1998
DOI: 10.1016/s0169-328x(98)00217-4
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Transforming growth factor-β inhibits apoptosis induced by β-amyloid peptide fragment 25–35 in cultured neuronal cells

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Cited by 43 publications
(32 citation statements)
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“…A similar transient expression pattern was previously reported in rat hippocampal neurons exposed to Ab [25][26][27][28][29][30][31][32][33][34][35] (Kim et al, 1998). It was proposed that this initial increase in Bcl-2 expression is a nonsustainable cellular response to the apoptotic pathways induced by Ab (Kim et al, 1998). Our observations indicate that when afobazole is applied along with Ab 25-35 , Bcl-2 levels do not drop below control at the 48-hour time point.…”
Section: Discussionsupporting
confidence: 76%
See 1 more Smart Citation
“…A similar transient expression pattern was previously reported in rat hippocampal neurons exposed to Ab [25][26][27][28][29][30][31][32][33][34][35] (Kim et al, 1998). It was proposed that this initial increase in Bcl-2 expression is a nonsustainable cellular response to the apoptotic pathways induced by Ab (Kim et al, 1998). Our observations indicate that when afobazole is applied along with Ab 25-35 , Bcl-2 levels do not drop below control at the 48-hour time point.…”
Section: Discussionsupporting
confidence: 76%
“…Our data indicate that there is a biphasic change in Bcl-2 levels in neurons following application of Ab [25][26][27][28][29][30][31][32][33][34][35] with an initial increase at 24 hours followed by a suppression of Bcl-2 expression at 48 hours. A similar transient expression pattern was previously reported in rat hippocampal neurons exposed to Ab [25][26][27][28][29][30][31][32][33][34][35] (Kim et al, 1998). It was proposed that this initial increase in Bcl-2 expression is a nonsustainable cellular response to the apoptotic pathways induced by Ab (Kim et al, 1998).…”
Section: Discussionsupporting
confidence: 75%
“…Inhibition of TGF-␤ activity facilitated cerebral inflammation and acute neuronal death in ME7-infected mice (9). IL-10 has been reported to have a neuroprotective role by blocking caspase-3-like activity (41), and TGF-␤ also promotes neuronal survival by upregulating anti-apoptotic Bcl-2 family proteins (42). Therefore, an earlier expression of these anti-inflammatory cytokines may partially contribute to the prolonged survival of CD14 Ϫ/Ϫ mice.…”
Section: Prolonged Survival Of Prion-infected Cd14mentioning
confidence: 99%
“…The previously demonstrated ability of ␣ 2 M to bind and neutralize the activity of TGF-␤ (12, 13, 27-29) may be detrimental in AD, because TGF-␤ stimulates A␤ clearance by microglial cells and reduces A␤ accumulation in the brain parenchyma of mice that overexpress human APP (30). Furthermore, TGF-␤ has been reported to antagonize the cytotoxic activity of A␤ (29,31,32).Another mechanism whereby ␣ 2 M may regulate AD progression involves its ability to bind A␤, forming a complex that is internalized by the ␣ 2 M receptor, low density lipoprotein receptor-related protein (LRP) and then degraded (33-35). Du et al.…”
mentioning
confidence: 99%
“…The previously demonstrated ability of ␣ 2 M to bind and neutralize the activity of TGF-␤ (12, 13, 27-29) may be detrimental in AD, because TGF-␤ stimulates A␤ clearance by microglial cells and reduces A␤ accumulation in the brain parenchyma of mice that overexpress human APP (30). Furthermore, TGF-␤ has been reported to antagonize the cytotoxic activity of A␤ (29,31,32).…”
mentioning
confidence: 99%