The effect of sucrose esters on a culture model of the nasal barrier

Kürti, Levente; Veszelka, Szilvia; Bocsik, Alexandra; Dung, Ngo Thi Khue; Ózsvári, Béla; Puskás, László G.; Kittel, Ágnes; Szabó‐Révész, Piroska; Deli, Mária A.

doi:10.1016/j.tiv.2012.01.015

Cited by 48 publications

(60 citation statements)

References 34 publications

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“…Growth and morphology of RPMI 2650 nasal epithelial cell line RPMI 2650 human nasal epithelial cells reached confluency in 2 days after seeding, which was confirmed by phase contrast microscopy (Kürti et al 2012). RPMI 2650 cells grew in mono-or multilayers as in vivo as demonstrated by the electron microscopic images.…”

Section: Resultsmentioning

confidence: 65%

“…We have used microelectric sensing to monitor the biological status of the RPMI 2650 cells in real-time and provide quantitative information on viability, adherence and permeability (Kürti et al 2012). RT-CES measures changes in the impedance of individual microelectronic wells, containing gold microelectrodes integrated into the bottom of the culturing plate.…”

Section: Resultsmentioning

confidence: 99%

“…Treatment with retinoic acid and hydrocortisone reinforced the paracellular barrier both morphologically and functionally. The presented in vitro nasal epithelial model may be applicable to test the toxicity and permeability of pharmaceutical excipients (Kürti et al 2012) and drug candidates.…”

Section: Conclusion Significancementioning

confidence: 99%

“…Although this cell line originates from an anaplastic nasal septum tumour, its properties are closely related to normal human nasal epithelium concerning its karyotype (Moorhead 1965), its cytokeratin polypeptide pattern (Moll et al 1983), and the presence of mucoid material on the cell surface (Moore and Sandberg 1964). This particular cell line has been mostly used for nasal metabolism studies and toxicity assays (Kürti et al 2012) and less for permeability studies, since there are conflicting reports with regard to the ability of these cells to form monolayer. Some experts claim that RPMI 2650 nasal epithelial cells do form monolayer (Bai et al 2008) while others described that they grow in clumps rather than in monolayer (De Fraissinette et al 1995).…”

Section: Introductionmentioning

confidence: 99%

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Retinoic acid and hydrocortisone strengthen the barrier function of human RPMI 2650 cells, a model for nasal epithelial permeability

et al. 2012

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The nasal pathway represents an alternative route for non-invasive systemic administration of drugs. The main advantages of nasal drug delivery are the rapid onset of action, the avoidance of the first-pass metabolism in the liver and the easy applicability. In vitro cell culture systems offer an opportunity to model biological barriers. Our aim was to develop and characterize an in vitro model based on confluent layers of the human RPMI 2650 cell line. Retinoic acid, hydrocortisone and cyclic adenosine monophosphate, which influence cell attachment, growth and differentiation have been investigated on the barrier formation and function of the nasal epithelial cell layers. Real-time cell microelectronic sensing, a novel label-free technique was used for dynamic monitoring of cell growth and barrier properties of RPMI 2650 cells. Treatments enhanced the formation of adherens and tight intercellular junctions visualized by electron microscopy, the presence and localization of junctional proteins ZO-1 and b-catenin demonstrated by fluorescent immunohistochemistry, and the barrier function of nasal epithelial cell layers. The transepithelial resistance of the RPMI 2650 cell model reached 50 to 200 X 9 cm 2 , the permeability coefficient for 4.4 kDa FITC-dextran was 9.3 to 17 9 10 -6 cm/s, in agreement with values measured on nasal mucosa from in vivo and ex vivo experiments. Based on these results human RPMI 2650 cells seem to be a suitable nasal epithelial model to test different pharmaceutical excipients and various novel formulations, such as nanoparticles for toxicity and permeability.

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Section: Resultsmentioning

confidence: 65%

Section: Resultsmentioning

confidence: 99%

Section: Conclusion Significancementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Retinoic acid and hydrocortisone strengthen the barrier function of human RPMI 2650 cells, a model for nasal epithelial permeability

et al. 2012

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“…The RTCA-SP instrument (ACEA Biosciences, US) measures impedance continuously and is automatized to non-invasively quantify adherent cell proliferation and viability in realtime. This method has been effectively utilized previously to quantify and measure the number, adherence, growth, and viability of cells [20][21][22][23][24]. 50 µL of cell culture medium was added to each well of the microtiter E-plates for impedance background measurements, and then 50 µL cell suspensions were dispensed at the density of 10 3 cells/well.…”

Section: Real Time Cell Impedance Measurementsmentioning

confidence: 99%

Role of GDF15 in radiosensitivity of breast cancer cells

et al. 2014

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The Growth Differentiation Factor-15 gene (GDF15) is a member of TGF-b superfamily and this cytokine family is considered to be a promising target for cancer therapy. The purpose of this study was to investigate the effect of tumor derived GDF15 on proliferation and radiosensitivity of breast cancer cells in vitro and in vivo. A mouse breast cancer LM2 cell line with stable transfection of full-length mouse GDF15 cDNA was established. Cell growth and proliferation was observed using WST assay and impedance-based method. Radiation induced GDF15 and TGF-b1 expression was determined by qRT-PCR. Radiosensitivity was measured by a colony formation assay in vitro and by a tumor growth delay assay in vivo. Cells with more than a 10-fold increase in GDF15 expression had a higher growth rate than parental control cells in vitro and in vivo. The radiation induced elevation of the expression of TGFb1 was reduced in GDF15 overexpressing cells. GDF15 may play a role in the radiation response of breast cancer cells by effecting cell survival, inhibiting radiation-induced cell death, and inhibiting the TGF-b1 related cytotoxic action.

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