Identification of prostaglandin D2 as a major prostaglandin in homogenates of rat brain

Abdel-Halim, M.Saeed; Hámberg, Mats; Sjöquist, Birgitta; Ångård, Erik

doi:10.1016/0090-6980(77)90190-3

Cited by 222 publications

(49 citation statements)

References 9 publications

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“…Studies with human lung tissue have shown that, after antigenic stimulation, essentially all of the PGD2 released is derived from the mast cells (24). Furthermore, until now, only human platelets and rat adrenocortical cells have been shown to produce PGD2, and the amount produced by human platelets is extremely small when compared with activated mast cells (28)(29)(30). The fact that TAME-esterase activity and kinins relate statistically to each other and to histamine and PGD2 (Table I) is consistent with their possible association with mast cell activation.…”

Section: Discussionmentioning

confidence: 99%

Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement.

et al. 1985

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The purpose of our study was to assess the effect of cold, dry air (CDA) on the nasal mucosa of selected individuals in relation to the release of inflammatory mediators associated with mast cells. 12 subjects with a history of nasal symptoms of rhinorrhea and congestion upon cold or dry environmental exposure were challenged by nasal breathing of CDA and warm, moist air (WMA). Each subject was tested on two occasions with the order of the challenges reversed. Symptom scores were recorded, and the levels of histamine, prostaglandin (PG) D2, kinins, and 1H1-N-a-tosyl-L-arginine methyl ester (TAME)-esterase activity in nasal lavage fluids were measured.CDA caused a significant increase in mediator levels and in symptom scores as compared to baseline or to WMA. No significant increase in symptom scores or mediators was noted after WMA challenge, with the exception of a marginal increase in kinins. The response to CDA was similar, regardless of challenge order. Changes in mediators correlated with one another, and symptom scores correlated significantly with the levels of histamine, kinins, and PGD2. Five subjects without a history of nasal symptoms on cold air exposure had no change in mediators or symptom scores after CDA or WMA challenge. We conclude that CDA causes the release of inflammatory mediators possibly associated with mast cells and speculate that such a mechanism may be involved in the bronchospasm induced by CDA in asthmatics.

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Section: Discussionmentioning

confidence: 99%

Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement.

et al. 1985

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“…Cell membranes are particularly vulnerable to the action of free radicals because of their high content of phosphol1pid-bound unsaturated fatty acids (24)(25)(26).…”

Section: Discussionmentioning

confidence: 99%

Free radicals-induced changes in mesenteric microvascular dimensions in the anesthetized cat.

et al. 1983

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Abstract-Effect of free radicals on microvascular dimensions was studied in anes thetized cat intestinal mesentery. Generation of free radicals by xanthine oxidase, acting on endogenous substrates (e.g., xanthine, hypoxanthine), produced sustained vasodilation at pH 7.4 or at pH 6.6. These effects were reversed by superoxide dismutase (SOD), a superoxide radical ('02-) scavenger, at pH 7.4, and by SOD plus hydroxyl radical ('OH) scavenger d-mannitol at pH 6.6. These findings suggest that the sustained vasodilation is caused by '02 and by 'OH derived from '02_ at low pH.

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“…Whereas the prostane ring on PGE 2 has a 9-keto and 11-hydroxy moiety, the positions of these substituents are reversed on PGD 2 . In the late 1970s, PGD 2 was identified as a major product in rat brain homogenates (45) and activated mast cells (46). PGD 2 is formed by two evolutionarily distinct, but functionally convergent, prostaglandin D synthases (PGDS): the lipocalin-type (l-PGDS) and hematopoietic-type (h-PGDS).…”

Section: Prostaglandin Dmentioning

confidence: 99%

Thematic Review Series: Proteomics. An integrated omics analysis of eicosanoid biology

Buczynski

Dumlao

Dennis

2009

Journal of Lipid Research

475

463

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Eicosanoids have been implicated in a vast number of devastating inflammatory conditions, including arthritis, atherosclerosis, pain, and cancer. Currently, over a hundred different eicosanoids have been identified, with many having potent bioactive signaling capacity. These lipid metabolites are synthesized de novo by at least 50 unique enzymes, many of which have been cloned and characterized. Due to the extensive characterization of eicosanoid biosynthetic pathways, this field provides a unique framework for integrating genomics, proteomics, and metabolomics toward the investigation of disease pathology. To facilitate a concerted systems biology approach, this review outlines the proteins implicated in eicosanoid biosynthesis and signaling in human, mouse, and rat. Applications of the extensive genomic and lipidomic research to date illustrate the questions in eicosanoid signaling that could be uniquely addressed by a thorough analysis of the entire eicosanoid proteome.-Buczynski, M. W., D. S. Dumlao, and E. A. Dennis. An integrated omics analysis of eicosanoid biology.

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Identification of prostaglandin D2 as a major prostaglandin in homogenates of rat brain

Cited by 222 publications

References 9 publications

Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement.

Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement.

Free radicals-induced changes in mesenteric microvascular dimensions in the anesthetized cat.

Thematic Review Series: Proteomics. An integrated omics analysis of eicosanoid biology

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