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Intracellular and Extracellular pH and Ca Are Bound to Control Mitosis in the Early Sea Urchin Embryo via ERK and MPF Activities  [PDF]
Brigitte Ciapa, Laetitia Philippe
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0066113
Abstract: Studies aiming to predict the impact on marine life of ocean acidification and of altered salinity have shown altered development in various species including sea urchins. We have analyzed how external Na, Ca, pH and bicarbonate control the first mitotic divisions of sea urchin embryos. Intracellular free Ca (Cai) and pH (pHi) and the activities of the MAP kinase ERK and of MPF regulate mitosis in various types of cells including oocytes and early embryos. We found that intracellular acidification of fertilized eggs by Na-acetate induces a huge activation of ERK at time of mitosis. This also stops the cell cycle and leads to cell death, which can be bypassed by treatment with the MEK inhibitor U0126. Similar intracellular acidification induced in external medium containing low sodium or 5-(N-Methyl-N-isobutyl) amiloride, an inhibitor of the Na+/H+ exchanger, also stops the cell cycle and leads to cell death. In that case, an increase in Cai and in the phosphorylation of tyr-cdc2 occurs during mitosis, modifications that depend on external Ca. Our results indicate that the levels of pHi and Cai determine accurate levels of Ptyr-Cdc2 and P-ERK capable of ensuring progression through the first mitotic cycles. These intracellular parameters rely on external Ca, Na and bicarbonate, alterations of which during climate changes could act synergistically to perturb the early marine life.
Intracellular and Extracellular Tau  [PDF]
Jesús Avila
Frontiers in Neuroscience , 2010, DOI: 10.3389/fnins.2010.00049
Abstract: In this short review is described the toxicity of modified intracellular tau and that of extracellular tau that could be released into the extracellular space after neuron death.
Study on mechanism of vasorelaxatory effect of Vitis vinifera leaf extract in rat aorta
Mohammad Kazem Gharib Naseri,Akbar Heidari
Physiology and Pharmacology , 2006,
Abstract: Introduction: Our previous studies showed that hydroalcoholic extract of leaf of Vitis vinifera relaxes the phenylephrine-induced contraction in rat thoracic aorta. This effect was dependent on endothelial integrity and NO-cGMP system. The vasorelaxant effect of extract was much lesser on KCl-induced contraction. We, therefore, postulated that K+ channels are involved. The main aim of the present study was to determine the type of K+ channels involved in this vasorelaxant effect. Methods: Thoracic aorta with intact endothelium was removed from adult male Wistar rats (170-220g). The aorta was mounted in an organ bath containing Krebs-Henseleit (37 oC, pH 7.4) bubbled with O2. Aortic contractions were recorded isometrically under 1 g resting tension. The aorta endothelium was considered intact if acetylcholine (1 μM) could induce more than 70% aorta relaxation on 1μM phenylephrine-induced contraction. Extract was prepared by maceration method using 70% alcohol and the solvent was then evaporated. Results: The results showed that in the presence of tetraethylammonium (10 mM), the vasorelaxant effect of extract (0.25, 0.5, 1 and 2 mg/ml) was reduced (P<0.001, n=7). In contrast, glibenclamide (1 μM) had no effect. In calcium-free (plus 0.1 mM of EDTA) Krebs-Henseleit solution, the vasorelaxant effect of extract (0.25, 0.5 and 1 mg/ml) was reduced (P<0.0001, n=8). Furthermore, the vasorelaxant effect of extract was unaffected by indomethacin (1 μM). Conclusion: These results suggest that Vitis vinifera leaf hydroalcoholic extract induces relaxation in rat aorta possibly by opening the Ca2+ -operated K+ channels but, not ATP- sensitive K+ channels and extracellular calcium was essential for inducing vasorelaxation by extract. Furthermore, cyclooxigenase was not involved in this vasorelaxant effect.
Hypotrophy of conduit artery walls of the offspring of nitric oxide-defective rats
Kristek, F.;Gerová, M.;
Brazilian Journal of Medical and Biological Research , 2004, DOI: 10.1590/S0100-879X2004000400018
Abstract: the objective of the present study was to investigate the structure of the arterial walls of the offspring stemming from nitric oxide (no)-defective hypertensive parents. the parents were treated with ng-nitro-l-arginine methyl ester (40 mg kg-1 day-1) for 5 weeks. blood pressure was measured noninvasively in six 30-day-old rats and nine age-matched controls. the cardiovascular system was perfused with glutaraldehyde at 120 mmhg. the thoracic aorta and carotid artery were processed for electron microscopy, and geometry was determined by light microscopy. endothelial cells, smooth muscle cells (smc) and extracellular matrix (ecm) were determined by the point counting method in electron micrographs of the carotid artery. the blood pressure of experimental offspring was 150.0 ± 2.3 vs 104.6 ± 2.1 mmhg (p < 0.01) for the controls and their heart/body weight ratio of 3.9 ± 0.1 vs 4.4 ± 0.2 (p < 0.05) for the controls indicated cardiac hypotrophy. the wall thickness (tunica intima and media) of the thoracic aorta and carotid artery of experimental offspring was decreased to 78.9% (p < 0.01) and 83.8% (p < 0.01), respectively, compared to controls, as confirmed by a respective cross-sectional area of 85.3% (p < 0.01) and 84.1% (p < 0.01). the wall thickness/inner diameter ratio was reduced to 75% (p < 0.01) in the thoracic artery and to 81.5% (p < 0.01) in the carotid artery. no change in endothelial cell volume density or ecm was observed in the tunica intima of the carotid artery, and smc volume density was lower in the tunica media (37.6 ± 0.9 vs 44.7 ± 1.1% for controls, p < 0.01), indicating compromised smc development. interference with arginine metabolism, a decrease in no, and other factors are possible mechanisms underlying the structural alterations of the cardiovascular system of offspring from no-defective hypertensive rats.
