Transforming growth factor β-related genes in human retinal pigment epithelial cells after tacrolimus treatment

Kimsa, Malgorzata W.; Strzałka‐Mrozik, Barbara; Kruszniewska‐Rajs, Celina; Gola, Joanna; Adamska, Jolanta; Mazurek, Urszula

doi:10.1016/j.pharep.2016.04.020

Cited by 5 publications

(2 citation statements)

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“…Their results showed that the mRNA levels for transforming growth factor b (TGFb) 2 and TGFbR3 were decreased after tacrolimus and LPS treatment. The TGFb family plays a pivotal role in the pathogenesis of various back of the eye diseases [60]. These studies warranted the investigation of TAC-NMF on D407 retinal cells to investigate the inflammatory changes after treating them with inflammatory and ROS-inducing agents such as SI.…”

Section: Discussionmentioning

confidence: 99%

“…An early stage of AMD constitutes an increase in oxidative stress and inflammation in the retinal pigment epithelium. In this study, we employed the use of SI to induce oxidative stress to the retinal pigment epithelium cells; D407 cells [57,60]. Here we postulated that SI can induce oxidative stress in D407 and can be used as an in-vitro model for early AMD.…”

Section: In-vitro Evaluation Of Tac-nmf Bioactivity Using Elisamentioning

confidence: 99%

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Self-Assembling Tacrolimus Nanomicelles for Retinal Drug Delivery

et al. 2020

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Neovascular age-related macular degeneration (AMD) is characterized by an increase in reactive oxygen species (ROS) and pro-inflammatory cytokines in the retinal pigment epithelium cells. The primary purpose of this study was the development of a clear, tacrolimus nanomicellar formulation (TAC-NMF) for AMD. The optimized formulation had a mean diameter of 15.41 nm, a zeta potential of 0.5 mV, and an entrapment efficiency of 97.13%. In-vitro cytotoxicity studies revealed the dose-dependent cytotoxicity of TAC-NMF on various ocular cell lines, such as human retinal pigment epithelium (D407), monkey retinal choroidal endothelial (RF/6A) cells, and human corneal epithelium (CCL 20.2) cells. Cellular uptake and in-vitro distribution studies using flow cytometry and confocal microscopy, respectively, indicated an elevated uptake of TAC-NMF in a time-dependent manner. Biocompatibility assay using macrophage RAW 264.7 cell line resulted in low production of inflammatory cytokines such as IL-6, IL-1β and TNF-α after treatment with TAC-NMF. There was a decrease in ROS in D407 cells pre-treated with sodium iodate (ROS inducing agent) after treating with TAC-NMF and tacrolimus drug. Similarly, there was a reduction in the pro-inflammatory cytokines and VEGF-A in D407 cells pretreated with sodium iodate. This indicates that TAC-NMF could lower pro-inflammatory cytokines and ROS commonly seen in AMD.

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Section: Discussionmentioning

confidence: 99%

Section: In-vitro Evaluation Of Tac-nmf Bioactivity Using Elisamentioning

confidence: 99%

Self-Assembling Tacrolimus Nanomicelles for Retinal Drug Delivery

et al. 2020

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Knockdown of survivin results in inhibition of epithelial to mesenchymal transition in retinal pigment epithelial cells by attenuating the TGFβ pathway

Zhang

Zhao

et al. 2018

Biochemical and Biophysical Research Communications

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Proliferative vitreoretinopathy (PVR) is a common complication of open globe injury and the most common cause of failed retinal detachment surgery. The response by retinal pigment epithelial (RPE) cells liberated into the vitreous includes proliferation and migration; most importantly, epithelial to mesenchymal transition (EMT) of RPE plays a central role in the development and progress of PVR. For the first time, we show that knockdown of BIRC5, a member of the inhibitor of apoptosis protein family, using either lentiviral vector based CRISPR/Cas9 nickase gene editing or inhibition of survivin using the small-molecule inhibitor YM155, results in the suppression of EMT in RPE cells. Knockdown of survivin or inhibition of survivin significantly reduced TGFβ-induced cell proliferation and migration. We further demonstrated that knockdown or inhibition of survivin attenuated the TGFβ signaling by showing reduced phospho-SMAD2 in BIRC5 knockdown or YM155-treated cells compared to controls. Inhibition of the TGFβ pathway using TGFβ receptor inhibitor also suppressed survivin expression in RPE cells. Our studies demonstrate that survivin contributes to EMT by cross-talking with the TGFβ pathway in RPE cells. Targeting survivin using small-molecule inhibitors may provide a novel approach to treat PVR disease.

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A static magnetic field changes the expression profile of the transforming growth factor β family genes in human cells that have been treated with fluoride ions

et al. 2021

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Transforming growth factor β-related genes in human retinal pigment epithelial cells after tacrolimus treatment

Abstract: These results can be important in regard to the treatment of proliferative vitreoretinopathy, pathogenesis of which is associated with processes regulated by TGFβ, such as inflammation, proliferation, epithelial-mesenchymal transition (EMT), and fibrosis.

Cited by 5 publications

References 38 publications

Self-Assembling Tacrolimus Nanomicelles for Retinal Drug Delivery

Self-Assembling Tacrolimus Nanomicelles for Retinal Drug Delivery

Knockdown of survivin results in inhibition of epithelial to mesenchymal transition in retinal pigment epithelial cells by attenuating the TGFβ pathway

A static magnetic field changes the expression profile of the transforming growth factor β family genes in human cells that have been treated with fluoride ions

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