PubMed · 14410450
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M P KOENIG, R GUBLER. 1959-04-04. [Hypercalcemia in hyperthyroidism].. https://pubmed.ncbi.nlm.nih.gov/14410450/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
We have further characterized the Ca2+ signalling properties of the NG115-401L (or 401L) neuroblastoma cell line, which has served as an important cell line for investigating SOC (store-operated channel) influx pathways. These cells possess an unusual Ca2+ signalling phenotype characterized by the absence of Ca2+ influx when Ca2+ stores are depleted by inhibitors of SERCA (sarcoplasmic/endoplasmic reticulum Ca2+-ATPase). Previous studies found that Ca2+-store depletion does not produce a CIF (Ca2+ influx factor) activity in 401L cells. These observations have prompted the question whether 401L cells possess the signalling machinery that permits non-voltage-gated Ca2+ influx to occur. We tested the hypothesis that ryanodine-sensitive Ca2+ pools and activation of RyRs (ryanodine receptors) constitute a signalling pathway capable of inducing Ca2+ influx in 401L cells. We found that 401L cells express mRNA for RyR1 and RyR2 and that RyR activators induced Ca2+ release. Activation of RyRs robustly couples with Ca2+ influx responses in 401L cells, in sharp contrast with absence of Ca2+ influx when cells are treated with SERCA inhibitors. Thus it is clear that 401L cells, despite lacking depletion-induced Ca2+ influx pathways, express the functional components of a Ca2+ influx pathway under the control of RyR function. These findings further support the importance of the 401L cell line as an important cell phenotype for deciphering Ca2+ influx regulation.
Zygosaccharomyces bailii is a commercially important spoilage yeast capable of growth at low pH in the presence of weak organic acid preservatives, such as benzoic acid. A patch-clamp electrophysiological analysis of plasma membrane K+ transport revealed a high conductance pathway for low-affinity K+ uptake. In contrast to the equivalent K+ transporter in Saccharomyces cerevisiae, this system remained operative at low extracellular pH and may therefore facilitate K+ uptake in K(+)-rich and acidic beverages. Benzoate inhibited growth, increased intracellular K+ content, yet decreased the magnitude of the K+ uptake conductance; specifically, the hyperpolarization-activated inwardly-rectifying component was reduced. It is proposed that this adaptation helps maintain a hyperpolarized membrane voltage to effect continued ATPase-mediated H+ extrusion and so combat preservative-induced cytosolic acidosis. Again in contrast to S. cerevisiae, the K+ conductance was relatively insensitive to increased extracellular Ca2+. Paradoxically (and unlike S. cerevisiae) increasing extracellular Ca2+ inhibited growth, suggesting a simple expedient to limit spoilage by Z. bailii.
A common feature in asthma is the induction of reactive oxygen species (ROS) and the AP-1 transcription factor during the inflammatory process. AP-1 induction leads to an increased expression of pro-inflammatory cytokines. Also, higher levels of the pro-inflammatory neuropeptide substance P (SP) have been reported in bronchoalveolar-lavage fluid of asthmatics. Here, the role of SP on ROS induction and the downstream activation of AP-1 in A549 airway epithelial cells was investigated by dichloroflourescein-diacetate method and reporter gene assays. The SP-mediated AP-1 induction was dependent on extracellular calcium and ROS. The likely source of ROS are the mitochondria as rotenone inhibited AP-1 induction and the p47phox subunit of the NADPH oxidase complex, responsible for ROS generation in phagocytotic cells, was not expressed in A549 cells assayed by RT-PCR. This is consistent with results obtained from cells of murine bronchial epithelium, isolated by laser capture microdissection. In summary, this study provides evidence for an SP-mediated induction of AP-1, which may contribute to the expression of pro-inflammatory cytokines.