Cholesterol modulates the interaction of sodium salt with negatively charged phospholipid membrane.

We present a systematic study on how alkali metal salts, like NaCl and NaI, affect negatively charged phospholipid vesicles using a range of experimental methods. Our goal was to find out how chain saturation and cholesterol affect the interaction between the ions and the membrane. An isothermal titration calorimetry study on large unilamellar vesicles made from dimyristoyl phosphatidylcholine (DMPC) revealed that Na shows higher binding affinity to the gel phase at 15 °C compared to the fluid phase at 30 °C.

Cholesterol-driven modulation of membrane-membrane interactions by an antimicrobial peptide, NK-2, in phospholipid vesicles.

Antimicrobial peptides (AMPs) are essential components of the innate immune system, demonstrating their antimicrobial effects primarily through the creation of transmembrane pores that result in membrane disruption. Cholesterol within the membrane can significantly affect the interaction between AMPs and the membrane, as it is known to alter both the permeability and elastic properties of the membrane. In this study, we have investigated the influence of cholesterol on the interaction of the AMP, NK-2 with phospholipid vesicles.

Effect of cholesterol on the ion-membrane interaction: Zeta potential and dynamic light scattering study.

Cholesterol in a bio-membrane plays a significant role in many cellular event and is known to regulate the functional activity of protein and ion channel. In this study we report a significant effect of cholesterol on the ion-membrane interaction. We prepare large unilamellar vesicles, composed of zwitterionic lipid DOPC and anionic lipid DOPG with different cholesterol concentration.

An evidence of pores in phospholipid membrane induced by an antimicrobial peptide NK-2.

NK-2, a peptide derived from a cationic core region of NK-lysin, has emerged as a promising candidate for new antibiotics. In contrast to classical antibiotics, antimicrobial peptides target bacterial membranes and disintegrate the membrane by forming the transmembrane pores. However, complete understanding of the precise mechanisms of cellular apoptosis and molecular basis of membrane selectivity is still in dispute.