Cloning and expression of a cDNA for mouse prostaglandin F receptor.

Sugimoto, Yukihiko; Hasumoto, Ken-yuh; Nambai, Tsunehisa; Irie, Atsushi; Katsuyama, Masato; Negishi, Manabu; Kakizuka, Akira; Narumiya, Shuh; Ichikawa, Atsushi

doi:10.1016/s0021-5198(19)50319-5

Cited by 6 publications

(6 citation statements)

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“…It exerts its biological functions by binding to a prostanoid receptor FP which has two differentially spliced variants (FP A , FP B ). The FP receptor couples with the G q protein for increasing the inositol phosphate accumulation, protein kinase C (PKC) activation, and intracellular calcium release [ 87 ]. In addition, stimulation of FP receptor leads to activation of G-protein Rho via a Gq-independent process, resulting in cytoskeleton rearrangement [ 88 ].…”

Section: Prostaglandins and Rheumatoid Arthritismentioning

confidence: 99%

Prostaglandins and Rheumatoid Arthritis

Fattahi

Mirshafiey

2012

Arthritis

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Rheumatoid arthritis (RA) is a chronic, autoimmune, and complex inflammatory disease leading to bone and cartilage destruction, whose cause remains obscure. Accumulation of genetic susceptibility, environmental factors, and dysregulated immune responses are necessary for mounting this self-reacting disease. Inflamed joints are infiltrated by a heterogeneous population of cellular and soluble mediators of the immune system, such as T cells, B cells, macrophages, cytokines, and prostaglandins (PGs). Prostaglandins are lipid inflammatory mediators derived from the arachidonic acid by multienzymatic reactions. They both sustain homeostatic mechanisms and mediate pathogenic processes, including the inflammatory reaction. They play both beneficial and harmful roles during inflammation, according to their site of action and the etiology of the inflammatory response. With respect to the role of PGs in inflammation, they can be effective mediators in the pathophysiology of RA. Thus the use of agonists or antagonists of PG receptors may be considered as a new therapeutic protocol in RA. In this paper, we try to elucidate the role of PGs in the immunopathology of RA.

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Section: Prostaglandins and Rheumatoid Arthritismentioning

confidence: 99%

Prostaglandins and Rheumatoid Arthritis

Fattahi

Mirshafiey

2012

Arthritis

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“…PGF 2 α has its own specific receptor (FP), which is expressed in endothelium and in vascular smooth muscle cells [ 139 – 143 ]. PGF 2 α can also interact with TP [ 54 ].…”

Section: Pgf 2 αmentioning

confidence: 99%

Aging-Shifted Prostaglandin Profile in Endothelium as a Factor in Cardiovascular Disorders

Qian

Luo

Chi

2012

Journal of Aging Research

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Age-associated endothelium dysfunction is a major risk factor for the development of cardiovascular diseases. Endothelium-synthesized prostaglandins and thromboxane are local hormones, which mediate vasodilation and vasoconstriction and critically maintain vascular homeostasis. Accumulating evidence indicates that the age-related changes in endothelial eicosanoids contribute to decline in endothelium function and are associated with pathological dysfunction. In this review we summarize currently available information on aging-shifted prostaglandin profiles in endothelium and how these shifts are associated with cardiovascular disorders, providing one molecular mechanism of age-associated endothelium dysfunction and cardiovascular diseases.

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“…In collaboration with Dr. Narumiya, we employed a homology screening strategy using mouse P-815, lung, kidney, and ovary cDNA libraries, and subsequently identified the structures of four subtypes of PGE receptors, 49 – 52 ) the PGI 2 receptor, 53 ) and PGF 2α receptor. 54 ) These receptors were expressed and their ligand binding properties and signal transduction were examined in homogenous populations in heterologous expression systems (reviewed in Refs. 55 , 56 ).…”

Section: Biochemical and Molecular Characterization Of Prostaglandin mentioning

confidence: 99%

Molecular biology of histidine decarboxylase and prostaglandin receptors

Ichikawa

Sugimoto

Tanaka

2010

Proc. Jpn. Acad., Ser. B

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Histamine and prostaglandins (PGs) play a variety of physiological roles as autacoids, which function in the vicinity of their sources and maintain local homeostasis in the body. They stimulate target cells by acting on their specific receptors, which are coupled to trimeric G proteins. For the precise understanding of the physiological roles of histamine and PGs, it is necessary to clarify the molecular mechanisms involved in their synthesis as well as their receptor-mediated responses. We cloned the cDNAs for mouse l-histidine decarboxylase (HDC) and 6 mouse prostanoid receptors (4 PGE2 receptors, PGF receptor, and PGI receptor). We then characterized the expression patterns and functions of these genes. Furthermore, we established gene-targeted mouse strains for HDC and PG receptors to explore the novel pathophysiological roles of histamine and PGs. We have here summarized our research, which should contribute to progress in the molecular biology of HDC and PG receptors.

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Cloning and expression of a cDNA for mouse prostaglandin F receptor.

Cited by 6 publications

References 0 publications

Prostaglandins and Rheumatoid Arthritis

Prostaglandins and Rheumatoid Arthritis

Aging-Shifted Prostaglandin Profile in Endothelium as a Factor in Cardiovascular Disorders

Molecular biology of histidine decarboxylase and prostaglandin receptors

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