Localization of Transforming Growth Factor-β1 and Receptor mRNA after Experimental Spinal Cord Injury

Transforming growth factor-β1 (TGFβ1) is a cytokine/growth factor found within the pathological central nervous system. TGFβ1 has been shown to inhibit the release of cytotoxic molecules from microglia and macrophages, decrease astrocyte proliferation, and promote neuron survival. Because of the rel...

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Bibliographic Details
Published inExperimental neurology Vol. 163; no. 1; pp. 220 - 230
Main Authors McTigue, Dana M., Popovich, Phillip G., Morgan, Todd E., Stokes, Bradford T.
Format Journal Article Conference Proceeding
LanguageEnglish
Published Amsterdam Elsevier Inc 01.05.2000
Elsevier
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Summary:Transforming growth factor-β1 (TGFβ1) is a cytokine/growth factor found within the pathological central nervous system. TGFβ1 has been shown to inhibit the release of cytotoxic molecules from microglia and macrophages, decrease astrocyte proliferation, and promote neuron survival. Because of the relevance of these actions to spinal cord injury, we examined TGFβ1 and its receptors βRI and βRII mRNA levels and localization within the contused rat spinal cord using in situ hybridization. At the lesion site, TGFβ1 mRNA peaked at 7 days postinjury and declined thereafter. Temporal and spatial localization of the βRI and βRII receptor mRNA closely mimicked that for TGFβ1 in the epicenter. TGFβ1, βRI, and βRII mRNAs also were elevated rostral and caudal to the injury, especially in regions known to contain activated microglia and degenerating axon profiles. Immunohistochemical staining of nearby sections confirmed that the highest levels of TGFβ1 and receptor mRNA corresponded to regions filled with activated microglia and macrophages. The similar expression pattern of TGFβ1, βRI, and βRII mRNA within the injured spinal cord suggests a local site of action. Since TGFβ1 can act as an immunosuppressant as well as a stimulant for growth factors and neurite sprouting, it likely plays an important role, both temporally and spatially, in orchestrating postinjury events within the spinal cord.
ISSN:0014-4886
1090-2430
DOI:10.1006/exnr.2000.7372