Dabigatran inhibits intravitreal thrombin activity

Bastiaans, Jeroen; Mulder, Verena C.; Meurs, Jan C. van; Nijenhuis, Marja Smits-Te; Holten-Neelen, Conny van; Hagen, P. Martin van; Dik, Willem A.

doi:10.1111/aos.13630

Cited by 5 publications

(2 citation statements)

References 39 publications

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“…A growing body of evidence indicates that the mechanisms of PVR are orchestrated by multiple elements ( Idrees, Sridhar & Kuriyan, 2019 ; Jin et al, 2017 ; Pastor et al, 2016 ), such as growth factors ( Charteris, 1998 ; Ni et al, 2020 ; Pennock et al, 2014 ; Wubben, Besirli & Zacks, 2016 ), cytokines ( Bastiaans et al, 2018 ; Harada, Mitamura & Harada, 2006 ; Limb et al, 1991 ), extracellular matrix proteins ( Feist et al, 2014 ; Miller et al, 2017 ) and various cells ( Eastlake et al, 2016 ; Pennock et al, 2011 ; Shu & Lovicu, 2017 ). According to the histopathology of PVR, the fibrocellular membrane of PVR is composed of excessive extracellular matrix (ECM) and multiple types of cells, and retinal pigment epithelial (RPE) cells have been indicated as the most consistently present and the most abundant ( Amarnani et al, 2017 ; Ding et al, 2017 ; Hiscott et al, 1989 ; Machemer & Laqua, 1975 ), proving that the RPE cell plays a crucial role in PVR.…”

Section: Introductionmentioning

confidence: 99%

Polarity and epithelial-mesenchymal transition of retinal pigment epithelial cells in proliferative vitreoretinopathy

Zou

Shan

et al. 2020

PeerJ

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Under physiological conditions, retinal pigment epithelium (RPE) is a cellular monolayer composed of mitotically quiescent cells. Tight junctions and adherens junctions maintain the polarity of RPE cells, and are required for cellular functions. In proliferative vitreoretinopathy (PVR), upon retinal tear, RPE cells lose cell-cell contact, undergo epithelial-mesenchymal transition (EMT), and ultimately transform into myofibroblasts, leading to the formation of fibrocellular membranes on both surfaces of the detached retina and on the posterior hyaloids, which causes tractional retinal detachment. In PVR, RPE cells are crucial contributors, and multiple signaling pathways, including the SMAD-dependent pathway, Rho pathway, MAPK pathways, Jagged/Notch pathway, and the Wnt/β-catenin pathway are activated. These pathways mediate the EMT of RPE cells, which play a key role in the pathogenesis of PVR. This review summarizes the current body of knowledge on the polarized phenotype of RPE, the role of cell-cell contact, and the molecular mechanisms underlying the RPE EMT in PVR, emphasizing key insights into potential approaches to prevent PVR.

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Section: Introductionmentioning

confidence: 99%

Polarity and epithelial-mesenchymal transition of retinal pigment epithelial cells in proliferative vitreoretinopathy

Zou

Shan

et al. 2020

PeerJ

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show abstract

“…A growing body of evidence indicates that the mechanisms of PVR are orchestrated by multiple elements (Idrees et al 2019;Jin et al 2017;Pastor et al 2016), such as growth factors (Charteris 1998;Ni et al 2020;Pennock et al 2014;Wubben et al 2016), cytokines (Bastiaans et al 2018;Harada et al 2006;Limb et al 1991), extracellular matrix proteins (Feist et al 2014;Miller et al 2017) and various cells (Eastlake et al 2016;Pennock et al 2011;Shu & Lovicu 2017). According to the histopathology of PVR, the fibrocellular membrane of PVR is composed of excessive extracellular matrix (ECM) and multiple types of cells, and retinal pigment epithelial (RPE) cells have been indicated as the most consistently present and the most abundant (Amarnani et al 2017;Ding et al 2017;Hiscott et al 1989;Machemer & Laqua 1975), proving that the RPE cell plays a crucial role in PVR.…”

Section: Introductionmentioning

confidence: 99%

Peer Review #1 of "Polarity and epithelial-mesenchymal transition of retinal pigment epithelial cells in proliferative vitreoretinopathy (v0.1)"

2020

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Under physiological conditions, retinal pigment epithelium (RPE) is a cellular monolayer composed of mitotically quiescent cells. Tight junctions and adherens junctions maintain the polarity of RPE cells, and are required for cellular functions. In proliferative vitreoretinopathy (PVR), upon retinal tear, RPE cells lose cell-cell contact, undergo epithelial-mesenchymal transition (EMT), and ultimately transform into myofibroblasts, leading to the formation of fibrocellular membranes on both surfaces of the detached retina and on the posterior hyaloids, which causes tractional retinal detachment. In PVR, RPE cells are crucial contributors, and multiple signaling pathways, including SMADdependent pathway, Rho pathway, MAPK pathways, Jagged/Notch pathway, and Wnt/βcatenin pathway, are activated. These pathways mediate the EMT of RPE cells, which play a key role in the pathogenesis of PVR. This review summarizes the current body of knowledge on the polarized phenotype of RPE, the role of cell-cell contact, and the molecular mechanisms underlying the RPE EMT in PVR, emphasizing key insights into potential approaches to prevent PVR.

show abstract

Development and validation of an ultra-high performance liquid chromatography with tandem mass spectrometry method for the simultaneous quantification of direct oral anticoagulants in human plasma

Zhang

Liu

et al. 2021

Journal of Chromatography B

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Dabigatran inhibits intravitreal thrombin activity

Abstract: Proliferative vitreoretinopathy (PVR) is associated with increased intravitreal thrombin activity that activates profibrotic and proinflammatory pathways in RPE cells. Our findings provide evidence that this activation pathway can potentially be inhibited by dabigatran.

Cited by 5 publications

References 39 publications

Polarity and epithelial-mesenchymal transition of retinal pigment epithelial cells in proliferative vitreoretinopathy

Polarity and epithelial-mesenchymal transition of retinal pigment epithelial cells in proliferative vitreoretinopathy

Peer Review #1 of "Polarity and epithelial-mesenchymal transition of retinal pigment epithelial cells in proliferative vitreoretinopathy (v0.1)"

Development and validation of an ultra-high performance liquid chromatography with tandem mass spectrometry method for the simultaneous quantification of direct oral anticoagulants in human plasma

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