IL-10 promotes survival of microglia without activating Akt

Klemen Strle; Jian Hua Zhou; Suzanne R. Broussard; Homer D. Venters; Rodney W. Johnson; Gregory G Freund; Robert Dantzer; Keith W. Kelley

doi:10.1016/S0165-5728(01)00444-1

IL-10 promotes survival of microglia without activating Akt

Klemen Strle, Jian Hua Zhou, Suzanne R. Broussard, Homer D. Venters, Rodney W. Johnson, Gregory G Freund, Robert Dantzer, Keith W. Kelley

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

Abstract

IL-10 is an anti-inflammatory cytokine that has recently been shown to promote survival of neurons and glia. Here we establish that IL-10 induces phosphorylation of Stat3 on Tyr⁷⁰⁵ and serves as a survival factor for N13 microglial cells. Recombinant IL-10 (10 ng/ml) decreases growth factor withdrawal-induced apoptosis by 50%, as assessed by TUNEL. In contrast to IL-10, IGF-I increases enzymatic activity of PI 3-kinase and causes phosphorylation on serine⁴⁷³ of Akt but does not prevent microglial apoptosis. These data establish that IL-10 activates Stat3 and inhibits the mitochondrial pathway of cell death without activating the Akt cell survival pathway.

Original language	English (US)
Pages (from-to)	9-19
Number of pages	11
Journal	Journal of Neuroimmunology
Volume	122
Issue number	1-2
DOIs	https://doi.org/10.1016/S0165-5728(01)00444-1
State	Published - 2002

Keywords

Akt
Apoptosis
IGF-I
IL-10
Phosphatidylinositol 3′ -kinase
Stat3

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

Online availability

10.1016/S0165-5728(01)00444-1

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@article{47db611955df4850a8205526450514a6,

title = "IL-10 promotes survival of microglia without activating Akt",

abstract = "IL-10 is an anti-inflammatory cytokine that has recently been shown to promote survival of neurons and glia. Here we establish that IL-10 induces phosphorylation of Stat3 on Tyr705 and serves as a survival factor for N13 microglial cells. Recombinant IL-10 (10 ng/ml) decreases growth factor withdrawal-induced apoptosis by 50%, as assessed by TUNEL. In contrast to IL-10, IGF-I increases enzymatic activity of PI 3-kinase and causes phosphorylation on serine473 of Akt but does not prevent microglial apoptosis. These data establish that IL-10 activates Stat3 and inhibits the mitochondrial pathway of cell death without activating the Akt cell survival pathway.",

keywords = "Akt, Apoptosis, IGF-I, IL-10, Phosphatidylinositol 3′ -kinase, Stat3",

author = "Klemen Strle and Zhou, {Jian Hua} and Broussard, {Suzanne R.} and Venters, {Homer D.} and Johnson, {Rodney W.} and Freund, {Gregory G} and Robert Dantzer and Kelley, {Keith W.}",

note = "Funding Information: This research was supported by grants from the National Institutes of Health to K.W.K. (MH-51569) and R.W.J. (AG-16710), and by the Pioneering Research Project in Biotechnology financed by the Japanese Ministry of Agriculture, Forestry and Fisheries to K.W.K. ",

year = "2002",

doi = "10.1016/S0165-5728(01)00444-1",

language = "English (US)",

volume = "122",

pages = "9--19",

journal = "Advances in Neuroimmunology",

issn = "0165-5728",

publisher = "Elsevier",

number = "1-2",

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TY - JOUR

T1 - IL-10 promotes survival of microglia without activating Akt

AU - Strle, Klemen

AU - Zhou, Jian Hua

AU - Broussard, Suzanne R.

AU - Venters, Homer D.

AU - Johnson, Rodney W.

AU - Freund, Gregory G

AU - Dantzer, Robert

AU - Kelley, Keith W.

N1 - Funding Information: This research was supported by grants from the National Institutes of Health to K.W.K. (MH-51569) and R.W.J. (AG-16710), and by the Pioneering Research Project in Biotechnology financed by the Japanese Ministry of Agriculture, Forestry and Fisheries to K.W.K.

PY - 2002

Y1 - 2002

N2 - IL-10 is an anti-inflammatory cytokine that has recently been shown to promote survival of neurons and glia. Here we establish that IL-10 induces phosphorylation of Stat3 on Tyr705 and serves as a survival factor for N13 microglial cells. Recombinant IL-10 (10 ng/ml) decreases growth factor withdrawal-induced apoptosis by 50%, as assessed by TUNEL. In contrast to IL-10, IGF-I increases enzymatic activity of PI 3-kinase and causes phosphorylation on serine473 of Akt but does not prevent microglial apoptosis. These data establish that IL-10 activates Stat3 and inhibits the mitochondrial pathway of cell death without activating the Akt cell survival pathway.

AB - IL-10 is an anti-inflammatory cytokine that has recently been shown to promote survival of neurons and glia. Here we establish that IL-10 induces phosphorylation of Stat3 on Tyr705 and serves as a survival factor for N13 microglial cells. Recombinant IL-10 (10 ng/ml) decreases growth factor withdrawal-induced apoptosis by 50%, as assessed by TUNEL. In contrast to IL-10, IGF-I increases enzymatic activity of PI 3-kinase and causes phosphorylation on serine473 of Akt but does not prevent microglial apoptosis. These data establish that IL-10 activates Stat3 and inhibits the mitochondrial pathway of cell death without activating the Akt cell survival pathway.

KW - Akt

KW - Apoptosis

KW - IGF-I

KW - IL-10

KW - Phosphatidylinositol 3′ -kinase

KW - Stat3

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U2 - 10.1016/S0165-5728(01)00444-1

DO - 10.1016/S0165-5728(01)00444-1

M3 - Article

C2 - 11777539

AN - SCOPUS:0036147475

SN - 0165-5728

VL - 122

SP - 9

EP - 19

JO - Advances in Neuroimmunology

JF - Advances in Neuroimmunology

IS - 1-2

ER -

IL-10 promotes survival of microglia without activating Akt

Abstract

Keywords

ASJC Scopus subject areas

Online availability

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