Modulation of canonical transient receptor potential channel 1 in the proliferation of oligodendrocyte precursor cells by the golli products of the myelin basic protein gene

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Modulation of canonical transient receptor potential channel 1 in the proliferation of oligodendrocyte precursor cells by the golli products of the myelin basic protein gene. / Paez, Pablo M; Fulton, Daniel; Spreuer, Vilma; Handley, Vance; Campagnoni, Anthony T.

In: The Journal of Neuroscience, Vol. 31, No. 10, 09.03.2011, p. 3625-37.

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@article{f6e4c6ee40654f439282aeecb2b29f80,
title = "Modulation of canonical transient receptor potential channel 1 in the proliferation of oligodendrocyte precursor cells by the golli products of the myelin basic protein gene",
abstract = "Golli proteins, products of the myelin basic protein gene, function as a new type of modulator of intracellular Ca(2+) levels in oligodendrocyte progenitor cells (OPCs). Because of this, they affect a number of Ca(2+)-dependent functions, such as OPC migration and process extension. To examine further the Ca(2+) channels regulated by golli, we studied the store-operated Ca(2+) channels (SOCCs) in OPCs and acute brain slice preparations from golli knock-out and golli-overexpressing mice. Our results showed that pharmacologically induced Ca(2+) release from intracellular stores evoked a significant extracellular Ca(2+) entry after store depletion in OPCs. They also indicated that, under these pharmacological conditions, golli promoted activation of Ca(2+) influx by SOCCs in cultured OPCs as well as in tissue slices. The canonical transient receptor potential family of Ca(2+) channels (TRPCs) has been postulated to be SOCC subunits in oligodendrocytes. Using a small interfering RNA knockdown approach, we provided direct evidence that TRPC1 is involved in store-operated Ca(2+) influx in OPCs and that it is modulated by golli. Furthermore, our data indicated that golli is probably associated with TRPC1 at OPC processes. Additionally, we found that TRPC1 expression is essential for the effects of golli on OPC proliferation. In summary, our data indicate a key role for golli proteins in the regulation of TRPC-mediated Ca(2+) influx, a finding that has profound consequences for the regulation of multiple biological processes in OPCs. More important, we have shown that extracellular Ca(2+) uptake through TRPC1 is an essential component in the mechanism of OPC proliferation.",
keywords = "Animals, Blotting, Western, Calcium, Cell Cycle, Cell Proliferation, Cells, Cultured, Cerebral Cortex, Immunohistochemistry, Mice, Mice, Transgenic, Myelin Basic Protein, Nerve Tissue Proteins, Oligodendroglia, Reverse Transcriptase Polymerase Chain Reaction, Stem Cells, TRPC Cation Channels, Transcription Factors",
author = "Paez, {Pablo M} and Daniel Fulton and Vilma Spreuer and Vance Handley and Campagnoni, {Anthony T}",
year = "2011",
month = mar,
day = "9",
doi = "10.1523/JNEUROSCI.4424-10.2011",
language = "English",
volume = "31",
pages = "3625--37",
journal = "The Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "10",

}

RIS

TY - JOUR

T1 - Modulation of canonical transient receptor potential channel 1 in the proliferation of oligodendrocyte precursor cells by the golli products of the myelin basic protein gene

AU - Paez, Pablo M

AU - Fulton, Daniel

AU - Spreuer, Vilma

AU - Handley, Vance

AU - Campagnoni, Anthony T

PY - 2011/3/9

Y1 - 2011/3/9

N2 - Golli proteins, products of the myelin basic protein gene, function as a new type of modulator of intracellular Ca(2+) levels in oligodendrocyte progenitor cells (OPCs). Because of this, they affect a number of Ca(2+)-dependent functions, such as OPC migration and process extension. To examine further the Ca(2+) channels regulated by golli, we studied the store-operated Ca(2+) channels (SOCCs) in OPCs and acute brain slice preparations from golli knock-out and golli-overexpressing mice. Our results showed that pharmacologically induced Ca(2+) release from intracellular stores evoked a significant extracellular Ca(2+) entry after store depletion in OPCs. They also indicated that, under these pharmacological conditions, golli promoted activation of Ca(2+) influx by SOCCs in cultured OPCs as well as in tissue slices. The canonical transient receptor potential family of Ca(2+) channels (TRPCs) has been postulated to be SOCC subunits in oligodendrocytes. Using a small interfering RNA knockdown approach, we provided direct evidence that TRPC1 is involved in store-operated Ca(2+) influx in OPCs and that it is modulated by golli. Furthermore, our data indicated that golli is probably associated with TRPC1 at OPC processes. Additionally, we found that TRPC1 expression is essential for the effects of golli on OPC proliferation. In summary, our data indicate a key role for golli proteins in the regulation of TRPC-mediated Ca(2+) influx, a finding that has profound consequences for the regulation of multiple biological processes in OPCs. More important, we have shown that extracellular Ca(2+) uptake through TRPC1 is an essential component in the mechanism of OPC proliferation.

AB - Golli proteins, products of the myelin basic protein gene, function as a new type of modulator of intracellular Ca(2+) levels in oligodendrocyte progenitor cells (OPCs). Because of this, they affect a number of Ca(2+)-dependent functions, such as OPC migration and process extension. To examine further the Ca(2+) channels regulated by golli, we studied the store-operated Ca(2+) channels (SOCCs) in OPCs and acute brain slice preparations from golli knock-out and golli-overexpressing mice. Our results showed that pharmacologically induced Ca(2+) release from intracellular stores evoked a significant extracellular Ca(2+) entry after store depletion in OPCs. They also indicated that, under these pharmacological conditions, golli promoted activation of Ca(2+) influx by SOCCs in cultured OPCs as well as in tissue slices. The canonical transient receptor potential family of Ca(2+) channels (TRPCs) has been postulated to be SOCC subunits in oligodendrocytes. Using a small interfering RNA knockdown approach, we provided direct evidence that TRPC1 is involved in store-operated Ca(2+) influx in OPCs and that it is modulated by golli. Furthermore, our data indicated that golli is probably associated with TRPC1 at OPC processes. Additionally, we found that TRPC1 expression is essential for the effects of golli on OPC proliferation. In summary, our data indicate a key role for golli proteins in the regulation of TRPC-mediated Ca(2+) influx, a finding that has profound consequences for the regulation of multiple biological processes in OPCs. More important, we have shown that extracellular Ca(2+) uptake through TRPC1 is an essential component in the mechanism of OPC proliferation.

KW - Animals

KW - Blotting, Western

KW - Calcium

KW - Cell Cycle

KW - Cell Proliferation

KW - Cells, Cultured

KW - Cerebral Cortex

KW - Immunohistochemistry

KW - Mice

KW - Mice, Transgenic

KW - Myelin Basic Protein

KW - Nerve Tissue Proteins

KW - Oligodendroglia

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Stem Cells

KW - TRPC Cation Channels

KW - Transcription Factors

U2 - 10.1523/JNEUROSCI.4424-10.2011

DO - 10.1523/JNEUROSCI.4424-10.2011

M3 - Article

C2 - 21389218

VL - 31

SP - 3625

EP - 3637

JO - The Journal of Neuroscience

JF - The Journal of Neuroscience

SN - 0270-6474

IS - 10

ER -