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- Ata, K A, et al.
(författare)
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Expression of transforming growth factor-beta1, 2, 3 isoforms and type I and II receptors in acute focal cerebral ischemia: an immunohistochemical study in rat after transient and permanent occlusion of middle cerebral artery.
- 1999
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Ingår i: Acta neuropathologica. - 0001-6322. ; 97:5, s. 447-55
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Tidskriftsartikel (refereegranskat)abstract
- Transforming growth factor beta (TGF-beta) is involved in the modulation of cell growth, differentiation and repair following injury of various organs. Previous studies on human autopsy material have indicated that TGF-beta isoforms-beta1, -beta2 and -beta3, and TGF-beta receptor type I are expressed in various cells of necrotizing brain lesions like infarction and abscess. The present immunohistochemical study was designed to investigate changes that may occur with regard to TGF-beta and its receptors type I and II in a rat model of focal brain ischemia induced by transient or permanent occlusion of the middle cerebral artery. Our findings indicate that at days 1 and 3 following such transient and permanent ischemia there is an up-regulation of TGF-beta isoforms -beta1, -beta2 and -beta3, and TGF-beta receptor types I and II mainly in the perifocal neurons, reactive astroglial cells, endothelial cells and macrophages.
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| 2. |
- Lennmyr, Fredrik, et al.
(författare)
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Expression of vascular endothelial growth factor (VEGF) and its receptors (Flt-1 and Flk-1) following permanent and transient occlusion of the middle cerebral artery in the rat.
- 1998
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Ingår i: Journal of neuropathology and experimental neurology. - 0022-3069 .- 1554-6578. ; 57:9, s. 874-82
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Tidskriftsartikel (refereegranskat)abstract
- Vascular endothelial growth factor (VEGF) is a known endothelial mitogen and a potent enhancer of vascular permeability although its role in focal cerebral ischemia is still not completely understood. The present report describes the immunohistochemical distribution of VEGF and its 2 receptors, Flt-1 and Flk-1 at day 1 and 3 following permanent and transient middle cerebral artery occlusion (MCAO) in the rat. A bilateral increase in VEGF immunoreactivity, particularly in neurons and blood vessels, was seen in both the experimental designs by day 1. By day 3, the immunoreactivity was restricted chiefly to the lesion side, where reaction was most prominent in the border zones of the infarcts. Immunoreaction to VEGF was more pronounced in cases of permanent MCAO than in transient MCAO. Flt-1 reaction was increased in neurons, glial and endothelial cells after both transient and permanent MCAO. Immunoreactivity to Flk-1 was prominent in glial cells and was present to some extent in endothelial cells. These findings indicate an early upregulation of VEGF and its receptors after permanent as well as transient focal cerebral ischemia in the rat.
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| 3. |
- Ata, A K, et al.
(författare)
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Expression of various TGF-beta isoforms and type I receptor in necrotizing human brain lesions.
- 1997
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Ingår i: Acta neuropathologica. - 0001-6322. ; 93:4, s. 326-33
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Tidskriftsartikel (refereegranskat)abstract
- It is known that transforming growth factor beta (TGF-beta) is involved in the modulation of cell growth, differentiation, and repair following injury. We performed an immunohistochemical study of human brain autopsy and biopsy material for the expression of TGF-beta isoforms beta 1, beta 2 and beta 3, and TGF-beta receptor (T beta R) type I in different cells of necrotizing lesions such as infarction and abscess, and compared them with controls. Various cell types, both inside and in the proximity of lesions, showed immunoreactivity indicating the presence of all three isoforms. Significant values of immunoreaction for various TGF-beta s and T beta R-I were observed in cells such as astrocytes, macrophages, neurons, microvascular endothelial cells, and granulocytes. In the control cases, comprising biopsy material without necrotizing lesions, a prominent TGF-beta 2 immunoreactivity was observed in glial cells and neurons. TGF-beta 1 and TGF-beta 3 reactivity in controls, when compared with TGF-beta 2, was less. T beta R-I antiserum showed clear and distinct signals in the same type of cells as for TGF-beta s in the necrotizing lesions with varying values of significance. Our findings suggest that TGF-beta s and their receptor type I are involved in reactive processes around necrotizing human brain lesions like glial and macrophage responses, angiogenesis, and deposition of extracellular matrix.
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