Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Yu, Albert Cheung Hoi; Lau, Lok Ting

doi:10.1016/s0197-0186(99)00145-x

Cited by 71 publications

(52 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These findings suggest that the induction of IL-1b by ischemia-reperfusion might be caused in the microglia and astrocytes. These observations are also supported by in vitro study that astrocytes contributed to the cytokines, such as IL-1a, TNFa, IL-6, released under ischemia [26].…”

Section: Discussionsupporting

confidence: 65%

Increased Expression of Interleukin-1.BETA. in Mouse Hippocampus after Global Cerebral Ischemia.

Imaizumi

Mizushima

Matsumoto

et al. 2001

Acta Histochem. Cytochem

View full text Add to dashboard Cite

We examined the in vivo expression of IL-1b and its transcript after cerebral ischemia produced in mice cardiac arrest model. The IL-1b mRNA in the hippocampal region reached a detectable level at 1 hr after ischemia and had a peak at 3 hr after ischemia recirculation. But it was markedly decreased at 1 day and reached the control levels at 4 day after ischemia recirculation. The IL-1b-like immunoreactivity was observed at 1, 2, 4 day after ischemia recirculation and its immunoreactivity was detected at 2 day. The IL-1b-like immunoreactivity was observed in both microglia and astrocytes after bran ischemia by double immunostaining. These results provide the direct evidence for the localization and induction of IL-1b expression in vivo in mice after ischemia. It is suggested that IL-1b, produced in both astrocytes and microglia cells after ischemia, directly affect on neurons as well as glial cells to induce delayed neuronal cell death.

show abstract

Section: Discussionsupporting

confidence: 65%

Increased Expression of Interleukin-1.BETA. in Mouse Hippocampus after Global Cerebral Ischemia.

Imaizumi

Mizushima

Matsumoto

et al. 2001

Acta Histochem. Cytochem

View full text Add to dashboard Cite

show abstract

“…Relatively few publications have reported changes in expression of the IL-1 family, such as IL-1␣ and IL-1RI, after stroke (Hill et al, 1999;Yu and Lau, 2000), yet it has been assumed that IL-1␤ is the primary form of IL-1 involved in ischemic brain damage (Buttini et al, 1994;Davies et al, 1999;Touzani et al, 1999), and in other local and systemic responses to peripheral injury (Luheshi et al, 1997;Eriksson et al, 1999). Indeed Horai Figure 3.…”

Section: Discussionmentioning

confidence: 99%

“…Despite the extensive evidence implicating IL-1 in ischemic brain damage, little information is available on the relative contribution of IL-1␣ and IL-1␤ (Hill et al, 1999;Yu and Lau, 2000). Both cytokines are induced in response to cerebral ischemia (Touzani et al, 1999) or excitotoxicity, and central administration of IL-1␤ exacerbates damage (Allan et al, , 2000Lawrence et al, 1998).…”

Section: Abstract: Interleukin-1; Cytokines; Stroke; Brain; Knock-oumentioning

confidence: 99%

Role of IL-1α and IL-1β in Ischemic Brain Damage

et al. 2001

View full text Add to dashboard Cite

The cytokine interleukin-1 (IL-1) has been strongly implicated in the pathogenesis of ischemic brain damage. Evidence to date suggests that the major form of IL-1 contributing to ischemic injury is IL-1␤ rather than IL-1␣, but this has not been tested directly.The objective of the present study was to compare the effects of transient cerebral ischemia [30 min middle cerebral artery occlusion (MCAO)] on neuronal injury in wild-type (WT) mice and in IL-1␣, IL-1␤, or both IL-1␣ and IL-1␤ knock-out (KO) mice.Mice lacking both forms of IL-1 exhibited dramatically reduced ischemic infarct volumes compared with wild type (total volume, 70%; cortex, 87% reduction). Ischemic damage compared with WT mice was not significantly altered in mice lacking either IL-1␣ or IL-1␤ alone. IL-1␤ mRNA, but not IL-1␣ or the IL-1 type 1 receptor, was strongly induced by MCAO in WT and IL-1␣ KO mice.Administration (intracerebroventricularly) of recombinant IL-1 receptor antagonist significantly reduced infarct volume in WT (-32%) and IL-1␣ KO (-48%) mice, but had no effect on injury in IL-1␤ or IL-1␣/␤ KO mice.These data confirm that IL-1 plays a major role in ischemic brain injury. They also show that chronic deletion of IL-1␣ or IL-1␤ fails to influence brain damage, probably because of compensatory changes in the IL-1 system in IL-1␣ KO mice and changes in IL-1-independent mediators of neuronal death in IL-1␤ KO mice.

show abstract

“…Evidence of proliferation of astrocytes with the morphological changes associated with activation has also been reported with age (Cotrina and Nedergaard, 2002;Maragakis and Rothstein, 2006). Although microglia are traditionally viewed as the most likely source of proinflammatory cytokines (Block et al, 2007;Garden and Moller, 2006), astrocytes also produce IL-1␤, IL-6 and TNF-␣ in response to stressors (Lau and Yu, 2001;Yu and Lau, 2000). Here we considered that the modulatory effect of rosiglitazone on the age-related deficit in LTP might be a consequence of an effect on astrocytes, rather than microglia.…”

Section: Introductionmentioning

confidence: 86%

Rosiglitazone attenuates the age-related changes in astrocytosis and the deficit in LTP

Cowley

O'Sullivan

Blau

et al. 2012

Neurobiology of Aging

View full text Add to dashboard Cite

Neuroinflammation is a significant and consistent feature of many neurodegenerative disorders, including Alzheimer's disease (AD) and Parkinson's disease (PD). The greatest risk factor for neurodegenerative disorders is age and a proinflammatory phenotype in the aged brain is believed to contribute to these neurodegenerative conditions. In animal models, neuroinflammatory changes, characterized by increased microglial activation, have been associated with a loss of synaptic plasticity and here we show that treatment of aged rats with the PPAR␥ agonist, rosiglitazone, modulates the inflammatory changes and restores synaptic function. The evidence presented highlights an important role for astrocytes in inducing inflammatory changes and suggests that the age-related astrogliosis and astrocytosis is responsible for the increase in the proinflammatory cytokine, tumor necrosis factor alpha (TNF-␣). Magnetic resonance (MR) imaging revealed an age-related increase in T1 relaxation time and, importantly, treatment of aged rats with rosiglitazone reversed the age-related increases in astrogliosis and astrocytosis, TNF-␣ concentration and T1 relaxation time. The evidence indicates that the site of action for rosiglitazone is endothelial cells, and suggests that its effect on astrocytes is secondary to its effect on endothelial cells.

show abstract

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Cited by 71 publications

References 29 publications

Increased Expression of Interleukin-1.BETA. in Mouse Hippocampus after Global Cerebral Ischemia.

Increased Expression of Interleukin-1.BETA. in Mouse Hippocampus after Global Cerebral Ischemia.

Role of IL-1α and IL-1β in Ischemic Brain Damage

Rosiglitazone attenuates the age-related changes in astrocytosis and the deficit in LTP

Contact Info

Product

Resources

About