Cyclooxygenase-2 expression is increased in frontal cortex of Alzheimer's disease brain

Pasinetti, Giulio Maria; Aisen, Paul S.

doi:10.1016/s0306-4522(98)00218-8

Cited by 420 publications

(261 citation statements)

References 20 publications

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“…The results are highly relevant because the generation of PGE 2 results from the combined actions of COX activity and PGE 2 synthesis enzymes. Nonetheless, as our Western blot analysis confirmed up-regulation of mPGES-1 in AD cortical tissue, other studies have also shown a corresponding up-regulation of COX-2 [32,33]. In light of the functional coupling of COX-2 and mPGES-1 [34], COX-2 might colocalize with mPGES-1 in pyramidal neurons.…”

Section: Discussionsupporting

confidence: 81%

Elevated microsomal prostaglandin‐E synthase‐1 in Alzheimer's disease

Chaudhry

Zhuang

Crain

et al. 2007

Alzheimer's & Dementia

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Section: Discussionsupporting

confidence: 81%

Elevated microsomal prostaglandin‐E synthase‐1 in Alzheimer's disease

Chaudhry

Zhuang

Crain

et al. 2007

Alzheimer's & Dementia

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“…Data obtained from several reports clearly indicate an agerelated increase in the expression of COX-2 and PGE2 (Baek et al 2001;Hayek et al 1997;Kim et al 2000), which is consistent with our results in the present study. Over-production of PGE2 eventually gives rise to the age-associated diseases, such as atherosclerosis, Alzheimer's disease, and arthritis (FitzGerald 2003;Mukherjee et al 2001;Pasinetti and Aisen 1998). Therefore, there might exist disordered regulation of COX-2 expression in the aging body.…”

Section: Tsa Suppresses Cox-2 Protein Expression By Upregulation Of Mmentioning

confidence: 99%

Dysregulated expression of miR-101b and miR-26b lead to age-associated increase in LPS-induced COX-2 expression in murine macrophage

Liú

Wang

et al. 2015

AGE

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Aging is the natural process of decline in physiological structure and function of various molecules, cells, tissues, and organs. Growing evidence indicates that increased immune genetic diversity and dysfunction of immune system cause aging-related pathophysiological process with the growth of age. In the present study, we observed that LPS-induced higher activation of cyclooxygenase (COX)-2 promoter is associated with the upregulated binding activity of nuclear factor kappa B (NF-κB) in peritoneal macrophages of aged mice than young ones. Additionally, COX-2 is a direct target of miR-101b and miR-26b in the macrophages. Significant upregulation of miR-101b and miR26b effectively prevented LPS-induced excessive expression of COX-2 in the young mice. Because these negative regulatory factors were unresponsive to LPS stimulation, the levels of COX-2 were markedly higher in the macrophages of aged mice. Further study showed that NF-κB activation contributed to the increase in the expression of miR-101b and miR-26b in the LPSstimulated macrophages of young mice, but not aged ones. Moreover, histone deacetylase (HDAC) inhibitor trichostatin A (TSA) upregulated expression of miR101b and miR-26b in the aged mouse macrophages only, but not the young cells. This demonstrated that HDAC suppressed the expression of miR-101b and miR-26b in the LPS-treated macrophages of aged mice and contributed to the aging process. TSA-induced increased expression of miR-101b and miR-26b could further suppress COX-2 expression. These findings provide novel evidence on the regulation of immune senescence and miR-101b and miR-26b, which might be promising targets in treating aged-related inflammatory diseases. Epigenetic regulation of the microRNAs (miRNAs) provides an important evidence for the treatment of innate inflammatory disease with HDAC inhibitors in elderly.

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“…COX-2 expression in the brain is dramatically increased in a wide range of neurological disorders including cerebral ischemia (Iadecola et al, 1999), Alzheimer disease (Pasinetti and Aisen, 1998), and amyotrophic lateral sclerosis (Drachman and Rothstein, 2000). It has also been suggested that COX-2 and prostaglandins may play a role in epilepsy.…”

Section: Introductionmentioning

confidence: 99%

Induction of astrocytic cyclooxygenase-2 in epileptic patients with hippocampal sclerosis

Desjardins

Sauvageau

Bouthillier

et al. 2003

Neurochemistry International

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Induction of cyclooxygenase-2 (COX-2) has been described in a wide range of neurological diseases including animal models of epilepsy. The present study was undertaken to assess COX-2 expression in hippocampal biopsies from patients with therapy-refractive temporal lobe epilepsy (TLE). For this purpose, hippocampal CA1 subfield was dissected from epileptic patients with (n=5) or without (n=2) hippocampal sclerosis (HS). COX-2 expression was investigated using immunohistochemistry and semi-quantitative RT-PCR. COX-2 immunoreactivity in TLE patient material in the absence of HS was restricted to a few neurons of the hippocampus. In the presence of HS, on the other hand, a significant induction of astrocytic COX-2 immunoreactivity associated with a concomitant increase in the steady-state level of COX-2 mRNA was observed in the CA1 subfield. These findings suggest that induction of astrocytic COX-2 is implicated in the pathogenesis of HS in TLE and is consistent with the previous findings of increased concentrations of prostaglandins in the cerebrospinal fluid of these patients.

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Cyclooxygenase-2 expression is increased in frontal cortex of Alzheimer's disease brain

Cited by 420 publications

References 20 publications

Elevated microsomal prostaglandin‐E synthase‐1 in Alzheimer's disease

Elevated microsomal prostaglandin‐E synthase‐1 in Alzheimer's disease

Dysregulated expression of miR-101b and miR-26b lead to age-associated increase in LPS-induced COX-2 expression in murine macrophage

Induction of astrocytic cyclooxygenase-2 in epileptic patients with hippocampal sclerosis

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