scholarly journals Signaling pathways in ascidian oocyte maturation: The roles of cAMP/Epac, intracellular calcium levels, and calmodulin kinase in regulating GVBD

2011 ◽  
Vol 78 (10-11) ◽  
pp. 726-733 ◽  
Author(s):  
Charles C. Lambert
Keyword(s):  
Intracellular Calcium ◽  
Signaling Pathways ◽  
Oocyte Maturation ◽  
Calmodulin Kinase

scholarly journals Mechanisms underlying oocyte activation and postovulatory ageing

Reproduction ◽  
2002 ◽  
pp. 745-754 ◽  
Author(s):  
RA Fissore ◽  
M Kurokawa ◽  
J Knott ◽  
M Zhang ◽  
J Smyth
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Intracellular Calcium ◽  
Oocyte Maturation ◽  
Abnormal Development ◽  
Oocyte Activation ◽  
Molecular Changes ◽  
Free Intracellular Calcium ◽  
Developmental Programme ◽  
Nuclear Modifications

Mammalian oocytes undergo significant growth during oogenesis and experience extensive cytoplasmic and nuclear modifications immediately before ovulation in a process commonly referred to as oocyte maturation. These changes are intended to maximize the developmental success after fertilization. Entry of a spermatozoon into the oocyte, which occurs a few hours after ovulation, initiates long-lasting oscillations in the free intracellular calcium ([Ca(2+)](i)) that are responsible for all events of oocyte activation and the initiation of the developmental programme that often culminates in the birth of young. Nevertheless, the cellular and molecular changes that occur during maturation to optimize development are transient, and exhibit rapid deterioration. Moreover, fertilization of oocytes after an extended residence in the oviduct (or in culture) initiates a different developmental programme, one that is characterized by fragmentation, programmed cell death, and abnormal development. Inasmuch as [Ca(2+)](i) oscillations can trigger both developmental programmes in mammalian oocytes, this review addresses one of the mechanism(s) possibly used by spermatozoa to initiate these persistent [Ca(2+)](i) responses, and the cellular and molecular changes that may underlie the postovulatory cellular fragmentation of ageing mammalian oocytes.

Several signaling pathways are involved in the control of cattle oocyte maturation

2004 ◽  
Vol 69 (4) ◽  
pp. 466-474 ◽  
Author(s):  
C�line Vigneron ◽  
Christine Perreau ◽  
Jo�lle Dupont ◽  
Svetlana Uzbekova ◽  
Claude Prigent ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Oocyte Maturation

scholarly journals Crotonaldehyde induces apoptosis in alveolar macrophages through intracellular calcium, mitochondria and p53 signaling pathways

2013 ◽  
Vol 38 (2) ◽  
pp. 225-235 ◽  
Author(s):  
Bi-cheng Yang ◽  
Xiu-jie Pan ◽  
Zhi-hua Yang ◽  
Feng-jun Xiao ◽  
Xing-yu Liu ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Signaling Pathways ◽  
Alveolar Macrophages ◽  
P53 Signaling

scholarly journals The Potassium Channel, Kir3.4 Participates in Angiotensin II-Stimulated Aldosterone Production by a Human Adrenocortical Cell Line

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4328-4335 ◽  
Author(s):  
Kenji Oki ◽  
Maria W. Plonczynski ◽  
Milay Luis Lam ◽  
Elise P. Gomez-Sanchez ◽  
Celso E. Gomez-Sanchez
Keyword(s):  
Cytochrome P450 ◽  
Angiotensin Ii ◽  
Potassium Channel ◽  
Intracellular Calcium ◽  
Regulatory Protein ◽  
Membrane Depolarization ◽  
Membrane Voltage ◽  
Aldosterone Secretion ◽  
Calmodulin Kinase ◽  
Kinase Cascade

