Role of thymus-eicosanoids in the immune response

Juzan, M.; Hostein, Isabelle; Gualde, N.

doi:10.1016/0952-3278(92)90030-m

Cited by 28 publications

(14 citation statements)

References 76 publications

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“…A third mechanism by which COX-2 could contribute to cell death is related to induction of apoptosis. In thymocytes, the COX-2 reaction product PGE 2 induces apoptosis (Juzan et al, 1992). This finding raises the possibility that COX-2 contributes to postischemic apoptosis (Li et al, 1995).…”

Section: Discussionmentioning

confidence: 91%

Cyclo-Oxygenase-2 Gene Expression in Neurons Contributes to Ischemic Brain Damage

et al. 1997

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Cyclo-oxygenase-2 (COX-2), a rate-limiting enzyme for prostanoid synthesis, is induced during inflammation and participates in inflammation-mediated cytotoxicity. Cerebral ischemia is followed by an inflammatory reaction that plays a role in the evolution of the tissue damage. We studied whether COX-2 is induced after cerebral ischemia and if so, whether such expression contributes to ischemic brain damage. The middle cerebral artery was occluded in rats, and the ischemic area was sampled for analysis 3-96 hr later. COX-2 mRNA was determined by the competitive reverse-transcription PCR. COX-2 mRNA was upregulated in the ischemic hemisphere, but not contralaterally, beginning 6 hr after ischemia. The upregulation reached a maximum at 12 hr, at which time a fivefold induction of the message occurred. Twenty-four hours after ischemia, the concentration of prostaglandin E 2 was elevated in the injured brain by 292 Ϯ 57% (n ϭ 6). COX-2 immunoreactivity was observed in neurons at the medial edge of the ischemic area. Administration of the COX-2 inhibitor NS-398 attenuated the elevation in prostaglandin E 2 in the postischemic brain and reduced the volume of the infarct by 29 Ϯ 6% ( p Ͻ 0.05). Thus, cerebral ischemia leads to upregulation of COX-2 message, protein, and reaction products in the injured hemisphere. The data implicate COX-2 in the mechanisms of delayed neuronal death at the infarct border and provide the rationale for neuroprotective strategies employing COX-2 inhibitors.

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Section: Discussionmentioning

confidence: 91%

Cyclo-Oxygenase-2 Gene Expression in Neurons Contributes to Ischemic Brain Damage

et al. 1997

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“…21 A third mechanism by which Cox-2 could contribute to cell death is related to the induction of apoptosis by PGE 2 in some cell systems. 49,50 This raises the possibility that Cox-2 contributes to the demise of motor neurons in ALS by promoting apoptosis, which is an active form of cell death. This prospect is of particular interest, because we have demonstrated previously that mSOD1 stimulates apoptosis in vitro and that several molecular pathways of apoptosis are activated in transgenic mSOD1 mice during the neurodegenerative process.…”

Section: (A) Cox-2 Immunoreactivity (Black Staining Indicated By the mentioning

confidence: 99%

Increased expression of the pro-inflammatory enzyme cyclooxygenase-2 in amyotrophic lateral sclerosis

et al. 2001

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“…LOX-derived eicosanoids have been shown to regulate the production and action of some cytokines including interferons [3], to regulate natural killer cell activity [4], to induce growth-related signals and to regulate cell proliferation [5,6]. Eicosanoids are involved in thymocyte maturation and/or differentiation and they modulate the activity of thymus-dependent lymphocytes [7]. Many pharmacological agents have been developed that inhibit the generation of eicosanoids with different potency and selectivity [8,9].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of ICE‐family cysteine proteases rescues murine lymphocytes from lipoxygenase inhibitor‐induced apoptosis

et al. 1996

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Role of thymus-eicosanoids in the immune response

Cited by 28 publications

References 76 publications

Cyclo-Oxygenase-2 Gene Expression in Neurons Contributes to Ischemic Brain Damage

Cyclo-Oxygenase-2 Gene Expression in Neurons Contributes to Ischemic Brain Damage

Increased expression of the pro-inflammatory enzyme cyclooxygenase-2 in amyotrophic lateral sclerosis

Inhibition of ICE‐family cysteine proteases rescues murine lymphocytes from lipoxygenase inhibitor‐induced apoptosis

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