Hypotrophy of conduit artery walls of the offspring of nitric oxide-defective rats  [cached]
Kristek F.,Gerová M.
Brazilian Journal of Medical and Biological Research , 2004,
Abstract: The objective of the present study was to investigate the structure of the arterial walls of the offspring stemming from nitric oxide (NO)-defective hypertensive parents. The parents were treated with N G-nitro-L-arginine methyl ester (40 mg kg-1 day-1) for 5 weeks. Blood pressure was measured noninvasively in six 30-day-old rats and nine age-matched controls. The cardiovascular system was perfused with glutaraldehyde at 120 mmHg. The thoracic aorta and carotid artery were processed for electron microscopy, and geometry was determined by light microscopy. Endothelial cells, smooth muscle cells (SMC) and extracellular matrix (ECM) were determined by the point counting method in electron micrographs of the carotid artery. The blood pressure of experimental offspring was 150.0 ± 2.3 vs 104.6 ± 2.1 mmHg (P < 0.01) for the controls and their heart/body weight ratio of 3.9 ± 0.1 vs 4.4 ± 0.2 (P < 0.05) for the controls indicated cardiac hypotrophy. The wall thickness (tunica intima and media) of the thoracic aorta and carotid artery of experimental offspring was decreased to 78.9% (P < 0.01) and 83.8% (P < 0.01), respectively, compared to controls, as confirmed by a respective cross-sectional area of 85.3% (P < 0.01) and 84.1% (P < 0.01). The wall thickness/inner diameter ratio was reduced to 75% (P < 0.01) in the thoracic artery and to 81.5% (P < 0.01) in the carotid artery. No change in endothelial cell volume density or ECM was observed in the tunica intima of the carotid artery, and SMC volume density was lower in the tunica media (37.6 ± 0.9 vs 44.7 ± 1.1% for controls, P < 0.01), indicating compromised SMC development. Interference with arginine metabolism, a decrease in NO, and other factors are possible mechanisms underlying the structural alterations of the cardiovascular system of offspring from NO-defective hypertensive rats.
Is intracellular pH a clock for mitosis?
Gagliardi L John,Shain Daniel H
Theoretical Biology and Medical Modelling , 2013, DOI: 10.1186/1742-4682-10-8
Abstract: Experiments have shown that the intracellular pH of many cells rises to a maximum at the onset of mitosis, subsequently decreasing 0.3 to 0.5 pH units by the end of mitosis. This result, and observations that tubulin net charge depends strongly on pH, may be critical for microtubule (MT) dynamics during mitosis. In vivo studies demonstrate that MT dynamics is sensitive to pH, with MT growth favored by higher pH values. Therefore it seems likely that the shift from the dominance of microtubule growth during prophase, and to a lesser extent during prometaphase, to a parity between MT polymerization and depolymerization during metaphase chromosome oscillations is a consequence of gradually decreasing intracellular pH during mitosis. Thus the timing and sequencing of prophase, prometaphase, and metaphase chromosome motions may be understood as an increase in the MT disassembly to assembly probability ratio resulting from a continuously declining intracellular pH.
