HoloMonitor ® M4FL

Chronic respiratory diseases, such as asthma, are an increaseing health issue worldwide and cause about 3.9 million deaths annually. Despite this, little is know about the molecular mechanisms underpinning disease pathogenesis. Bronchial and alveolar remodeling and impaired epithelial function are typical characteristics of chronic respiratory diseases. In these patients, an increased number of mast cells, positive for the serine proteases; tryptase and chymase, infiltrate the epithelium and the alveolar parenchyma. While it is likely that the epithelial cells are exposed to various amounts of released tryptase and chymase, the interaction between mast cells and epithelial cells remains unknown. This thesis aimed to investigate the impact of mast cell proteases on bronchial and alveolar remodelling. Human bronchial and alveolar epithelial cells were treated with tryptase and chymase. Holographic live cell imaging, fluorescent microscopy, and gene and protein assays were used to analyze various parameters such as proliferation patterns, protein expressions and distributions. The results showed that both tryptase and chymase promoted epithelial remodelling in several ways. Tryptase induced cell growth, cell survival, and wound healing, whereas chymase reduced cell growth, altered cell morphology and impaired epithelial barrier proprties. In conclusion, our results suggest that intraepithelial and alveolar mast cell release of proteases plays a crucial role in epithelial homeostasis, and that an inbalance of the protease release may be involved in respiratory disease progression and in disruption of critical epithelial functions.

Glioblastoma (GBM) is the most common malignant tumor of the central nervous system. Vasculogenic mimicry (VM) is a hematological system composed of tumor cells that exert blood perfusion without relying on vascular endothelial cells. The current poor results of anti-vascular therapy for clinical GBM are associated with the presence of VM; therefore, it is important to investigate VM formation in GBM. The results demonstrate thatSTK24P1 encodes P1-121aa with a kinase structural domain, and in vitro kinase assays demonstrated that P1-121aa mediates modification of ELF2 phosphorylation. ChIP and dual luciferase reporter gene assays demonstrated that the transcription factor ELF2 binds to VE-cadherin and the VEGFR2 promoter region, thereby promoting VM formation in glioma cells. P1-121aa, encoded by the pseudogene STK24P1, phosphorylates ELF2 at S107, increasing the stability of the ELF2 protein. ELF2 promotes VEGFR2 and VE-cadherin expression at the transcriptional level, which in turn promotes VM in GBM. This study demonstrates the important roles of STK24P1, P1-121aa, and ELF2 in regulating VM in GBM, which could provide potential targets for GBM treatment.HoloMonitor M4 is used to study the effect of different mutations on the migration ability of human glioma cell.

The regulation of cellular adhesion is a crucial aspect in the development of biomaterials and cell-based biosensing assays. In this study, synthetic poly(diallyldimethylammonium chloride) (PDADMAC), natural chitosan, and heparin were utilized to assemble PDADMAC/heparin and chitosan/heparin films. The physicochemical properties of these macroion multilayers were characterized using streaming potential measurements (SPM), quartz crystal microbalance (QCM-D), and optical waveguide lightmode spectroscopy (OWLS), while their topography was imaged using atomic force microscopy (AFM). The adhesion of the preosteoblastic cell line MC3T3-E1 on these well-characterized polysaccharide-based multilayers was evaluated using a resonant waveguide grating (RWG) based optical biosensor and digital holographic microscopy HoloMonitor M4. Results showed that PDADMAC/heparin films were the most effective in inducing cellular adhesion, while chitosan/heparin-based multilayers exhibited negligible cell attachment. These findings suggest that polysaccharide-based multilayers have potential for use in medical applications.HoloMonitor M4 is used to study the cell proliferation and morphological parameters of preosteoblastic cells on different coatings.

The article investigates the role of mast cell tryptase in bronchial and alveolar remodeling and the mechanisms of regulation during inflammation. The study found that mast cell tryptase enhanced human bronchial and alveolar epithelial cell growth and shortened the cell division intervals. The elevated cell growth induced by tryptase remained in a pro-inflammatory state. Tryptase also increased the expression of the anti-apoptotic protein BIRC3, as well as growth factor release in epithelial cells1. HoloMonitor is used to investigate the cell growth and cell division effects of mast cell tryptase on bronchial and alveolar epithelial cells.