinity ◽  
Sprague Dawley Rats ◽  
Rate Kinetics ◽  
Isolated Renal Tubule

Isolated renal tubule preparations were made from newborn Sprague-Dawley rats and used to study initial entry rate kinetics of glycine. The results were compared to those obtained in the isolated tubule preparation from the adult rat kidney. While initial rates of glycine uptake were identical for newborn and adult tubules, significant differences in influx kinetics were demonstrated. Of the two apparent transport Km systems shown to be present in the newborn tubule, the high-affinity, low-capacity system accounts for about 40% of total glycine uptake at physiologic concentrations. The high-affinity, low-capacity system of the adult tissue accounts for about 10% of total uptake at the same concentration range. The data lend strength to the argument against the concept that the physiologic hyperglycinuria of the newborn rat is due to either impaired ability to concentrate glycine intracellularly or to absence of one or more transport mechanisms for glycine.

Oxygen or glucose deprivation-induced neuronal injury in cortical cell cultures is reduced by tetanus toxin

Neuron ◽  
1992 ◽  
Vol 8 (5) ◽  
pp. 967-973 ◽  
Author(s):  
H. Monyer ◽  
R.G. Giffard ◽  
D.M. Hartley ◽  
L.L. Dugan ◽  
M.P. Goldberg ◽  
...  
Keyword(s):  
Cell Cultures ◽  
Tetanus Toxin ◽  
Cortical Cell ◽  
Neuronal Injury ◽  
Glucose Deprivation ◽  
Cortical Cell Cultures

Neuroprotective MK801 is associated with nitric oxide synthase during hypoxia/reoxygenation in rat cortical cell cultures

2002 ◽  
Vol 84 (2) ◽  
pp. 367-376 ◽  
Author(s):  
Hsueh-Meei Huang ◽  
Chiung-Chyi Shen ◽  
Hsiu-Chung Ou ◽  
Jean-Yuan Yu ◽  
Huan-Lian Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cell Cultures ◽  
Cortical Cell ◽  
Cortical Cell Cultures ◽  
Oxide Synthase ◽  
Hypoxia Reoxygenation

Neuroprotective Effects of Propofol in a Model of Ischemic Cortical Cell Cultures

2003 ◽  
Vol 99 (2) ◽  
pp. 368-375 ◽  
Author(s):  
Lionel J. Velly ◽  
Benjamin A. Guillet ◽  
Frederique M. Masmejean ◽  
André L. Nieoullon ◽  
Nicolas J. Bruder ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Cell Cultures ◽  
Glutamate Uptake ◽  
Neuroprotective Effect ◽  
Glutamate Release ◽  
Cortical Cell ◽  
Neuroprotective Effects ◽  
Mk 801 ◽  
Lactate Dehydrogenase Release ◽  
Cortical Cell Cultures

Background During cerebral ischemia, excess of glutamate release and dysfunction of its high affinity transport induce an accumulation of extracellular glutamate, which plays an important role in neuronal death. The authors studied the relationship among propofol neuroprotection, glutamate extracellular concentrations, and glutamate transporter activity in a model of ischemic cortical cell cultures. Methods Thirteen-day-old primary cortical neuronal-glial cultures were exposed to a 90-min combined oxygen-glucose deprivation (OGD) in an anaerobic chamber, followed by reoxygenation. Propofol was added only during the OGD period, and its effect was compared to that of the N-methyl-d-aspartate receptor antagonist dizocilpine (MK-801). Twenty-four hours after the injury, cell death was quantified by lactate dehydrogenase release and cell viability by reduction of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). Extracellular concentrations of glutamate in culture supernatants and glutamate uptake were performed at the end of OGD period by high-performance liquid chromatography and incorporation of l-[3H]glutamate into cells, respectively. Results At clinically relevant concentrations (0.05-10 microm), propofol offered protection equivalent to that of MK-801. It significantly reduced lactate dehydrogenase release and increased the reduction of MTT. At the end of the ischemic injury, propofol was able to reverse the OGD-induced increase in glutamate extracellular concentrations and decrease of glutamate uptake. The inhibition of the glial GLT1 transporter by 3-methyl-glutamate did not further modify the effect of propofol on glutamate uptake, suggesting that GLT1 was not the major target of propofol. Conclusion Propofol showed a neuroprotective effect in this in vitro model of OGD, which was apparently mediated by a GLT1-independent restoration of the glutamate uptake impaired during the injury.

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