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Type 3 inositol 1,4,5-trisphosphate receptor modulates cell death.

S Blackshaw¹, A Sawa, A H Sharp

¹Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|July 6, 2000

Summary

Type 3 inositol trisphosphate receptors (IP(3)R3) play a key role in programmed cell death (apoptosis). Increased IP(3)R3 levels are observed across diverse tissues undergoing apoptosis, suggesting a broad involvement in cell death mechanisms.

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Area of Science:

Cell Biology
Molecular Biology
Neuroscience

Background:

The cellular mechanisms of calcium entry regulating cell proliferation and apoptosis remain unclear.
Previous research indicated selective augmentation of type 3 inositol (1,4,5) trisphosphate receptors (IP(3)R3) in lymphocytes during programmed cell death.

Purpose of the Study:

To investigate the role of IP(3)R3 in various apoptotic paradigms across different tissues.
To determine if IP(3)R3 augmentation is a common feature of apoptosis.

Main Methods:

Analysis of IP(3)R3 mRNA and protein levels in diverse apoptotic models.
Utilizing antisense oligonucleotides to inhibit IP(3)R3 function in specific cell types.

Main Results:

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IP(3)R3 mRNA and protein levels were found to increase in multiple tissues undergoing apoptosis, including cerebellar granule cells, dorsal root ganglia, hair follicles, and intestinal villi.

Elevated IP(3)R3 levels were also observed in neurotoxic damage induced by kainate.

In chick dorsal root ganglia neurons, antisense inhibition of IP(3)R3 selectively prevented nerve growth factor deprivation-induced apoptosis.

Conclusions:

Type 3 inositol trisphosphate receptors (IP(3)R3) are actively involved in the process of cell death (apoptosis).
The augmentation of IP(3)R3 is a conserved mechanism observed in diverse tissues during apoptosis.