Enhanced Expression of the Developmentally Regulated Extracellular Matrix Molecule Tenascin Following Adult Brain Injury

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 89; no. 7; pp. 2634 - 2638
• Main Authors: Laywell, Eric D., Dorries, Ulrich, Bartsch, Udo, Faissner, Andreas, Schachner, Melitta, Steindler, Dennis A.
• Format: Journal Article
• Language: English
• Published: Washington, DC National Academy of Sciences of the United States of America 01.04.1992; National Acad Sciences; National Academy of Sciences
• Subjects: Adults; Age Factors; Animals; Antibodies; Astrocytes; Biological and medical sciences; Brain; Brain Injuries - physiopathology; Cell Adhesion Molecules, Neuronal - metabolism; Cellular biology; Central nervous system; Cerebellar Cortex - metabolism; Cerebellum; Cerebral Cortex - metabolism; Complementary RNA; Epithelial cells; Extracellular Matrix Proteins - metabolism; Fundamental and applied biological sciences. Psychology; Gene Expression; Glial Fibrillary Acidic Protein - metabolism; Immunoenzyme Techniques; In situ hybridization; Injuries; Lesions; Mice; Mice, Inbred Strains; Molecular and cellular biology; Molecular genetics; Molecules; Nervous system; Nucleic Acid Hybridization; RNA, Messenger - genetics; Tenascin; Neurite; Rodentia; Glycoproteins; Gene expression; Regeneration; Vertebrata; Regulation(control); Mammalia; Mouse; Development; Extracellular matrix; Lesion; Brain (vertebrata)
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.89.7.2634

Tenascin is an extracellular matrix molecule synthesized and released by young astrocytes during embryonic and early postnatal development of the nervous system, and it is concentrated in boundaries around emerging functional neuronal units. In the adult nervous system, tenascin can be detected only in very low levels. Distinct spatial and temporal distributions of tenascin during developmental events suggest a role in the guidance and/or segregation of neurons and their processes within incipient functional patterns. We show here, using in situ hybridization and immunocytochemistry, that stab wounds of the adult mouse cerebellar and cerebral cortices result in an enhanced expression of tenascin in a discrete region around the lesion site that is associated with a subset of glial fibrillary acidic protein-positive astrocytes. Tenascin up-regulation in the lesioned adult brain may be directly involved in failed regeneration or indirectly involved through its interactions with other glycoconjugates that either inhibit or facilitate neurite growth.