Glial CellsInjury selectively down-regulates the gene encoding for the Id4 transcription factor in primary cultures of forebrain astrocytesAndres-Barquin, Pedro J.1; Hernandez, Maria-Clemencia1; Israel, Mark A.1,2Author Information 1Preuss Laboratory for Molecular Neuro-Oncology, Brain Tumor Research Center, Department of Neurological Surgery, HSE 722, School of Medicine, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA 2Corresponding Author: Mark A. Israel ACKNOWLEDGEMENTS: We thank Lucy Avila and Norma Shipp for help with the manuscript, and Mark Galdo for technical support. This work was supported in part by grants from the Pediatric Brain Tumor Foundation of the United States, the Preuss Foundation, and the Nissen Foundation. P.J.A.-B. was supported by a postdoctoral research fellowship from the Spanish Ministry of Education and Culture. We regret we could not include many relevant citations due to space limitations. Received 30 September 1998; accepted 20 October 1998 NeuroReport: December 21st, 1998 - Volume 9 - Issue 18 - p 4075-4080 Buy Abstract ASTROGLIOSIS is an important component of the response to injury of the central nervous system (CNS). The Id family of helix-loop-helix (HLH) transcription factors has been implicated in the regulation of cellular differentiation in several different lineages and may contribute to the regulation of astrogliosis. We examined the expression of Id genes in primary cultures of mouse forebrain astrocytes under experimental conditions in which astrogliosis was elicited by mechanical injury. Astrocyte cultures expressed the four known members of the Id gene family, Id1, Id2, Id3, and Id4. After injury, at a time when astrocytes developed the characteristic phenotypic changes of astrogliosis, Id4 expression decreased dramatically. Id1, Id2, and Id3 mRNA levels did not change. These results identify Id4 as a candidate marker of astroglial activation in culture and suggest that Id4 expression plays a role in the process of astrogliosis. © 1998 Lippincott Williams & Wilkins, Inc.