Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intracellular microelectrode recordings were made from smooth muscle cells in cross-sectional preparations of equine ileum, superfused in vitro. Membrane potential oscillations and spike potentials were recorded in all preparations, but recordings were made more readily from cells in the longitudinal muscle layer than from cells in the circular layer. The mean (se) resting membrane potential (RMP) of smooth muscle cells in the longitudinal muscle layer was -51.9 (1.2) mV, and the membrane potential oscillations in this layer had a mean amplitude of 4.8 (0.4) mV, a frequency of 9.0 (0.1) cycles per minute and a duration of 5.8 (0.2) seconds. The membrane potential oscillations were preserved in the presence of tetrodotoxin. A waxing and waning pattern of membrane potential oscillation activity was observed. Nifedipine abolished the spiking contractile activity of the smooth muscle, did not abolish the membrane potential oscillations but did alter their temporal characteristics.
Vet Rec 2001 Dec 08
PMID:In vitro microelectrode study of the electrical properties of smooth muscle in equine ileum. 1178 83

Autoantibodies against recoverin, a Ca2+-binding protein found in patients with cancer-associated retinopathy (CAR syndrome), penetrate retinal cells and induce their apoptosis via a mitochondrial pathway. The goal of this study was to investigate whether the entry of anti-recoverin antibody into E1A.NR3 retinal cells causes a change in intracellular Ca2+. Intracellular Ca2+ was measured using the Ca2+-sensitive fluorescent dye Fura-2 AM in living E1A.NR3 retinal cells treated with anti-recoverin antibody Rec-1, patients' autoantibodies, and control rat and human IgG. The exposure of retinal cells to Rec-1 antibody and to the CAR patients' autoantibodies in vitro caused a significant increase in intracellular Ca2+, while non-specific antibodies did not induce such an effect. Co-treatment of the E1A.NR3 cells with Rec-1 in the presence of nifedipine, a L-type Ca2+ channel blocker, significantly suppressed the increase of Ca2+. Treatment with nifedipine also blocked changes in the anti-apoptotic protein bcl-xL and in expressions of the pro-apoptotic protein bax. Nifedipine-treated cells also showed a decrease in cytosolic cytochrome c release and a decrease in caspase 3 activation, compared to cells treated only with Rec-1 antibody. The increase in the antibody-induced Ca2+ is at least in part dependent on extracellular Ca2+. Nifedipine was found to inhibit the entry of Ca2+ into the cells and to protect them from Rec-1-induced apoptosis. Increased levels of intracellular Ca2+ may lead to retinal dysfunction and degeneration in the CAR syndrome. Our results provide a molecular basis for the use of Ca2+ blockers in the treatment of the CAR syndrome.
 ...
PMID:Anti-recoverin antibodies induce an increase in intracellular calcium, leading to apoptosis in retinal cells. 1642 15

We have previously demonstrated that nitric oxide (NO) is involved in the regulation of the lymphatic stomata. However, the related mechanisms are still unknown. The present study was designed to test the hypothesis that NO-cyclic guanosine monophosphate (cGMP) -mediated cytosolic Ca(2+) concentration ([Ca(2+)]i) signaling may contribute to the regulation of the lymphatic stomata and lymph drainage. Using trypan blue as a tracer, the effects of NO-cGMP-Ca(2+) signal cascade on the lymphatic stomata and lymph absorption were examined by means of scanning electron microscopy. Then, the role of NO in cGMP and [Ca(2+)]i of rat peritoneal mesothelial cells (RPMCs) was measured by radioimmunoassay and a confocal laser scanning microscope. Our results showed that NO-donor spermine/nitric oxide complex (Sper/NO) could broaden the opening area of the lymphatic stomata and enhance lymph absorption in a dose-dependent manner. These NO-mediated changes could be blocked by 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), a specific inhibitor of soluble guanylyl cyclase, and mimicked by calcium channel blocker nifedipine. Furthermore, Sper/NO enhanced the cGMP level and lessened [Ca(2+)](i) in RPMCs, which was completely abrogated at the presence of ODQ. Nifedipine induced an immediate and marked decrease of [Ca(2+)](i) in the RPMCs, which was not attenuated by addition of Sper/NO, indicating that the Sper/NO-cGMP signaling system induced [Ca(2+)](i) change was related to the L-type voltage-gated calcium channel in the RPMCs. Our results suggest that NO enlarges the opening area of the lymphatic stomata to strengthen the lymph drainage of tracer by means of NO-cGMP-[Ca(2+)]i signal transduction pathway in the RPMCs.
Anat Rec (Hoboken) 2008 Feb
PMID:Cell signal transduction mechanism for nitric oxide regulating lymphatic stomata and its draining capability. 1821 6