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- Czigner, Andrea, et al.
(författare)
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Dynamics and regional distribution of c-fos protein expression in rat brain after a closed head injury
- 2004
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Ingår i: International Journal of Molecular Medicine. - : Spandidos Publications. - 1107-3756 .- 1791-244X. ; 14:2, s. 247-252
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Tidskriftsartikel (refereegranskat)abstract
- The objective of this study was to define the time- and brain-area-related distribution of c-fos expression in the brain during the first 24 h following a closed head injury in rats. In the control groups (n = 32), only a few c-fos positive nuclei were observed in the brain and the c-fos staining did not change during the next 24 h. In the closed head injury group c-fos-positive cells were rare in the brain regions during the first 30 min. During the next 2 h, the number of c-fos-positive cells increased rapidly in the basal ganglions, the ventricular ependyma cells the corticospinal tract, the area postrema, the cerebral neocortex, and the corpus callosum. The increase was highest in the corpus callosum (317 +/- 44.5 mm(-2)), in the thalamic reticular nucleus (474.8 +/- 49.2 mm(-2)), in the dentate hilus (1090 +/- 187 mm(-2)) and in the cerebral neocortex (992 +/- 93 mm(-2)). Thereafter, the elevated c-fos expression gradually decreased and at 6 h post-closed head injury no significant differences were observed between the controls and the trauma group. We conclude that a closed head injury induces a large, transient increase of c-fos expression in the brain. Since the observed time course and regional differences in c-fos expression are in good agreement with the cognitive and memory deficits observed after human TBI it can be utilized in further investigations, especially to test the effects of various forms of pharmacological or cellular therapy.
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- Dimberg, J, et al.
(författare)
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Decreased levels of precursor transforming growth factor beta(1) in human colorectal cancer
- 2001
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Ingår i: International Journal of Molecular Medicine. - 1107-3756 .- 1791-244X. ; 7:6, s. 597-601
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Tidskriftsartikel (refereegranskat)abstract
- Transforming growth factor (TGF) beta (1) is a growth factor with wide-ranging effects on proliferation, differentiation, immunosuppression, apoptosis and matrix remodelling. TGF beta (1) seems to have an antitumorigenic role in the gastrointestinal tract but may also be associated with the development of colorectal cancer. Initially, TGF beta (1) is produced in a latent (precursor) form in epithelial cells and then is activated by a not clearly understood multistep process. In this study, we analysed precursor TGF beta (1) protein expression (n=40) and TGF beta (1) gene expression (n=49) in human colorectal adenocarcinomas and 49 normal adjacent tissue. Out of these 49 normal tissues 40 were matched. Western blot analysis revealed that the precursor TGF beta (1) protein levels were generally lower in colorectal cancerous tissue compared to adjacent noncancerous tissue (P <0.001). Furthermore, with real-time PCR our results cannot reflect a statistically significant difference in TGF beta (1) gene expression between the tumour tissue and normal tissue. These finds indicate that it is likely that there are mechanisms which control precursor TGF beta (1) protein expression by factor(s) at the level of pre-translation of the TGF beta (1) transcript and/or at the level of post-translation of the TGF beta (1) protein in the tumours. This process may be related to carcinogenesis and poses the question whether the suppression of the precursor TGF beta (1) is an early event, in vivo, in the human colorectal adenoma-carcinoma sequence.
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- Hägg, Maria, et al.
(författare)
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EGF and dextran-conjugated EGF induces differential phosphorylation of the EGF receptor
- 2002
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Ingår i: International Journal of Molecular Medicine. - 1107-3756 .- 1791-244X. ; 10:5, s. 655-659
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Tidskriftsartikel (refereegranskat)abstract
- Dextran-conjugated EGF (EGF-dextran) has a potential use for targeted radionuclide therapy of tumors that overexpress the epidermal growth factor receptor (EGFR). There are plans to treat both bladder carcinomas and malignant gliomas with local injections of radiolabeled EGF-dextran since these tumors often express high levels of EGFR. In this report we show that EGF and EGF-dextran differentially activate the EGFR. In the human glioma cell line U-343, activation of the serine/threonine kinases Erk and Akt is identical upon stimulation with EGF or EGF-dextran. However, the effect on phospholipase Cgamma1 (PLCgamma1) phosphorylation differs. In cells stimulated with EGF-dextran, the PLCgamma1 phosphorylation is lower than in cells stimulated with EGF. This observation could be explained by the fact that the PLCgamma1 association sites in the EGFR, tyrosine residues 992 and 1173, were phosphorylated to a lower degree when the receptor was stimulated with EGF-dextran as compared to with EGF.
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