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Olof Gidlöf

Research project participant

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LL-37-induced caspase-independent apoptosis is associated with plasma membrane permeabilization in human osteoblast-like cells


  • Elisabeth Bankell
  • Sara Dahl
  • Olof Gidlöf
  • Daniel Svensson
  • Bengt Olof Nilsson

Summary, in English

The host defense peptide LL-37 is active against both gram-positive and gram-negative bacteria, but it has also been shown to reduce human host cell viability. However, the mechanisms behind LL-37-induced human host cell cytotoxicity are not yet fully understood. Here, we assess if LL-37-evoked attenuation of human osteoblast-like MG63 cell viability is associated with apoptosis, and if the underlying mechanism may involve LL-37-induced plasma membrane permeabilization. MG63 cell viability and plasma membrane permeabilization were investigated by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method and by measuring lactate dehydrogenase (LDH) release, respectively. Apoptosis was assessed by the terminal deoxynucleotidyl dUTP nick end labeling (TUNEL) assay and Annexin V flow cytometry, and caspase-3 and poly (ADP-ribose) polymerase (PARP) cleavage were determined by Western blot. LL-37 (4 and 10 μM) reduced both cell number and cell viability, and these effects were associated with a pro-apoptotic effect demonstrated by positive TUNEL staining and Annexin V flow cytometry. LL-37-induced apoptosis was not coupled to either caspase-3 or PARP cleavage, suggesting that LL-37 causes caspase-independent apoptosis in MG63 cells. Both LL-37 and the well-known plasma membrane permeabilizer Triton X-100 reduced cell viability and stimulated LDH release. Triton X-100-treated cells showed positive TUNEL staining, and the detergent accumulated cells in late apoptosis/necrosis. Similar to LL-37, Triton X-100 caused no PARP cleavage. We conclude that LL-37 promotes caspase-independent apoptosis, and that this effect seems coupled to plasma membrane permeabilization in human MG63 cells.


  • Vascular Physiology
  • Cardiovascular Epigenetics
  • Molecular Cardiology
  • Molecular Epidemiology and Cardiology
  • Cardiology
  • Department of Experimental Medical Science

Publishing year








Document type

Journal article




  • Cell and Molecular Biology


  • Antimicrobial peptides (AMP)
  • Apoptosis
  • Cathelicidin
  • Cytotoxicity
  • Innate immunity



Research group

  • Vascular Physiology
  • Cardiovascular Epigenetics
  • Molecular Cardiology
  • Molecular Epidemiology and Cardiology


  • ISSN: 0196-9781