MO015ANALYZING THE EFFECT OF MICROPLASTIC PARTICLES ON HUMAN PODOCYTES

Background and Aims Despite increasing use of plastic based products and their potential health risks on the humans, very little is known about their possible accumulation in the food chain and their further long-term effect on the human health. Recently, there are increasing reports related to the potential risk of polystyrene microplastics to the human respiratory system and human intestinal epithelia cell line. In this study, we assayed the primary effect of microplastic particles on the human kidney cells. To that aim, we used human podocytes cells and four different types of plastic particles including; polyvinyl chloride (PVC), polypropylene (PP), polyamide (PA) and tyre wear particles to evaluate the effects of microplastics on the viability and morphology of human podocytes in vitro. Method In this study, we applied different biological methods such as, cell viability test and phalloidin staining, to assay the toxicity of particles and their further effects on the actin cytoskeleton organization in human podocytes, respectively. Furthermore, Raman imaging is used to track particle attachment on the cells and to evaluate the possible changes in the cell compartment following the particle treatment. The particle uptake by the cells and changes in cellular biological features were visualized with the use of scanning electron microscopy (SEM). Results As a primary result, the cytotoxicity response of particle treatment was found to be dependent on the polymer type. As an example higher concentration of PP particle as compared to PVC, PA, and tyre wear caused a similar rate of cell mortality. Furthermore, the degree of particle attachment on the cells depended on their adhesion properties, which was higher in PA, PVC and tyre wear in comparison to PP particles. These particles remained attached to the cell surface even after two-three times of washing with PBS. Based on the phalloidin staining results, particle treatment induced cytoskeleton reorganization in podocytes in vitro. With the use of Raman imaging particle attachment was confirmed based on the fingerprint spectra related to each particle. Conclusion This study suggests that exposure duration and particle concentrations are two of the key factors to evaluate the toxicological effect of particles on podocytes as a highly-specialized epithelial cells in the kidney. It is supposed that two mechanisms can be related to the harmful effects of plastic particles on podocytes. First, particle attachment on the cell surface leading to limitation of nutrient uptake by the cells. Second, uptake of smaller size particles into the cells through phagocytosis. More studies are necessary to determine the direct effect of microplastics on human kidney cells.

Identification of the SHREK family of proteins as broad-spectrum host antiviral factors

ABSTRACTMucins and mucin-like molecules are highly glycosylated, high-molecular-weight cell surface proteins that possess a semi-rigid and highly extended extracellular domain. P-selectin glycoprotein ligand-1 (PSGL-1), a mucin-like glycoprotein, has recently been found to restrict HIV-1 infectivity through virion incorporation that sterically hinders virus particle attachment to target cells. Here, we report the identification of a family of antiviral cellular proteins, named the Surface-Hinged, Rigidly-Extended Killer (SHREK) family of virion inactivators (PSGL-1, CD43, TIM-1, CD34, PODXL1, PODXL2, CD164, MUC1, MUC4, and TMEM123), that share similar structural characteristics with PSGL-1. We demonstrate that SHREK proteins block HIV-1 infectivity by inhibiting virus particle attachment to target cells. In addition, we demonstrate that SHREK proteins are broad-spectrum host antiviral factors that block the infection of diverse viruses such as influenza A. Furthermore, we demonstrate that a subset of SHREKs also blocks the infectivity of a hybrid alphavirus-SARS-CoV-2 virus-like particle. These results suggest that SHREK proteins may be a part of host innate immunity against enveloped viruses.

From particle attachment to space-filling coral skeletons

Reef-building corals and their aragonite (CaCO3) skeletons support entire reef ecosystems, yet their formation mechanism is poorly understood. Here we used synchrotron spectromicroscopy to observe the nanoscale mineralogy of fresh, forming skeletons from six species spanning all reef-forming coral morphologies: Branching, encrusting, massive, and table. In all species, hydrated and anhydrous amorphous calcium carbonate nanoparticles were precursors for skeletal growth, as previously observed in a single species. The amorphous precursors here were observed in tissue, between tissue and skeleton, and at growth fronts of the skeleton, within a low-density nano- or microporous layer varying in thickness from 7 to 20 µm. Brunauer-Emmett-Teller measurements, however, indicated that the mature skeletons at the microscale were space-filling, comparable to single crystals of geologic aragonite. Nanoparticles alone can never fill space completely, thus ion-by-ion filling must be invoked to fill interstitial pores. Such ion-by-ion diffusion and attachment may occur from the supersaturated calcifying fluid known to exist in corals, or from a dense liquid precursor, observed in synthetic systems but never in biogenic ones. Concomitant particle attachment and ion-by-ion filling was previously observed in synthetic calcite rhombohedra, but never in aragonite pseudohexagonal prisms, synthetic or biogenic, as observed here. Models for biomineral growth, isotope incorporation, and coral skeletons’ resilience to ocean warming and acidification must take into account the dual formation mechanism, including particle attachment and ion-by-ion space filling.