Biology subjects

Tse, H.

Publications and source records attributed to Tse, H..

3 recordsLinked to original sources

bioRxiv2024

Electrospun Fiber Surface Roughness Modulates Human Monocyte-Derived Macrophage Phenotype

Injuries to fibrous connective tissues have very little capacity for self-renewal and exhibit poor healing after injury. Phenotypic shifts in macrophages play a vital role in mediating the healing response, creating an opportunity to design immunomodulatory biomaterials which control macrophage polarization and promote regeneration. In this study, electrospun poly(-caprolactone) fibers with increasing surface roughness (SR) were produced by increasing relative humidity and inducing vapor-induced phase separation during the electrospinning process. The impact of surface roughness on macrophage phenotype was assessed using human monocyte-derived macrophages in vitro and in vivo using B6.Cg-Tg(Csf1r-EGFP)1Hume/J (MacGreen) mice. In vitro experiments showed that macrophages cultured on mesh with increasing SR exhibited decreased release of both pro- and anti-inflammatory cytokines potentially driven by increased protein adsorption and biophysical impacts on the cells. Further, increasing SR led to an increase in the expression of the pro-regenerative cell surface marker CD206 relative to the pro-inflammatory marker CD80. Mesh with increasing SR were implanted subcutaneously in MacGreen mice, again showing an increase in the ratio of cells expressing CD206 to those expressing CD80 visualized by immunofluorescence. SR on implanted biomaterials is sufficient to drive macrophage polarization, demonstrating a simple feature to include in biomaterial design to control innate immunity. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=86 SRC="FIGDIR/small/610568v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@1b40283org.highwire.dtl.DTLVardef@1110307org.highwire.dtl.DTLVardef@1ddc63eorg.highwire.dtl.DTLVardef@1021581_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

bioRxiv2022

Numerical investigation of the dynamics of a rigid spherical particle in a vortical cross-slot flow at moderate inertia

The study of flow and particle dynamics in microfluidic cross-slot channels is of high relevance for lab-on-a-chip applications. In this work we investigate the dynamics of a rigid spherical particle in a cross-slot junction for a channel height-to-width ratio of 0.6 and at a Reynolds number of 120 for which a steady vortex exists in the junction area. Using an in-house immersed- boundary-lattice-Boltzmann code, we analyse the effect of the entry position of the particle in the junction and the particle size on the dynamics and trajectory shape of the particle. We find that the dynamics of the particle depends strongly on its lateral entry position in the junction and weakly on its vertical entry position; particles that enter close to the centre show trajectory oscillations. Larger particles have longer residence times in the junction and tend to oscillate less due to their confinement. Our work contributes to the understanding of the particle dynamics in intersecting flows and enables the design of optimised geometries for cytometry and particle manipulation.

biophysics↗

bioRxiv2019

Inhibition of mTORC1 signaling in aged rats counteracts the decline in muscle mass and reverses multiple parameters of muscle signaling associated with sarcopenia

There is a lack of pharmacological interventions available for sarcopenia, a progressive age-associated loss of muscle mass, leading to a decline in mobility and quality of life. We found mTORC1 (mammalian target of rapamycin complex 1), a well-established critical positive modulator of mass, to be hyperactivated in sarcopenic muscle. Furthermore, inhibition of the mTORC1 pathway counteracted sarcopenia as determined by observing an increase in muscle mass and fiber type cross sectional area, surprising because mTORC1 signaling has been shown to be required for muscle mass gains in some settings. Additionally, several genes related to senescence were downregulated, while gene expression indicators of neuromuscular junction denervation were diminished using a low dose of a rapalog. Therefore mTORC1 inhibition may delay the progression of sarcopenia by directly and indirectly modulating multiple age-associated pathways, implicating mTORC1 as a therapeutic target to treat sarcopenia.

physiology↗