Angiotensin II (A-II) regulation of aldosterone secretion is initiated by inducing cell membrane depolarization, thereby increasing intracellular calcium and activating the calcium calmodulin/calmodulin kinase cascade. Mutations in the selectivity filter of the KCNJ5 gene coding for inward rectifying potassium channel (Kir)3.4 has been found in about one third of aldosterone-producing adenomas. These mutations result in loss of selectivity of the inward rectifying current for potassium, which causes membrane depolarization and opening of calcium channels and activation of the calcium calmodulin/calmodulin kinase cascade and results in an increase in aldosterone secretion. In this study we show that A-II and a calcium ionophore down-regulate the expression of KCNJ5 mRNA and protein. Activation of Kir3.4 by naringin inhibits A-II-stimulated membrane voltage and aldosterone secretion. Overexpression of KCNJ5 in the HAC15 cells using a lentivirus resulted in a decrease in membrane voltage, intracellular calcium, expression of steroidogenic acute regulatory protein, 3-β-hydroxysteroid dehydrogenase 3B2, cytochrome P450 11B1 and cytochrome P450 11B2 mRNA, and aldosterone synthesis. In conclusion, A-II appears to stimulate aldosterone secretion by depolarizing the membrane acting in part through the regulation of the expression and activity of Kir3.4.

Cyclopiazonic acid induces accelerated progress of meiosis in pig oocytes

Zygote ◽  
1997 ◽  
Vol 5 (3) ◽  
pp. 193-205 ◽  
Author(s):  
Jaroslav Petr ◽  
Jirří Rozinek ◽  
František Jílek
Keyword(s):  
Intracellular Calcium ◽  
Oocyte Maturation ◽  
Ryanodine Receptors ◽  
Cyclopiazonic Acid ◽  
Cumulus Cells ◽  
Ruthenium Red ◽  
Sensitive Period ◽  
Calcium Deposits ◽  
Transient Elevation

SummaryIn mammalian oocytes, calcium plays an important role in the regulation of meiotic maturation. In our study, we used the mycotoxin cyclopiazonic acid (CPA), an inhibitor of calcium-dependent ATPases, to mobilise intracellular calcium deposits during in vitro maturation of pig oocytes. The CPA treatment of maturing oocytes significantly accelerated the progress of their maturation. Oocytes entered the CPA-sensitive period after 21 h of in vitro culture. A very short (5 min) exposure to CPA (100 mM) is sufficient to accelerate maturation and it seems that accelerated maturation can be triggered by a transient elevation of intracellular calcium levels. The effect of CPA is not mediated through the cumulus cells, because maturation is accelerated by CPA treatment even in oocytes devoid of cumulus cells. Culture of oocytes with the calcium channel blocker verapamil (concentrations ranging from 0.01 to 0.04 mM) blocked the progress of oocyte maturation beyond the stage of metaphase I. This block can be overcome by the mobilisation of intracellular calcium deposits after CPA treatment (100 nM). The microinjection of heparin (20 pl, 50.1 mg/;ml), the inhibitor of inositol triphosphate receptors, before CPA treatment prevented the acceleration of oocyte maturation. This indicates that CPA mobilises the release of calcium deposits through inositol trisphosphate receptors. On the other hand, the microinjection of procaine (20 pl, 200 nM) or the microinjection of ruthenium red (20 pl, 50 mM), both inhibitors of ryanodine receptors, did not prevent accelerated maturation in CPA-treated oocytes. If present in pig oocytes, ryanodine receptors evidently play no part in the liberation of calcium from intracellular stores after CPA treatment.

Negative Regulation of Gq-Mediated Pathways in Platelets by G12/13 Pathways through Fyn Kinase

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2854-2854
Author(s):  
Soochong Kim ◽  
Satya P. Kunapuli
Keyword(s):  
Platelet Aggregation ◽  
Intracellular Calcium ◽  
Signaling Pathways ◽  
Platelet Function ◽  
Shape Change ◽  
Wild Type Mouse ◽  
Calcium Mobilization ◽  
Negative Regulator ◽  
Platelet Response ◽  
Calcium Response

