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Published online on May 21, 2004, 10.1073/pnas.0402140101
PNAS | June 1, 2004 | vol. 101 | no. 22 | 8384-8389


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Developmental Biology
Molecular diversity of astrocytes with implications for neurological disorders

Robert M. Bachoo *, {dagger} {ddagger}, Ryung S. Kim {ddagger}, §, Keith L. Ligon ¶, Elizabeth A. Maher *, Cameron Brennan *, Nathan Billings ¶, Suzanne Chan *, Cheng Li §, David H. Rowitch ¶, Wing H. Wong ||, and Ronald A. DePinho *, **, {dagger}{dagger}

Departments of *Medical Oncology and Pediatric Oncology, Dana–Farber Cancer Institute, 44 Binney Street, Boston, MA 02115; {dagger}Department of Neurology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115; Departments of §Biostatistics and ||Statistics, Harvard University, Boston, MA 02115; **Departments of Medicine and Genetics, Harvard Medical School, 25 Shattuck Street, Boston, MA 02115

Communicated by Webster K. Cavenee, University of California at San Diego, La Jolla, CA, March 29, 2004 (received for review January 5, 2004)

The astrocyte represents the most abundant yet least understood cell type of the CNS. Here, we use a stringent experimental strategy to molecularly define the astrocyte lineage by integrating microarray datasets across several in vitro model systems of astrocyte differentiation, primary astrocyte cultures, and various astrocyterich CNS structures. The intersection of astrocyte data sets, coupled with the application of nonastrocytic exclusion filters, yielded many astrocyte-specific genes possessing strikingly varied patterns of regional CNS expression. Annotation of these astrocyte-specific genes provides direct molecular documentation of the diverse physiological roles of the astrocyte lineage. This global perspective in the normal brain also provides a framework for how astrocytes may participate in the pathogenesis of common neurological disorders like Alzheimer's disease, Parkinson's disease, stroke, epilepsy, and primary brain tumors.

Abbreviations: NSC, neural stem cell; ISH, in situ hybridization; En, embryonic day n; Pn, postnatal day n; CNTF, ciliary neurotrophic factor; BMP, bone morphogenetic protein; PACAP, pituitary adenylate cyclase-activating polypeptide; LBFC, lower-bound fold change; SVM, support vector machine; SVZ, subventricular zone; GFAP, glial fibrillary acidic protein; ApoE, apolipoprotein E, UHC, unsupervised hierarchical clustering; R-SVM, recursive-supervised machine; CC, corpus callosum; GL, glial limitans; GM, gray matter; WM, white matter.

{ddagger} R.M.B. and R.S.K. contributed equally to this work.

{dagger}{dagger} To whom correspondence should be addressed at: Dana–Farber Cancer Institute, Harvard Medical School, 44 Binney Street (M413), Boston, MA 02115. E-mail: ron_depinho{at}dfci.harvard.edu.

© 2004 by The National Academy of Sciences of the USA


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