Signal transduction in red bloodcells of the lizards Ameiva ameiva and Tupinambis merianae (Squamata, Teiidae)

Beraldo, Flávio H.; Sartorello, R.; Lanari, R.D.; Garcia, Célia Regina da Silva

doi:10.1054/ceca.2001.0207

Cited by 17 publications

(20 citation statements)

References 29 publications

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“…These data are in agreement with previous observations indicating that chloroquine causes a substantial Ca 2ϩ release in the parasite Plasmodium chabaudi (30). Similarly, it has been shown that bafilomycin alters cytosolic Ca 2ϩ by discharging intracellular Ca 2ϩ pools in lizard red blood cells (31). Therefore, taken together, our results clearly indicate that Ca 2ϩ is a key participant in the exosome release process.…”

Section: Discussionsupporting

confidence: 84%

“…We tested the effect of two agents known to alter the pH of vacuolar compartments, the weak base chloroquine and the vacuolar proton pump inhibitor bafilomycin A1 (29). Previous work has shown that these compounds may also discharge intracellular Ca 2ϩ pools from acidic compartments (30,31). We have evidence that chloroquine elevated intracellular Ca 2ϩ in a similar manner to MON (not shown).…”

Section: Monensin Induces the Formation Of Large Mvbs And Stim-mentioning

confidence: 95%

See 1 more Smart Citation

Exosome Release Is Regulated by a Calcium-dependent Mechanism in K562 Cells

Savina

Furlán

Vidal

et al. 2003

Journal of Biological Chemistry

730

614

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Section: Discussionsupporting

confidence: 84%

Section: Monensin Induces the Formation Of Large Mvbs And Stim-mentioning

confidence: 95%

Exosome Release Is Regulated by a Calcium-dependent Mechanism in K562 Cells

Savina

Furlán

Vidal

et al. 2003

Journal of Biological Chemistry

730

614

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“…However, it is still unknown how a calcium signal is triggered and how particular metabolites derived from the host are central in providing signalling molecules to facilitate parasite growth. The host hormone, melatonin [27] and its derivatives that elicit a rise in cytosolic calcium in Plasmodium [17,28-30] also induce proteolysis in Plasmodium falciparum and Plasmodium chabaudi [31]. …”

Section: Introductionmentioning

confidence: 99%

Extracellular ATP triggers proteolysis and cytosolic Ca2+ rise in Plasmodium berghei and Plasmodium yoelii malaria parasites

Cruz

Juliano

Budu

et al. 2012

Malar J

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BackgroundPlasmodium has a complex cell biology and it is essential to dissect the cell-signalling pathways underlying its survival within the host.MethodsUsing the fluorescence resonance energy transfer (FRET) peptide substrate Abz-AIKFFARQ-EDDnp and Fluo4/AM, the effects of extracellular ATP on triggering proteolysis and Ca2+ signalling in Plasmodium berghei and Plasmodium yoelii malaria parasites were investigated.ResultsThe protease activity was blocked in the presence of the purinergic receptor blockers suramin (50 μM) and PPADS (50 μM) or the extracellular and intracellular calcium chelators EGTA (5 mM) and BAPTA/AM (25, 100, 200 and 500 μM), respectively for P. yoelii and P. berghei. Addition of ATP (50, 70, 200 and 250 μM) to isolated parasites previously loaded with Fluo4/AM in a Ca2+-containing medium led to an increase in cytosolic calcium. This rise was blocked by pre-incubating the parasites with either purinergic antagonists PPADS (50 μM), TNP-ATP (50 μM) or the purinergic blockers KN-62 (10 μM) and Ip5I (10 μM). Incubating P. berghei infected cells with KN-62 (200 μM) resulted in a changed profile of merozoite surface protein 1 (MSP1) processing as revealed by western blot assays. Moreover incubating P. berghei for 17 h with KN-62 (10 μM) led to an increase in rings forms (82% ± 4, n = 11) and a decrease in trophozoite forms (18% ± 4, n = 11).ConclusionsThe data clearly show that purinergic signalling modulates P. berghei protease(s) activity and that MSP1 is one target in this pathway.

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“…Furthermore, bafilomycin A1, which prevents vesicular neurotransmitter release (Floor et al, 1990;Kuromi & Kidokoro, 2000) and reduced stimulation-evoked calcium transients in neurons (present study), was inefficient in reducing stimulationinduced calcium influx into OECs. In contrast, bafilomycin A1 leads to an increase in the amplitude of the calcium transients, which may be due to an impairment of calcium uptake into acidic organelles during elevated calcium concentrations resulting in a reduced calcium buffer capacity (Beraldo et al, 2001;Lopez et al, 2005). Bafilomycin A1 may also affect H + pumps of the plasma membrane (Pappas & Ransom, 1993), but whether this may account for the increase in amplitude of the stimulation-induced calcium transients in OECs remains unclear.…”

Section: Calcium Signalling In Oecs Is Neurotransmitter-independentmentioning

confidence: 99%

A novel neurotransmitter‐independent communication pathway between axons and glial cells

Hartl

Heil

Hirsekorn

et al. 2007

Eur J of Neuroscience

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Recent studies have provided evidence that transmitters released by neurons can activate glial receptors and stimulate calcium signalling in glial cells. Glial calcium signalling, in turn, may affect neuronal performance such as long-term changes in synaptic efficacy. Olfactory ensheathing cells (OECs) are a special glial cell type in vertebrates and insects and promote axon growth in the developing and mature nervous system. Physiological properties of OECs, however, have not been studied so far in detail. We measured changes in the calcium concentration in OECs of the moth Manduca sexta, in situ and in vivo. Electrical stimulation of olfactory receptor neurons in pupae or odour stimulation of receptor neurons in adults resulted in calcium transients in OECs. Olfactory receptor axons release acetylcholine; however, application of acetylcholine or other transmitters such as glutamate, GABA or nitric oxide did not induce calcium transients in OECs. Upon nerve stimulation, extracellular potassium rose by several millimolar as measured with potassium-sensitive microelectrodes. When potassium in the perfusion saline was increased from 4 to 10 mM or higher, voltage-dependent calcium transients in OECs that resembled stimulation-induced calcium transients were evoked. Blocking neuronal potassium channels with TEA reduced both the stimulation-induced increases in extracellular potassium and the calcium transients in OECs, whereas calcium transients in receptor axons were augmented. Our results show for the first time that accumulation of potassium, released by electrically active axons, is sufficient to evoke voltage-dependent calcium influx into glial cells, whereas neurotransmitters appear not to be involved in this neuron-glia communication in Manduca.

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Signal transduction in red bloodcells of the lizards Ameiva ameiva and Tupinambis merianae (Squamata, Teiidae)

Cited by 17 publications

References 29 publications

Exosome Release Is Regulated by a Calcium-dependent Mechanism in K562 Cells

Exosome Release Is Regulated by a Calcium-dependent Mechanism in K562 Cells

Extracellular ATP triggers proteolysis and cytosolic Ca2+ rise in Plasmodium berghei and Plasmodium yoelii malaria parasites

A novel neurotransmitter‐independent communication pathway between axons and glial cells

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