Calbindin-D(28k) buffers intracellular calcium and promotes resistance to degeneration in PC12 cells

Anne McMahon; Brendan S. Wong; Anthony M. Iacopino; May C. Ng; Susan Chi; Dwight C. German

doi:10.1016/S0169-328X(97)00305-7

Calbindin-D(28k) buffers intracellular calcium and promotes resistance to degeneration in PC12 cells

Anne McMahon, Brendan S. Wong, Anthony M. Iacopino, May C. Ng, Susan Chi, Dwight C. German

Research output: Contribution to journal › Article › peer-review

20 Scopus citations

Abstract

The calcium-binding protein calbindin-D(28k) (CB) has been hypothesized to function, in part, as a neuroprotective protein. CB is localized within nerve cells that are often less vulnerable to degeneration in patients with Alzheimer's disease and Parkinson's disease, and cells containing CB can buffer intracellular calcium concentrations ([Ca²⁺](i). The present study was designed to directly test the hypothesis that CB can protect cells from degeneration by reducing [Ca²⁺](i). PC12 cells, transfected to express different levels of CB, were found to be significantly less vulnerable to degeneration caused by serum withdrawal, glutamate, and the neurotoxin 1-methyl-4-phenylpyridinium (MPP⁺). However, CB did not protect cells from degeneration caused by the calcium ionophore A23187. CB-transfected cells exhibited reduced elevations in [Ca²⁺](i) following treatment with bradykinin, or ATP compared to non-CB-containing cells. These data indicate that CB can protect cells from degeneration caused by certain conditions, and it reduces elevations in [Ca²⁺](i) caused by influx from extracellular sources.

Original language	English (US)
Pages (from-to)	56-63
Number of pages	8
Journal	Molecular Brain Research
Volume	54
Issue number	1
DOIs	https://doi.org/10.1016/S0169-328X(97)00305-7
State	Published - Feb 1998

Keywords

A23187
Calcium imaging
Glutamate
Serum withdrawal

ASJC Scopus subject areas

Molecular Biology
Cellular and Molecular Neuroscience

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10.1016/S0169-328X(97)00305-7

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title = "Calbindin-D(28k) buffers intracellular calcium and promotes resistance to degeneration in PC12 cells",

abstract = "The calcium-binding protein calbindin-D(28k) (CB) has been hypothesized to function, in part, as a neuroprotective protein. CB is localized within nerve cells that are often less vulnerable to degeneration in patients with Alzheimer's disease and Parkinson's disease, and cells containing CB can buffer intracellular calcium concentrations ([Ca2+](i). The present study was designed to directly test the hypothesis that CB can protect cells from degeneration by reducing [Ca2+](i). PC12 cells, transfected to express different levels of CB, were found to be significantly less vulnerable to degeneration caused by serum withdrawal, glutamate, and the neurotoxin 1-methyl-4-phenylpyridinium (MPP+). However, CB did not protect cells from degeneration caused by the calcium ionophore A23187. CB-transfected cells exhibited reduced elevations in [Ca2+](i) following treatment with bradykinin, or ATP compared to non-CB-containing cells. These data indicate that CB can protect cells from degeneration caused by certain conditions, and it reduces elevations in [Ca2+](i) caused by influx from extracellular sources.",

keywords = "A23187, Calcium imaging, Glutamate, Serum withdrawal",

author = "Anne McMahon and Wong, {Brendan S.} and Iacopino, {Anthony M.} and Ng, {May C.} and Susan Chi and German, {Dwight C.}",

note = "Funding Information: Research supported by NIH grant NS30406, and the Carl J. and Hortense M. Thomsen Chair in Alzheimer's Disease Research. The authors wish to thank Mike Lee for technical assistance, and Judy Burdette for secretarial assistance.",

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AU - Iacopino, Anthony M.

AU - Ng, May C.

AU - Chi, Susan

AU - German, Dwight C.

N1 - Funding Information: Research supported by NIH grant NS30406, and the Carl J. and Hortense M. Thomsen Chair in Alzheimer's Disease Research. The authors wish to thank Mike Lee for technical assistance, and Judy Burdette for secretarial assistance.

PY - 1998/2

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N2 - The calcium-binding protein calbindin-D(28k) (CB) has been hypothesized to function, in part, as a neuroprotective protein. CB is localized within nerve cells that are often less vulnerable to degeneration in patients with Alzheimer's disease and Parkinson's disease, and cells containing CB can buffer intracellular calcium concentrations ([Ca2+](i). The present study was designed to directly test the hypothesis that CB can protect cells from degeneration by reducing [Ca2+](i). PC12 cells, transfected to express different levels of CB, were found to be significantly less vulnerable to degeneration caused by serum withdrawal, glutamate, and the neurotoxin 1-methyl-4-phenylpyridinium (MPP+). However, CB did not protect cells from degeneration caused by the calcium ionophore A23187. CB-transfected cells exhibited reduced elevations in [Ca2+](i) following treatment with bradykinin, or ATP compared to non-CB-containing cells. These data indicate that CB can protect cells from degeneration caused by certain conditions, and it reduces elevations in [Ca2+](i) caused by influx from extracellular sources.

AB - The calcium-binding protein calbindin-D(28k) (CB) has been hypothesized to function, in part, as a neuroprotective protein. CB is localized within nerve cells that are often less vulnerable to degeneration in patients with Alzheimer's disease and Parkinson's disease, and cells containing CB can buffer intracellular calcium concentrations ([Ca2+](i). The present study was designed to directly test the hypothesis that CB can protect cells from degeneration by reducing [Ca2+](i). PC12 cells, transfected to express different levels of CB, were found to be significantly less vulnerable to degeneration caused by serum withdrawal, glutamate, and the neurotoxin 1-methyl-4-phenylpyridinium (MPP+). However, CB did not protect cells from degeneration caused by the calcium ionophore A23187. CB-transfected cells exhibited reduced elevations in [Ca2+](i) following treatment with bradykinin, or ATP compared to non-CB-containing cells. These data indicate that CB can protect cells from degeneration caused by certain conditions, and it reduces elevations in [Ca2+](i) caused by influx from extracellular sources.

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Calbindin-D(28k) buffers intracellular calcium and promotes resistance to degeneration in PC12 cells

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