Effect of WSSV infection on cell cycle regulation, respiratory burst and cytoplasmic free calcium concentration in Penaeus vannamei

2021 ◽  
Author(s):  
Mudagandur Shashi Shekhar ◽  
Swathi Anandan ◽  
Vinaya Kumar Katneni ◽  
Ashok Kumar Jangam ◽  
Jesudhas Raymond Jani Angel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Respiratory Burst ◽  
Cell Cycle Regulation ◽  
Calcium Concentration ◽  
Free Calcium ◽  
Penaeus Vannamei ◽  
Free Calcium Concentration ◽  
Cycle Regulation ◽  
Cytoplasmic Free Calcium

Calcium and cell cycle control

Development ◽  
1990 ◽  
Vol 108 (4) ◽  
pp. 525-542 ◽  
Author(s):  
M. Whitaker ◽  
R. Patel
Keyword(s):  
Cell Cycle ◽  
Sea Urchin ◽  
Mammalian Cells ◽  
Cell Cycle Regulation ◽  
Sea Urchins ◽  
Cell Cycle Control ◽  
Control Point ◽  
Control Cell ◽  
Free Calcium ◽  
Cycle Regulation

The cell division cycle of the early sea urchin embryo is basic. Nonetheless, it has control points in common with the yeast and mammalian cell cycles, at START, mitosis ENTRY and mitosis EXIT. Progression through each control point in sea urchins is triggered by transient increases in intracellular free calcium. The Cai transients control cell cycle progression by translational and post-translational regulation of the cell cycle control proteins pp34 and cyclin. The START Cai transient leads to phosphorylation of pp34 and cyclin synthesis. The mitosis ENTRY Cai transient triggers cyclin phosphorylation. The motosis EXIT transient causes destruction of phosphorylated cyclin. We compare cell cycle regulation by calcium in sea urchin embryos to cell cycle regulation in other eggs and oocytes and in mammalian cells.

Cytoplasmic free calcium concentration in porcine platelets

1984 ◽  
Vol 800 (2) ◽  
pp. 178-187 ◽  
Author(s):  
A. David Purdon ◽  
James L. Daniel ◽  
Gwendolyn J. Stewart ◽  
Holm Holmsen
Keyword(s):  
Calcium Concentration ◽  
Free Calcium ◽  
Free Calcium Concentration ◽  
Cytoplasmic Free Calcium

The Effects of Chloride Channel Blockers on Platelet Cytoplasmic Free Calcium Concentration and Platelet Aggregation.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3879-3879
Author(s):  
Songmei Yin ◽  
Xiaolin Chen ◽  
Danian Nie ◽  
Shuangfeng Xie ◽  
Liping Ma ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Chloride Channel ◽  
Calcium Concentration ◽  
Disulfonic Acid ◽  
Free Calcium ◽  
Channel Blockers ◽  
Free Calcium Concentration ◽  
Cytoplasmic Free Calcium

Abstract Objective To explore the effects of chloride channels on the regulations of platelet cytoplasmic free calcium concentration ([Ca2+]i) and platelet aggregation (PAG). Methods Platelet were separated freshly and then activated by thrombin; The chloride channel blockers 4,4′-diisothiocyano-2, 2′-disulfonic acid stilbene (DIDS) or niflumic acid (NFA), and calcium channel blockers 1-{β-[3-(4-methoxyphenyl)propoxy]- 4-methoxyphenethyl}- 1H - imidazole hydrochloride (SK&F96365) or Nifedipine were added to react with the activated platelets. The effects of each agent on platelet [Ca2+]i and PAG were detected. The combine effects and the interactions among chloride channel blockers (DIDS, NFA) and calcium channel blockers (SK&F96365, Nifedipine) were also investigated. Results Both DIDS and NFA [the concentration were12.5, 25, 50, 100 and 200μmol•L−1 respectively] could inhibit the PAG induced by thrombin (1U/ml) and the effect was dose-dependent. Compared with the control, they had no significant effects on resting [Ca2+]i. Compare with the control group, DIDS (100μmol•L−1), SK&F96365 (100μmol•L−1) and Nifedipine (100μmol•L−1) could significantly reduce the PAG, Ca2+ release and Ca2+ influx activated by thrombin in platelet (P<0.05). DIDS (100μmol•L−1) and SK&F96365 (100μmol•L−1) could enhance each other’s effect on reducing the PAG, Ca2+ release and Ca2+ influx (P<0.05). DIDS (100μmol•L−1) and Nifedipine (100μmol•L−1) could enhance each other’s effect on reducing Ca2+ release (P<0.05). NFA (100μmol•L−1) and SK&F96365 (100μmol•L−1) could weaken each other’s effect on Ca2+ release (P<0.05). NFA (100μmol•L−1) and Nifedipine (100μmol•L−1) could weaken each other’s effect on PAG, Ca2+ release and Ca2+ influx activated by thrombin in platelet (P<0.05). Conclusion The chloride channel blockers DIDS and NFA have no effect on the resting [Ca2+]i and the leak calcium influx of platelet. DIDS can inhibit the Ca2+ release, Ca2+ influx and PAG of platelet induced by thrombin, while NFA can only inhibit the Ca2+ release of platelet induced by thrombin. There are interactions between chloride channel blockers and calcium channel blockers in resting [Ca2+]i and PAG of platelet. The opening of chloride channel can influence the cellular calcium movement of platelet.

Oscillation of cytoplasmic free calcium concentration induced by insulin-like growth factor I

1992 ◽  
Vol 262 (3) ◽  
pp. E307-E311
Author(s):  
I. Kojima ◽  
H. Mogami ◽  
E. Ogata
Keyword(s):  
Growth Factor ◽  
Calcium Concentration ◽  
Calcium Entry ◽  
Free Calcium ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Free Calcium Concentration ◽  
Growth Factor I ◽  
Cytoplasmic Free Calcium

The effect of insulin-like growth factor I (IGF-I) on cytoplasmic free calcium concentration ([Ca2+]c) was studied in single BALB/c 3T3 cells by monitoring fura-2 fluorescence. In primed competent cells, IGF-I (1 nM) increased [Ca2+]c in approximately 60% of the cells tested. IGF-I-mediated elevation of [Ca2+]c was observed after a 4- to 17-min lag period. Elevation of [Ca2+]c was only transient but was followed by repetitive increases in [Ca2+]c. The interval between each peak was quite constant in each cell at a given concentration of IGF-I. When the concentration of IGF-I was reduced, both the latent period and interval of each peak were prolonged, whereas amplitude of the increase in [Ca2+]c was not altered. In medium containing 10 microM extracellular calcium, IGF-I did not cause any increase in [Ca2+]c. Likewise, blockade of IGF-induced calcium entry by either cobalt or tetramethrin abolished IGF-I action on [Ca2+]c. IGF-I-mediated oscillation was not affected by either ryanodine or caffeine, compounds that affect calcium-induced calcium release. In addition, pretreatment of the cell with neomycin did not affect IGF-I-mediated oscillation. In agreement with this, IGF-I did not augment production of [3H]inositol trisphosphate in cells prelabeled with [3H]inositol. These results indicate that IGF-I induces oscillation of [Ca2+]c in a single primed competent cell and that the oscillation is totally dependent on IGF-I-mediated calcium entry.

Sign in / Sign up

Export Citation Format

Share Document