4.4 Article

The effect of LDL particles on the behaviour of epithelial noncancer and cancer cell lines after in vitro induced injury

Journal

PROTOPLASMA
Volume 252, Issue 6, Pages 1537-1550

Publisher

SPRINGER WIEN
DOI: 10.1007/s00709-015-0784-7

Keywords

LDL particles; Epithelial cell; Cancer cells; Re-epithelisation; Cell spreading; Proliferation

Funding

  1. Slovenian Research Agency ARRS [P3-0108]

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Cell spreading capability and cell proliferation are the major processes in wound healing of injured epithelia as well as in tumour progression. The effect of low-density lipoprotein (LDL) particles as a major extracellular source of cholesterol was evaluated in the re-epithelisation assay of in vitro induced injury. We selected two noncancer cell lines with different dependence on LDL concentrations, the kidney epithelial cells (MDCK) with higher dependence and keratinocytes (HaCaT) with lower dependence on LDL, and three cancer cell lines originating from epithelial cells: A549 (alveolar), CaCo-2 (intestinal) and RT4 (urothelial). All cells were incubated in a control medium, in an LDL-enriched medium or in an LDL-deficient medium. The LDL-enriched medium stimulated cell spreading of MDCK cells which, together with increased proliferation of these cells, resulted in an enhanced re-epithelisation of in vitro induced injury. LDL deficiency caused lower cell spreading which resulted in a decreased re-epithelisation despite the higher proliferation of MDCK cells in this medium. The re-epithelisation of keratinocytes (HaCaT) was not affected by altered LDL concentrations. In cancer cell lines A549, CaCo-2 and RT4, wide heterogeneity regarding cell proliferation and spreading capability was observed after treatment with different LDL concentrations. LDL had no influence on actin filament and tight junction distribution in any of the tested cell lines. The cholesterol content of all cell types, except for CaCo-2 cells, proved to be independent of the LDL level. Further research of the beneficial effects of LDL is needed to prove LDL as a safe enhancer of epithelial wound healing.

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