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Expression of transforming growth factor-?1 and interleukin-1? mRNA in rat brain following transient forebrain ischemia

Wie�ner, C., Gehrmann, J., Lindholm, D., T�pper, R., Kreutzberg, G.W., Hossmann, K.A.·1993·Acta Neuropathologica
DOI 10.1007/bf00228578
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Abstract

Transforming growth factor-beta 1 (TGF-beta 1) and interleukin-1 beta mRNA expression were studied in rat brains after 30 min of global ischemia by in situ hybridization. Ischemia was produced by four-vessel occlusion followed by different recirculation times ranging between 15 min and 7 days. TGF-beta 1 mRNA could first be detected 3 days after ischemia in the hippocampus, in layers II/III of cortex, in the striatum and in parts of the ventral thalamus. At 7 days after recirculation a prominent increase in TGF-beta 1 mRNA was observed in the CA1 sector of the hippocampus. Induction of interleukin-1 beta mRNA, however, was less marked and limited to the rostral striatum 3 and 7 days after ischemia. TGF-beta 1 expression 7 days after ischemia correlated well with the histological localization of regions where neuronal degeneration and subsequent astrocytic and microglial activation had occurred. In adjacent brain sections, the distribution of TGF-beta 1 mRNA after 7 days closely resembled that of the immunostaining pattern of activated microglia, indicating that at this time point TGF-beta 1 mRNA was mainly produced by microglial cells. The late induction of TGF-beta 1 mRNA after ischemia points to an involvement in the persistent glial response rather than the initial glial activation. The differential pattern of interleukin-1 beta mRNA induction indicates regional variations of cytokine production after ischemic brain lesions.

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  • TGF-β and their receptors are expressed at low levels by both neurons and glial cells, and their expression is upregulated in response to a wide range of neuronal insults and during aging.

    “TGF-β and their receptors are expressed at low levels by both neurons and glial cells42,43, and their expression is upregulated in response to a wide range of neuronal insults and during aging44,45.”

    From Identification of a unique TGF-β–dependent molecular and functional signature in microglia (2014) · cites this paper as [45]

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Authors
Wie�ner, C., Gehrmann, J., Lindholm, D., T�pper, R., Kreutzberg, G. W., & Hossmann, K. A.
Venue
Acta Neuropathologica
Publisher
Springer Science and Business Media LLC
Published
1993-10
Volume
86
Issue
5
ISSN
  • 0001-6322
  • 1432-0533
DOI
10.1007/bf00228578
Cited by
94
References
0
Language
en
Licence
www.springer.com/tdm (tdm)

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