A functional study of platelets in menstrual fluid

Rees, Margaret; Demers, Laurence M.; Anderson, Anne B. M.; Turnbull, A. C.

doi:10.1111/j.1471-0528.1984.tb04828.x

Cited by 22 publications

(7 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…During contractions, endometrial blood flow decreases and there is now good correlation between minimal blood flow and maximal pain, indicating that ischaemia due to hypercontractility is the primary cause (Rees, 1989;Rees and Turnbull, 1989). In addition, PGE 2 and PGF 2α concentrations are higher in the menstrual fluid of women with dysmenorrhoea than in women with painless periods (Rees et al, 1984b;Rees, 1989). Studies in vitro have demonstrated that endometrial explants from women with dysmenorrhoea produce more PGF 2α in response to arachidonic acid compared with endometrium from pain-free women (Lundstrom and Green, 1978).…”

Section: Dysmenorrhoeamentioning

confidence: 99%

Cyclooxygenase enzymes and prostaglandins in pathology of the endometrium

Sales¹

2003

Reproduction

View full text Add to dashboard Cite

Prostaglandins are bioactive lipids produced from arachidonic acid by cyclooxygenase (COX) enzymes and specific terminal prostanoid synthase enzymes. After biosynthesis, prostaglandins exert an autocrine-paracrine function by coupling to specific prostanoid G protein-coupled receptors to activate intracellular signalling and gene transcription. For many years, prostaglandins have been recognized as key molecules in reproductive biology by regulating ovulation, endometrial physiology and proliferation of endometrial glands and menstruation. More recently, a role for COX enzymes and prostaglandins has been ascertained in reproductive tract pathology, including carcinomas, menorrhagia, dysmenorrhoea and endometriosis. Although the mechanism by which prostaglandins modulate these pathologies is still unclear, a large body of evidence supports a role for COX enzymes, prostaglandins and prostaglandin receptor signalling pathways in angiogenesis, apoptosis and proliferation, tissue invasion and metastases and immunosuppression. Here, an overview is provided of some of the findings from these studies with specific emphasis on the role of COX enzymes, prostaglandin E 2 and F 2α in disorders of endometrial proliferation and menstruation in non-pregnant women.The arachidonic acid cascade generates a family of bioactive lipids, including prostaglandins, thromboxanes and leukotrienes that modulate diverse physiological and pathophysiological responses in the reproductive tract. There has been a great deal of interest over the past few years in the involvement of arachidonic acid metabolites in pathology. However, there is still much uncertainty about the manner in which they contribute to specific phenotypic cellular changes that may precipitate pathophysiology. The focus of this review is to provide some insight into the role of cyclooxygenase (COX) enzymes, prostaglandin E 2 (PGE 2 ) and PGF 2α and their respective receptors in reproductive pathophysiology, with specific regard to disorders of endometrial proliferation and dysfunctional menstruation.The kinetics of the prostaglandin biosynthetic pathway is driven by the availability of free arachidonic acid. When released from plasma membrane phospholipids or dietary fatty acids, after activation of phospholipase A2 (PLA2) or PLC, arachidonic acid is cyclized and oxygenated by COX enzymes by addition of the 15-hydroperoxy group to form prostaglandin G 2 (PGG 2 ). The hydroperoxy group of PGG 2 is reduced to the hydroxy group of PGH 2 (Marnett, 1992) (Fig. 1). This intermediate serves as the substrate for terminal prostanoid synthase enzymes. These enzymes are named according to the prostaglandin they produce, such that prostaglandin D 2 is synthesized by prostaglandin-D-synthase (PGDS), prostaglandin E 2 (PGE 2 ) by prostaglandin-E-synthase (PGES); prostaglandin F 2α by

show abstract

Section: Dysmenorrhoeamentioning

confidence: 99%

Cyclooxygenase enzymes and prostaglandins in pathology of the endometrium

Sales¹

2003

Reproduction

View full text Add to dashboard Cite

show abstract

“…VEGF stimulates tPA synthesis by endothelial cells and increases vascular permeability, resulting in activation of the extravascular coagulation cascade with the consumption of fibrin (Pepper et al, 1991). The release of VEGF by activated platelets provides a further means by which VEGF increases tPA release, as menstrual platelets are activated in the uterine cavity (Rees et al, 1984).…”

Section: Role Of Vegf In Menorrhagiamentioning

confidence: 99%

Effect of Polyherbal Drug on Menorrhagia and Its Evaluation by Assesing Biomarker Serum VEGF-A

Mishra¹,

Tjprc²

2018

IJEEFUS

View full text Add to dashboard Cite

show abstract

“…Prothrombin is converted to thrombin which degrades fibrinogen. Moreover, the platelets in menstruum are fewer in number and do not aggregate to produce the signals necessary for clotting to begin [11,38]. As such, there was no clot formation and the fibrinogen was easily extracted from the bloodstain.…”

Section: Liquid Samplesmentioning

confidence: 99%