Abstract Platelets contain high levels of Src family kinases (SFKs) suggesting an important role for these enzymes in platelet function. In this study, we have investigated the regulation of platelet function by SFKs downstream of G12/13 pathways. Calcium-independent platelet shape change induced by selective G12/13 stimulation with YFLLRNP was potentiated with a small mobilization of intracellular calcium in the presence of SFK inhibitors PP1 or PP2, which was abolished by the chelation of intracellular calcium, suggesting that SFKs downstream of G12/13 negatively regulate calcium mobilization in platelets. In addition, PP1 or PP2 caused a leftward shift of human platelet aggregation, secretion, and calcium response induced by low concentrations of agonists that activate platelets through G12/13 signaling such as PAR1-activating peptide SFLLRN and PAR4-activating peptide AYPGKF. However, 2-MeSADP-induced calcium response and platelet aggregation were not affected by the presence of PP1 or PP2, suggesting that SFKs downstream of G12/13, but not Gq/Gi, pathways are involved in this platelet response. Moreover, platelet aggregation and secretion caused by combined stimulation of G12/13 and Gi/Gz (YFLLRNP + 2-MeSADP with P2Y1 antagonist/epinephrine) were also potentiated in the presence of PP1 or PP2 confirming the contribution of SFKs downstream of G12/13 as a negative regulator to platelet activation. Potentiation of platelet aggregation in the presence of SFK inhibitors was not affected in the presence of GF109203X, while PP2 failed to potentiate platelet aggregation in the presence of 5,5′-dimethyl-BAPTA indicating that potentiation of cytosolic calcium may have an important role in this enhanced platelet responses by SFK inhibition. Moreover, PP1 or PP2 failed to potentiate platelet responses in the presence of Gq selective inhibitor YM-254890 or in Gq-deficient platelets, indicating that SFKs negatively regulate platelet responses through modulation of Gq signaling pathways. Importantly, AYPGKF-induced platelet aggregation, secretion, and calcium response were potentiated in Fyn-, but not in Lyn-, deficient platelets compared to the wild-type mouse platelets, whereas 2-MeSADP-induced platelet response was not affected in these platelets. We conclude that SFKs activated downstream of G12/13, but not Gq/Gi, pathways negatively regulate platelet responses by inhibiting intracellular calcium mobilization in platelets through Gq signaling pathways. Specifically, we define that Fyn plays a major role in this negatively regulatory pathway.

Comprehensive identification of signaling pathways for idiopathic pulmonary arterial hypertension

2020 ◽  
Vol 318 (5) ◽  
pp. C913-C930
Author(s):  
Bingxun Liu ◽  
Liping Zhu ◽  
Ping Yuan ◽  
Glenn Marsboom ◽  
Zhigang Hong ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Intracellular Calcium ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Cell Function ◽  
Idiopathic Pulmonary Arterial Hypertension ◽  
Channel Blockers ◽  
Gpcr Signaling ◽  
Pulmonary Arterial

Whole exome sequencing (WES) was used in the research of familial pulmonary arterial hypertension (FPAH). CAV1 and KCNK3 were found as two novel candidate genes of FPAH. However, few pathogenic genes were identified in idiopathic pulmonary arterial hypertension (IPAH). We conducted WES in 20 unrelated IPAH patients who did not carry the known PAH-pathogenic variants among BMPR2, CAV1, KCNK3, SMAD9, ALK1, and ENG. We found a total of 4,950 variants in 3,534 genes, including 4,444 single-nucleotide polymorphisms and 506 insertions/deletions (InDels). Through the comprehensive and multilevel analysis, we disclosed several novel signaling cascades significantly connected to IPAH, including variants related to cadherin signaling pathway, dilated cardiomyopathy, glucose metabolism, immune response, mucin-type O-glycosylation, phospholipase C (PLC)-activating G protein-coupled receptor (GPCR) signaling pathway, vascular contraction and generation, and voltage-dependent Ca2+ channels. We also conducted validation studies in five mutant genes related to PLC-activating GPCR signaling pathway potentially involved in intracellular calcium regulation through Sanger sequencing for mutation accuracy, qRT-PCR for mRNA stability, immunofluorescence for subcellular localization, Western blotting for protein level, Fura-2 imaging for intracellular calcium, and proliferation analysis for cell function. The validation experiments showed that those variants in CCR5 and C3AR1 significantly increased the rise of intracellular calcium and the variant in CCR5 profoundly enhanced proliferative capacity of human pulmonary artery smooth muscle cells. Thus, our study suggests that multiple genetically affected signaling pathways take effect together to cause the formation of IPAH and the development of right heart failure and may further provide new therapy targets or putative clues for the present treatments such as limited therapeutic effectiveness of Ca2+ channel blockers.

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