![]() ![]() | [Frontiers in Bioscience 1, d324-339, November 1, 1996] Reprints PubMed CAVEAT LECTOR |
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INVASION OF HUMAN GLIOMA: ROLE OF EXTRACELLULAR MATRIX PROTEINS Shravan K. Chintala, Ph.D. and Jasti S. Rao, Ph.D. Department of Neurosurgery, Box 064, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA.
Received 9/28/96; Accepted 10/17/96; On-line 11/01/96
![]() The extracellular matrix (ECM) is a dynamic milieu that plays a pivotal role in regulating cellular functions during normal and pathological remodeling processes such as embryonic development, tissue repair, inflammation, tumor invasion, and metastasis. Although the ECM contains mainly collagens and noncollagenous glycoproteins such as glycosaminoglycans and proteoglycans, its composition is probably unique for each cell type within an organ. In the nervous system, in contrast to other organ systems, the structure and function of the ECM have not yet been completely determined. The brain is largely free of a well-defined ECM, except where mesodermally derived endothelial cells invade the CNS to establish vasculature. The parenchyma of the CNS, however, appear to be filled with a relatively amorphous matrix that contains mainly hyaluronic acid (1) and little collagen and other fibrous proteins. A well-defined ECM exists in the form of a true basement membrane, cerebral vasculature, and the glial limitans externa. The latter is a basement membrane that covers the brain's entire cortical surface and also separates astrocyte foot processes from pial cells and the subarachnoid space (2). The cerebral vascular basement membrane, which surrounds the blood vessels of the brain, contains type I, III, and IV collagens, fibronectin, laminin, and heparan sulfate proteoglycans (Table 1). Recent in vitro studies have shown that both immature astrocytes and normal leptomeningial cells can synthesize basement membrane molecules. For this review we limit our focus to the ECM components of the human brain that have been proposed as potential candidates for mediating glioma cell invasion.
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