Expression of tumor necrosis factor alpha after focal cerebral ischaemia in the rat

Buttini, Manuel; Appel, Kurt; Sauter, André; Gebicke-Haerter, P.J.; Boddeke, Hendrikus

doi:10.1016/0306-4522(95)00414-9

Cited by 236 publications

(140 citation statements)

References 59 publications

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“…The increase in cytokine expression following stroke has previously been documented by 15 others [4], [20], [27], [36]. Levels of IL-1β mRNA were 34 times higher in ipsilateral hemisphere compared to the contralateral hemisphere in the present study.…”

Section: Discussionsupporting

confidence: 79%

“…ADAMTS-1 and -4 was found to be constitutively expressed by western blotting in sham operated and MCAo tissue however using a number of commercially antibodies available we were unable to detect ADAMTS-5 by western blotting (Figure 2). Basal expression of ADAMTS-4 mRNA was higher than that of ADAMTS-1 and -5 whereas TIMP-3 was expressed higher levels than the IL-1β, IL-1RA and TNF have all previously been shown to be increased in stroke [4], [16], [20]. We therefore examined the expression of these genes as evidence of the (Figure 5a).…”

Section: Adamts-1 -4 -5 and Timp-3 Mrna Were All Constitutively Exprmentioning

confidence: 97%

“…ADAMTS expression has been detected in the CNS [1], [17], [37] and is known to be altered in disease states [10], [22], [23]. 4 The chondroitin sulphate proteoglycans (CSPGs), aggrecan, brevican, neurocan, phosphacan, appican and versican are expressed in the brain [3], [12], [26], [28], [46] and are potential substrates for ADAMTSs. These CSPGs are important to brain structure through maintenance of the correct hydrodynamics and in their interactions with other ECM components.…”

Section: Introductionmentioning

confidence: 99%

“…The purpose of this study was to identify any changes in the expression of ADAMTS- [4], [20] and we have therefore included these genes in the study to confirm the extent of ischaemia and to allow comparison with ADAMTS and TIMP-3 expression. 6…”

Section: Introductionmentioning

confidence: 99%

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ADAMTS-1 and -4 are up-regulated following transient middle cerebral artery occlusion in the rat and their expression is modulated by TNF in cultured astrocytes

et al. 2006

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ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) enzymes are a recently described group of metalloproteinases. The substrates degraded by ADAMTS-1, -4 and -5 suggests that they play a role in turnover of extracellular matrix in the central nervous system (CNS). ADAMTS-1 is also known to exhibit anti-angiogenic activity. Their main endogenous inhibitor is tissue inhibitor of metalloproteinases (TIMP)-3.The present study was designed to investigate ADAMTS-1, -4 and -5 and TIMP-3 expression after experimental cerebral ischaemia and to examine whether cytokines known to be up-regulated in stroke could alter their expression by astrocytes in vitro.Focal cerebral ischaemia was induced by transient middle cerebral artery occlusion in the rat using the filament method.Our results demonstrate a significant increase in expression of ADAMTS-1 and -4 in the occluded hemisphere but no significant change in TIMP-3. This was accompanied by an increase in mRNA levels for interleukin (IL)-1β, IL-1 receptor antagonist (IL1ra) and tumour necrosis factor (TNF). ADAMTS-4 mRNA and protein was upregulated by TNF in primary human astrocyte cultures. The increased ADAMTS-1 and -4 in experimental stroke, together with no change in TIMP-3, may promote ECM breakdown after stroke, enabling infiltration of inflammatory cells and contribute to brain injury. In vitro studies suggest that the in vivo modulation of ADAMTS-1 and -4 may be controlled in part by TNF.3

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Section: Discussionsupporting

confidence: 79%

Section: Adamts-1 -4 -5 and Timp-3 Mrna Were All Constitutively Exprmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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ADAMTS-1 and -4 are up-regulated following transient middle cerebral artery occlusion in the rat and their expression is modulated by TNF in cultured astrocytes

et al. 2006

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“…Caspase-8, a protease triggering the proteolytic activation of downstream caspases and apoptosis resulting from overstimulation of p55 TNF or Fas/APO-1 receptors (Boldin et al, 1996;Muzio et al, 1996), recently has been demonstrated to cleave caspase-3 zymogen in a cell-free system (Muzio et al, 1997). Whether caspase-8 activation occurs as a result of TBI has not been determined; however, the early induction of TNF␣, the cytokine suggested to induce activation of caspase-8 (Boldin et al, 1996), has been well documented in various models of CNS trauma (Shohami et al, 1994;Yakovlev and Faden, 1995;Buttini et al, 1996;Fan et al, 1996;Wang et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Activation of CPP32-Like Caspases Contributes to Neuronal Apoptosis and Neurological Dysfunction after Traumatic Brain Injury

et al. 1997

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We examined the temporal profile of apoptosis after fluid percussion-induced traumatic brain injury (TBI) in rats and investigated the potential pathophysiological role of caspase-3-like proteases in this process. DNA fragmentation was observed in samples from injured cortex and hippocampus, but not from contralateral tissue, beginning 4 hr after TBI and continuing for at least 3 d. Double labeling of brain with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and an antibody directed to neuronal nuclear protein identified apoptotic neurons with high frequency in both traumatized rat cortex and hippocampus. Cytosolic extracts from injured cortex and hippocampus, but not from contralateral or control tissue, induced internucleosomal DNA fragmentation in isolated nuclei with temporal profiles consistent with those of DNA fragmentation observed in vivo. Caspase-3 mRNA levels, estimated by semiquantitative RT-PCR, were elevated fivefold in ipsilateral cortex and twofold in hippocampus by 24 hr after TBI. Caspase-1 mRNA content also was increased after trauma, but to a lesser extent in cortex. Increased caspase-3-like, but not caspase-1-like, enzymatic activity was found in cytosolic extracts from injured cortex. Intracerebroventricular administration of z-DEVD-fmk-a specific tetrapeptide inhibitor of caspase-3-before and after injury markedly reduced post-traumatic apoptosis, as demonstrated by DNA electrophoresis and TUNEL staining, and significantly improved neurological recovery. Together, these results implicate caspase-3-like proteases in neuronal apoptosis induced by TBI and suggest that the blockade of such caspases can reduce post-traumatic apoptosis and associated neurological dysfunction.

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Inflammation After Stroke

Zoppo

Becker²,

Hallenbeck³

2001

Arch Neurol

129

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Expression of tumor necrosis factor alpha after focal cerebral ischaemia in the rat

Cited by 236 publications

References 59 publications

ADAMTS-1 and -4 are up-regulated following transient middle cerebral artery occlusion in the rat and their expression is modulated by TNF in cultured astrocytes

ADAMTS-1 and -4 are up-regulated following transient middle cerebral artery occlusion in the rat and their expression is modulated by TNF in cultured astrocytes

Activation of CPP32-Like Caspases Contributes to Neuronal Apoptosis and Neurological Dysfunction after Traumatic Brain Injury

Inflammation After Stroke

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