The Journal of Neuroscience, October 22, 2008, 28(43):10983-10989; doi:10.1523/JNEUROSCI.3545-08.2008
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Brief Communications
The Basic Helix-Loop-Helix Transcription Factor Olig2 Is Critical for Reactive Astrocyte Proliferation after Cortical Injury
Ying Chen,1,4 *
Darryl K. Miles,1,4 *
ThaoNguyen Hoang,1,4
Jian Shi,1,4
Edward Hurlock,1,4
Steven G. Kernie,1,2,4 and
Q. Richard Lu1,3,4
Departments of 1Developmental Biology, 2Pediatrics, and 3Molecular Biology, and 4Kent Waldrep Foundation Center for Basic Neuroscience Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390
Correspondence should be addressed to Q. Richard Lu at the above address. Email: qrichard.lu{at}utsouthwestern.edu
The mechanisms underlying the formation of the glial scar after injury are poorly understood. In this report, we demonstrate that after cortical injury Olig2 is upregulated in reactive astrocytes coincident with proliferation of these cells. Short-term lineage tracing studies with glial subtype-restricted transgenic reporter lines indicate that Olig2-expressing cells in the astroglial but not the oligodendroglial lineage are the essential source of reactive astrocytes. In addition, cortical Olig2 ablation results in a decrease in proliferation of reactive astrocytes in response to injury. Cell-type-specific mutagenesis indicates that Olig2 ablation in GFAP+ astrocytes and their precursors rather than in neuronal or oligodendroglial cells is responsible for the reduction of reactive astrocyte proliferation. Thus, our studies suggest that Olig2 is critical for postinjury gliosis.
Key words: bHLH transcription factor; Olig2; conditional knock-out mice; reactive astrocytes; proliferation; cortical injury
Received July 28, 2008;
revised Sept. 16, 2008;
accepted Sept. 22, 2008.
Correspondence should be addressed to Q. Richard Lu at the above address. Email: qrichard.lu{at}utsouthwestern.edu
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