Eighth Gaddum Memorial Lecture University of London Institute of Education December 1980: Biological Importance of Prostacyclin

Moncada, Salvador

doi:10.1111/j.1476-5381.1982.tb09186.x

Cited by 267 publications

(12 citation statements)

References 250 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, PGI 2 analogs iloprost and cicaprost have been used to treat patients with peripheral ischemia (Beischer et al, 1998; Ciuffetti et al, 2003) and as therapeutic agents for ischemic CNS injury (Moncada, 1982; Gryglewski et al, 1983). A clinical trial of cicaprost failed to help patients with a specific disease such as Raynaud’s syndrome (Lau et al, 1991), but evidence suggests that PGI 2 is effective in treating heart failure that occurs as a result of cardiac bypass surgery (Ocal et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Prostacyclin receptor deletion aggravates hippocampal neuronal loss after bilateral common carotid artery occlusion in mouse

Kibler

Koehler

et al. 2008

Neuroscience

View full text Add to dashboard Cite

Transient global cerebral ischemia causes delayed neuronal death in the hippocampal CA1 region. It also induces an increase in cyclooxygenase 2 (COX-2), which generates several metabolites of arachidonic acid, known as prostanoids, including prostacyclin (PGI2). To determine the role of the PGI2 receptor (IP) in post-ischemic delayed cell death, wild-type and IP knockout (IP−/−) C57Bl/6 mice were subjected to 12-min bilateral common carotid artery occlusion or sham surgery, followed by 7 days of reperfusion. In the sham-operated mice, no statistical difference in CA1 hip-pocampal neuronal density was observed between the wild-type (2836±18/mm2) and IP−/− (2793±43/mm2) mice. Interestingly, in animals subjected to ischemia, surviving neuronal density in wild-type mice decreased to 50.5±7.9% and that of IP−/− mice decreased to 23.0±4.5% of their respective sham-operated controls (P<0.05). The results establish a role for the IP receptor in protecting pyramidal hippocampal neurons after this global ischemic model and suggest that IP receptor agonists could be developed to prevent delayed pyramidal neuronal cell death.

show abstract

Section: Discussionmentioning

confidence: 99%

Prostacyclin receptor deletion aggravates hippocampal neuronal loss after bilateral common carotid artery occlusion in mouse

Kibler

Koehler

et al. 2008

Neuroscience

View full text Add to dashboard Cite

show abstract

“…Of particular interest are the observations that VEGF can regulate the production both of nitric oxide and of prostacyclin, two agents which have diverse effects on vascular tone and reactivity, including vasodilatation, inhibition of platelet aggregation, and the inhibition of vascular smooth muscle cell proliferation [59, 60]. The finding that VEGF-induced PGI 2 production and cPLA 2 activation may be mediated through the p42/p44 MAP kinase pathway also suggests a novel function for this kinase cascade in the action of VEGF distinct from its well-established role in mitogenic signalling.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Vascular Endothelial Growth Factor: How It Transmits Its Signal

Zachary¹

1998

Nephron Exp Nephrol

View full text Add to dashboard Cite

Vascular endothelial growth factor (VEGF) is an essential molecule in the development and formation of mammalian blood vessels in health and disease. VEGF is also increasingly implicated in other biological processes including renal development and pathophysiology. The biological activities of VEGF in vivo and in its target cells in culture are mediated through two receptor protein tyrosine kinases, KDR/Flk-1 and Flt-1. KDR/Flk-1 is able to mediate the tyrosine phosphorylation of several cellular components as well as the generation of second messengers. Recent findings have revealed novel signaling mechanisms which may mediate the biological actions of VEGF. In contrast, the signal transduction mechanisms triggered by Flt-1 remain largely unknown.

show abstract

“…It is very labile and undergoes spontaneous transformation to 6-keto-PGF 1α within minutes in vivo [54]. Prostacyclin is a potent endogenous anticoagulator for platelets and a strong vasodilator [53].…”

Section: Prostanoid Signalingmentioning

confidence: 99%

Non-steroid anti-inflammatory drugs, prostaglandins, and cancer

2013

View full text Add to dashboard Cite

Fatty acids are involved in multiple pathways and play a pivotal role in health. Eicosanoids, derived from arachidonic acid, have received extensive attention in the field of cancer research. Following release from the phospholipid membrane, arachidonic acid can be metabolized into different classes of eicosanoids through cyclooxygenases, lipoxygenases, or p450 epoxygenase pathways. Non-steroid anti-inflammatory drugs (NSAIDs) are widely consumed as analgesics to relieve minor aches and pains, as antipyretics to reduce fever, and as anti-inflammatory medications. Most NSAIDs are nonselective inhibitors of cyclooxygenases, the rate limiting enzymes in the formation of prostaglandins. Long term use of some NSAIDs has been linked with reduced incidence and mortality in many cancers. In this review, we appraise the biological activities of prostanoids and their cognate receptors in the context of cancer biology. The existing literature supports that these lipid mediators are involved to a great extent in the occurrence and progression of cancer.

show abstract

Eighth Gaddum Memorial Lecture University of London Institute of Education December 1980: Biological Importance of Prostacyclin

Cited by 267 publications

References 250 publications

Prostacyclin receptor deletion aggravates hippocampal neuronal loss after bilateral common carotid artery occlusion in mouse

Prostacyclin receptor deletion aggravates hippocampal neuronal loss after bilateral common carotid artery occlusion in mouse

Vascular Endothelial Growth Factor: How It Transmits Its Signal

Non-steroid anti-inflammatory drugs, prostaglandins, and cancer

Contact Info

Product

Resources

About