Signal transducers and activators of transcription: STATs-mediated mitochondrial neuroprotection

Hung Wen Lin, John W. Thompson, Kahlilia C. Morris, Miguel Perez-Pinzon

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Cerebral ischemia is defined as little or no blood flow in cerebral circulation, characterized by low tissue oxygen and glucose levels, which promotes neuronal mitochondria dysfunction leading to cell death. A strategy to counteract cerebral ischemia-induced neuronal cell death is ischemic preconditioning (IPC). IPC results in neuroprotection, which is conferred by a mild ischemic challenge prior to a normally lethal ischemic insult. Although many IPC-induced mechanisms have been described, many cellular and subcellular mechanisms remain undefined. Some reports have suggested key signal transduction pathways of IPC, such as activation of protein kinase C epsilon, mitogen-activated protein kinase, and hypoxia-inducible factors, that are likely involved in IPC-induced mitochondria mediated-neuroprotection. Moreover, recent findings suggest that signal transducers and activators of transcription (STATs), a family of transcription factors involved in many cellular activities, may be intimately involved in IPC-induced ischemic tolerance. In this review, we explore current signal transduction pathways involved in IPC-induced mitochondria mediated-neuroprotection, STAT activation in the mitochondria as it relates to IPC, and functional significance of STATs in cerebral ischemia.

Original languageEnglish
Pages (from-to)1853-1861
Number of pages9
JournalAntioxidants and Redox Signaling
Volume14
Issue number10
DOIs
StatePublished - May 15 2011

Fingerprint

Ischemic Preconditioning
Mitochondria
Transcription
Transducers
Signal transduction
Cell death
Brain Ischemia
Chemical activation
Protein Kinase C-epsilon
Mitogen-Activated Protein Kinases
Signal Transduction
Cerebrovascular Circulation
Blood
Cell Death
Transcription Factors
Tissue
Oxygen
Glucose
Neuroprotection
Transcriptional Activation

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology
  • Physiology
  • Clinical Biochemistry

Cite this

Signal transducers and activators of transcription : STATs-mediated mitochondrial neuroprotection. / Wen Lin, Hung; Thompson, John W.; Morris, Kahlilia C.; Perez-Pinzon, Miguel.

In: Antioxidants and Redox Signaling, Vol. 14, No. 10, 15.05.2011, p. 1853-1861.

Research output: Contribution to journalArticle

Wen Lin, Hung ; Thompson, John W. ; Morris, Kahlilia C. ; Perez-Pinzon, Miguel. / Signal transducers and activators of transcription : STATs-mediated mitochondrial neuroprotection. In: Antioxidants and Redox Signaling. 2011 ; Vol. 14, No. 10. pp. 1853-1861.
@article{d1008c8ed3bb42229a8ce9ad0a105334,
title = "Signal transducers and activators of transcription: STATs-mediated mitochondrial neuroprotection",
abstract = "Cerebral ischemia is defined as little or no blood flow in cerebral circulation, characterized by low tissue oxygen and glucose levels, which promotes neuronal mitochondria dysfunction leading to cell death. A strategy to counteract cerebral ischemia-induced neuronal cell death is ischemic preconditioning (IPC). IPC results in neuroprotection, which is conferred by a mild ischemic challenge prior to a normally lethal ischemic insult. Although many IPC-induced mechanisms have been described, many cellular and subcellular mechanisms remain undefined. Some reports have suggested key signal transduction pathways of IPC, such as activation of protein kinase C epsilon, mitogen-activated protein kinase, and hypoxia-inducible factors, that are likely involved in IPC-induced mitochondria mediated-neuroprotection. Moreover, recent findings suggest that signal transducers and activators of transcription (STATs), a family of transcription factors involved in many cellular activities, may be intimately involved in IPC-induced ischemic tolerance. In this review, we explore current signal transduction pathways involved in IPC-induced mitochondria mediated-neuroprotection, STAT activation in the mitochondria as it relates to IPC, and functional significance of STATs in cerebral ischemia.",
author = "{Wen Lin}, Hung and Thompson, {John W.} and Morris, {Kahlilia C.} and Miguel Perez-Pinzon",
year = "2011",
month = "5",
day = "15",
doi = "10.1089/ars.2010.3467",
language = "English",
volume = "14",
pages = "1853--1861",
journal = "Antioxidants and Redox Signaling",
issn = "1523-0864",
publisher = "Mary Ann Liebert Inc.",
number = "10",

}

TY - JOUR

T1 - Signal transducers and activators of transcription

T2 - STATs-mediated mitochondrial neuroprotection

AU - Wen Lin, Hung

AU - Thompson, John W.

AU - Morris, Kahlilia C.

AU - Perez-Pinzon, Miguel

PY - 2011/5/15

Y1 - 2011/5/15

N2 - Cerebral ischemia is defined as little or no blood flow in cerebral circulation, characterized by low tissue oxygen and glucose levels, which promotes neuronal mitochondria dysfunction leading to cell death. A strategy to counteract cerebral ischemia-induced neuronal cell death is ischemic preconditioning (IPC). IPC results in neuroprotection, which is conferred by a mild ischemic challenge prior to a normally lethal ischemic insult. Although many IPC-induced mechanisms have been described, many cellular and subcellular mechanisms remain undefined. Some reports have suggested key signal transduction pathways of IPC, such as activation of protein kinase C epsilon, mitogen-activated protein kinase, and hypoxia-inducible factors, that are likely involved in IPC-induced mitochondria mediated-neuroprotection. Moreover, recent findings suggest that signal transducers and activators of transcription (STATs), a family of transcription factors involved in many cellular activities, may be intimately involved in IPC-induced ischemic tolerance. In this review, we explore current signal transduction pathways involved in IPC-induced mitochondria mediated-neuroprotection, STAT activation in the mitochondria as it relates to IPC, and functional significance of STATs in cerebral ischemia.

AB - Cerebral ischemia is defined as little or no blood flow in cerebral circulation, characterized by low tissue oxygen and glucose levels, which promotes neuronal mitochondria dysfunction leading to cell death. A strategy to counteract cerebral ischemia-induced neuronal cell death is ischemic preconditioning (IPC). IPC results in neuroprotection, which is conferred by a mild ischemic challenge prior to a normally lethal ischemic insult. Although many IPC-induced mechanisms have been described, many cellular and subcellular mechanisms remain undefined. Some reports have suggested key signal transduction pathways of IPC, such as activation of protein kinase C epsilon, mitogen-activated protein kinase, and hypoxia-inducible factors, that are likely involved in IPC-induced mitochondria mediated-neuroprotection. Moreover, recent findings suggest that signal transducers and activators of transcription (STATs), a family of transcription factors involved in many cellular activities, may be intimately involved in IPC-induced ischemic tolerance. In this review, we explore current signal transduction pathways involved in IPC-induced mitochondria mediated-neuroprotection, STAT activation in the mitochondria as it relates to IPC, and functional significance of STATs in cerebral ischemia.

UR - http://www.scopus.com/inward/record.url?scp=79954579966&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79954579966&partnerID=8YFLogxK

U2 - 10.1089/ars.2010.3467

DO - 10.1089/ars.2010.3467

M3 - Article

C2 - 20712401

AN - SCOPUS:79954579966

VL - 14

SP - 1853

EP - 1861

JO - Antioxidants and Redox Signaling

JF - Antioxidants and Redox Signaling

SN - 1523-0864

IS - 10

ER -