Comparison of Prostaglandin F2α, Bimatoprost (Prostamide), and Butaprost (EP2 Agonist) on Cyr61 and Connective Tissue Growth Factor Gene Expression

Liang, Yuanbo; Li, Chen; Guzmán, Víctor; Evinger, Albert J.; Protzman, Charles E.; Krauss, Achim H.-P.; Woodward, David F.

doi:10.1074/jbc.m301009200

Cited by 70 publications

(57 citation statements)

References 33 publications

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“…EP 2 -mediated CCN1/Cyr61 expression is via Rho and MAP kinase pathways. Butaprost triggers G s protein-coupled receptor activation mechanism, which involves activation of adenylate cyclase and initiation of the cAMP pathway with resultant activation of protein kinase A [Liang et al, 2003].…”

Section: Pathways Involved In Ccn1/cyr61 Inductionmentioning

confidence: 99%

Functional properties and intracellular signaling of CCN1/Cyr61

Chen

2006

J of Cellular Biochemistry

149

128

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CCN1/Cyr61 is a member of the protein family that can be promptly induced by growth factors. CCN1/Cyr61 promotes cell proliferation, adhesion, and differentiation. It plays important roles in angiogenesis and extracellular matrix production. In addition, CCN1/Cyr61 has many potential functions in tumorigenesis, development, embryo implantation, as well as formation of endometriotic lesions. Expression of CCN1/Cyr61 is regulated by a variety of agents including cytokines, growth factors, steroid hormones, and some drugs. These inducers regulate the transcription of CCN1/Cyr61 through several signaling transduction pathways. CCN1/Cyr61 is able to interact either with the cell itself or the surrounding cells through an autocrine-paracrine mechanism. It has been reported that CCN1/Cyr61 exerts its functions via interacting with at least five integrins as well as heparan sulfate proteoglycan. By activating Wnt, NF-kappaB, or tyrosine kinase signaling pathways, CCN1/Cyr61 is not only able to control the growth of epithelial cells and fibroblasts, but also induce or suppress apoptosis in a cell type-specific manner.

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Section: Pathways Involved In Ccn1/cyr61 Inductionmentioning

confidence: 99%

Functional properties and intracellular signaling of CCN1/Cyr61

Chen

2006

J of Cellular Biochemistry

149

128

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“…It was reported that Cyr61 mRNA (factor involved in tissue remodeling) expression was upregulated through EP 2 receptor stimulation in the isolated cat iris [69] and human ciliary smooth muscle cells and that a non-selective EP receptors agonist induced proMMP-1 and -3 secretion in ciliary muscle cells [70]. Currently unknown is whether EP 2 specifically mediates the secretion of MMPs and ECM turnover in TM cells.…”

Section: Prostaglandin Ementioning

confidence: 99%

“…Bimatoprost activates signaling pathways in different cells from PGF 2α in the same cat iris sphincter preparation by mechanisms unrelated to conversion to prostaglandins, activation of prostanoid receptors, enhancement of anandamide levels or gating of TRPV1 vanilloid receptors [87,88]. Bimatoprost also potently contracts tissues, such as uterus [89] and stimulates Cyr 61 expression in ciliary muscle cells, with mechanisms that are distinct from that of PGF 2α [69]. Additionally, prostamide F 2α and its analogue bimatoprost exhibit activities at recombinant FP and native FP receptors, including those in TM cells, with a concentration 1000 times higher than PGF 2α and its derivatives.…”

Section: Prostamidesmentioning

confidence: 99%

Endogenous bioactive lipids and the regulation of conventional outflow facility

Wan

Woodward

Stamer

2008

Expert Review of Ophthalmology

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SummaryPerturbation of paracrine signaling within the human conventional outflow pathway influences tissue homeostasis and outflow function. For example, exogenous introduction of the bioactive lipids, sphingosine-1-phosphate, anandamide or prostaglandin F 2α , to conventional outflow tissues alters the rate of drainage of aqueous humor through the trabecular meshwork, and into Schlemm's canal. This review summarizes recent data that characterizes endogenous bioactive lipids, their receptors and associated signaling partners in the conventional outflow tract. We also discuss the potential of targeting such signaling pathways as a strategy for the development of therapeutics to treat ocular hypertension and glaucoma.

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“…Es wird angenommen, dass die Wirkung auf den trabekulären und den uveoskleralen Abflussweg nicht alleine über Prostaglandin-Rezeptoren erfolgt, sondern auch über eigene Prostamid-Rezeptoren [9]. Neben den häufig beschriebenen Nebenwirkungen wie Hyperpigmentierung der periokulären Haut und der Iris, gesteigertem Zilienwachstum, konjunktivaler Hyperämie und zystoidem Makulaçdem gibt es auch Berichte über HSV-Keratitis-Reaktivierungen und Iritiden [7,8,14].…”

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