Protective Role of Acidic pH-Activated Chloride Channel in Severe Acidosis-Induced Contraction from the Aorta of Spontaneously Hypertensive Rats  [PDF]
Zhiyong Ma, Jia Qi, Zhijie Fu, Mingying Ling, Li Li, Yun Zhang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0061018
Abstract: Severe acidic pH-activated chloride channel (ICl,acid) has been found in various mammalian cells. In the present study, we investigate whether this channel participates in reactions of the thoracic aorta to severe acidosis and whether it plays a role in hypertension. We measured isometric contraction in thoracic aorta rings from spontaneously hypertensive rats (SHRs) and normotensive Wistar rats. Severe acidosis induced contractions of both endothelium-intact and -denuded thoracic aorta rings. In Wistar rats, contractions did not differ at pH 6.4, 5.4 and 4.4. However, in SHRs, contractions were higher at pH 5.4 or 4.4 than pH 6.4, with no difference between contractions at pH 5.4 and 4.4. Nifedipine, ICl,acid blockers 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and 4,4′-diisothiocyanatostilbene-2, 2′-disulfonic acid (DIDS) inhibited severe acidosis-induced contraction of aortas at different pH levels. When blocking ICl,acid, the remnant contraction was greater at pH 4.4 than pH 5.4 and 6.4 for both SHRs and Wistar rats. With nifedipine, the remnant contraction was greatly reduced at pH 4.4 as compared with at pH 6.4 and 5.4. With NPPB or DIDS, the ratio of remnant contractions at pH 4.4 and 5.4 (R4.4/5.4) was lower for SHRs than Wistar rats (all <1). However, with nifedipine, the R4.4/5.4 was higher for SHRs than Wistar rats (both >1). Furthermore, patch clamp recordings of ICl,acid and intracellular Ca2+ measurements in smooth muscle cells confirmed these findings. ICl,acid may protect arteries against excess vasoconstriction under extremely acidic extracellular conditions. This protective effect may be decreased in hypertension.
CO2chemotransduction in central neurons: role of intracellular pH (pHi) and extracellular pH (pHo)
Putnam RW
Respiratory Research , 2001, DOI: 10.1186/rr122
Abstract:
Reversal of doxorubicin-induced vascular dysfunction by resveratrol in rat thoracic aorta: Is there a possible role of nitric oxide synthase inhibition?  [cached]
Murat Olukman,Cenk Can,Ay?e Erol,Gülperi ?ktem
Anadolu Kardiyoloji Dergisi , 2009,
Abstract: Objective: The natural antioxidant, resveratrol has been suggested to protect against doxorubicin-induced cardiotoxicity. Although derangements in nitric oxide (NO) synthesis contribute to vascular endothelial dysfunction caused by doxorubicin, the effects of resveratrol on these parameters have not been evaluated yet. We investigated the impact of resveratrol on doxorubicin-induced vascular dysfunction in rat thoracic aorta with regard to NO synthesis in an experimental, prospective, controlled study. Methods: Wistar rats were assigned to 5 groups; doxorubicin (n=9), vehicle (dimethylsulphoxide) (n=8), resveratrol (n=8), doxorubicin+resveratrol (n=10), controls (n=9). Contractile and relaxant responses were evaluated on the isolated thoracic aortas. The expressions of endothelial (eNOS) and inducible (iNOS) isoforms of NO-synthase were also examined histopathologically on the aortas. Statistical analysis was performed by ANOVA for repeated measures for the response curves and one-way ANOVA for the pD2 (-log EC50) and Emax (maximum phenylephrine contraction) values with subsequent Bonferroni test.Results: Doxorubicin (20 mg/kg, i.p), not only decreased the contractile responses to phenylephrine (p<0.001), but also attenuated the relaxant responses to acetylcholine (ACh) (p=0.002), calcium ionophore (A23187) (p=0.002) and sodium nitroprusside (SNP) (p=0.007). Immunohistochemistry revealed increased (p<0.05) eNOS and iNOS protein expressions after doxorubicin treatment. Coadministration of resveratrol (10 mg/kg/i.p.) reversed the increased expression of both NOS isoforms (p<0.05). Similarly, it prevented the doxorubicin-induced attenuation in ACh- (p=0.013) and A23187- (p=0.038) induced responses. In healthy rats the antioxidant did not cause significant changes.Conclusion: Prevention of excessive NO formation through eNOS and iNOS overexpression by resveratrol might contribute to the reversal of vascular endothelial dysfunction associated with doxorubicin treatment.
Acidic Extracellular pH Promotes Activation of Integrin αvβ3  [PDF]
Ranjani K. Paradise,Douglas A. Lauffenburger,Krystyn J. Van Vliet
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015746
Abstract: Acidic extracellular pH is characteristic of the cell microenvironment in several important physiological and pathological contexts. Although it is well established that acidic extracellular pH can have profound effects on processes such as cell adhesion and migration, the underlying molecular mechanisms are largely unknown. Integrin receptors physically connect cells to the extracellular matrix, and are thus likely to modulate cell responses to extracellular conditions. Here, we examine the role of acidic extracellular pH in regulating activation of integrin αvβ3. Through computational molecular dynamics simulations, we find that acidic extracellular pH promotes opening of the αvβ3 headpiece, indicating that acidic pH can thereby facilitate integrin activation. This prediction is consistent with our flow cytometry and atomic force microscope-mediated force spectroscopy assays of integrin αvβ3 on live cells, which both demonstrate that acidic pH promotes activation at the intact cell surface. Finally, quantification of cell morphology and migration measurements shows that acidic extracellular pH affects cell behavior in a manner that is consistent with increased integrin activation. Taken together, these computational and experimental results suggest a new and complementary mechanism of integrin activation regulation, with associated implications for cell adhesion and migration in regions of altered pH that are relevant to wound healing and cancer.
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