Molecularly imprinted nanoparticles with recognition properties towards diphtheria toxin for ELISA applications.

Plastic antibodies can be used for in vitro neutralization of biomacromolecules with different fragments due to their potential in separation, purification, chemical sensor, catalysis and drug production studies. These polymer nanoparticles with binding affinity and selectivity comparable to natural antibodies were prepared using functional monomer synthesis and copolymerization of acrylic monomers via miniemulsion polymerization. As a result, the in vitro cytotoxic effect from diphtheria toxin was reduced by MIPs. In vitro imaging experiments of polymer nanoparticles (plastic antibodies) were performed to examine the interaction of diphtheria toxin with actin filaments, and MIPs inhibited diphtheria toxin damage on actin filaments. The enzyme-linked immunosorbent assay (ELISA) was performed with plastic antibodies labeled with biotin, and it was determined that plastic antibodies could also be used for diagnostic purposes. We report that molecularly imprinted polymers (MIPs), which are biocompatible polymer nanoparticles, can capture and reduce the effect of diphtheria toxic and its fragment A.

Macromolecules can be imprinted by using their fragments as template molecules.MIPs gain an affinity for the template molecule by covalent binding, non-covalent interactions or ligand interactions, as well as the ability to bind, release and recognize the template molecule.The viability of cells treated with DT, NIPs and MIPs was determined by MTT assay.Immunofluorescence staining studies examined structural changes in actin filaments in HUVEC treated with DT, NIPs and MIPs.FA imprinted polymer has the ability to bind whole diphtheria toxin.FA-MIP gave significant results in terms of specificity in ELISA using diphtheria toxin.

Mitochondrial dynamic alterations regulate melanoma cell progression.

Research on mitochondrial fusion and fission (mitochondrial dynamics) has gained much attention in recent years, as it is important for understanding many biological processes, including the maintenance of mitochondrial functions, apoptosis, and cancer. The rate of mitochondrial biosynthesis and degradation can affect various aspects of tumor progression. However, the role of mitochondrial dynamics in melanoma progression remains controversial and requires a mechanistic understanding to target the altered metabolism of cancer cells. Therefore, in our study, we disrupted mitochondrial fission with mdivi-1, the reported inhibitor of dynamin related protein 1 (Drp1), and knocked down Drp1 and Mfn2 to evaluate the effects of mitochondrial dynamic alterations on melanoma cell progression. Our confocal study results showed that mitochondrial fission was inhibited both in mdivi-1 and in Drp1 knockdown cells and, in parallel, mitochondrial fusion was induced. We also found that mitochondrial fission inhibition by mdivi-1 induced cell death in melanoma cells. However, silencing Drp1 and Mfn2 did not affect cell viability, but enhanced melanoma cell migration. We further show that dysregulated mitochondrial fusion by Mfn2 knockdowns suppressed the oxygen consumption rate of melanoma cells. Together, our findings suggest that mitochondrial dynamic alterations regulate melanoma cell migration and progression.