What is the clinical evidence from this study?

Study design: Other. Intervention: Ins(2,4,5)P3 vs. ionomycin. Primary outcome: Ca2+ efflux rate and permeability.

What question did this study set out to answer?

To investigate the mechanism governing calcium permeability and release from undischarged intracellular stores in permeabilized L1210 cells stimulated by inositol 2,4,5-trisphosphate.

February 1, 1993Biochemical JournalOpen Access

A steady-state mechanism can account for the properties of inositol 2,4,5-trisphosphate-stimulated Ca2+ release from permeabilized L1210 cells

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Key result

Sub-maximal Ins(2,4,5)P3 concentrations stimulated Ca2+ efflux in permeabilized L1210 cells, indicating increased Ca2+ permeability consistent with a steady state model of Ca2+ release.

Population

Electroporated or digitonin-permeabilized L1210 cells

Comparison

Sub-maximal Ins(2,4,5)P3 concentrations vs Ionomycin

Design

Preclinical

Authors

JLJ W Loomis-HusselbeeUniversity of Cambridge ADA P DawsonJohn Innes Centre

Discussion

Member takes

Implication

Favors steady-state IP3 Ca2+ release in lymphoma cells; leaves open relevance to cardiomyocytes.

Key Points

To investigate the mechanism governing calcium permeability and release from undischarged intracellular stores in permeabilized L1210 cells stimulated by inositol 2,4,5-trisphosphate.
Permeabilized L1210 cells via electroporation or digitonin treatment.
Measured calcium-efflux rates after applying sub-maximal inositol 2,4,5-trisphosphate concentrations and inhibiting active transport with thapsigargin.
Compared efflux kinetics against ionomycin treatment in the presence and absence of an extravesicular calcium-buffering system.
Sub-maximal inositol 2,4,5-trisphosphate substantially accelerated calcium efflux following thapsigargin addition, consistent with an active steady-state pump-leak mechanism rather than quantal release.
Ionomycin induced comparable elevations in passive calcium permeability, although with markedly slower initial release rates than inositol 2,4,5-trisphosphate.
Buffering extravesicular calcium aligned inositol 2,4,5-trisphosphate release kinetics with ionomycin, demonstrating that initial rapid efflux depends partly on positive feedback from external calcium.

Structured PICO

Population

Electroporated or digitonin-permeabilized L1210 cells

Intervention

Sub-maximal Ins(2,4,5)P3 concentrations

Comparator

Ionomycin

Outcome

Ca2+-efflux rate after addition of thapsigarginsurrogate

The study demonstrates that Ins(2,4,5)P3-stimulated Ca2+ release in L1210 cells is more consistent with a steady state mechanism than a quantal model.

Cite This Study

Loomis-Husselbee et al. (1993) studied this question. Ins(2,4,5)P3 vs. ionomycin was evaluated on Ca2+ efflux rate and permeability. Sub-maximal Ins(2,4,5)P3 concentrations stimulated Ca2+ efflux in permeabilized L1210 cells, indicating increased Ca2+ permeability consistent with a steady state model of Ca2+ release.

synapsesocial.com/papers/6a975d47713b4e110fe32c0e https://doi.org/10.1042/bj2890861

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A steady-state mechanism can account for the properties of inositol 2,4,5-trisphosphate-stimulated Ca2+ release from permeabilized L1210 cells

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

A steady-state mechanism can account for the properties of inositol 2,4,5-trisphosphate-stimulated Ca2+ release from permeabilized L1210 cells

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

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