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Leptin affects filopodia and cofilin in NK-92 cells in a dose- and time-dependent manner

Jana Oswald, Maximilian Büttner, Simon Jasinsky-Bergner and 3 more

European Journal of Histochemistry · 2018

doi:10.4081/ejh.2018.2848 (opens in a new tab)

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Abstract

Hyperleptinemia, associated with obesity, is related with immune dysfunction and carcinogenesis. Natural Killer (NK) cells, a major component of the innate immune system are mediators of anti-tumor immunity and the most actively migrating cells among leukocytes. Actin rearrangement, promoted by cofilin plays a central role in cellular migration. Leptin affects the phosphorylation-dependent activity of cofilin and thus actin remodeling. We used human NK-92 cells to explore the in vitro effects of leptin on co-localization of cofilin and F-actin and on morphological changes in NK cells. NK-92 cells were incubated with different leptin concentrations (10 and 100 ng/mL) for 30 min and 24 h and immunocytochemically stained. Results demonstrate a dose- and time-dependent influence of leptin on cellular morphology. Utilizing confocal microscopy, we observed that the co-localization of cofilin-1 and F-actin was slightly influenced by leptin. In summary, the present study demonstrates an impact of a physiological leptin stimulation on the filopodia length, and a time-dependent effect on the co-localization of cofilin and F-actin in NK-92 cells.

Abstract licence: CC BY-NC

References47

  1. 11.
  2. 17.
  3. 39.
  4. 40.

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