Biology subjects

Wang, S.-J.

Publications and source records attributed to Wang, S.-J..

4 recordsLinked to original sources

bioRxiv2026

MRI-Trackable Mesenchymal Stem Cells for Oncolytic Therapy: A Clinically Feasible Dual-Labeling Protocol

Non-invasive imaging of oncolytic virus-loaded mesenchymal stem cells (MSCs) could help evaluate cell trafficking and delivery in cancer therapy. Labeling MSCs with iron oxide particles (IOPs) enables in vivo tracking using magnetic resonance imaging (MRI). This study evaluated a dual-labeling strategy that loads MSCs with MegaPro IOPs and the oncolytic virus Delta-24-RGD (DNX-2401; tasadenoturev) and assessed cellular function and MRI detectability. MSCs were labeled with IOPs alone or in combination with the oncolytic virus. We compared cell viability and intracellular iron content among IOP-labeled, dual-labeled, and naive MSCs, and evaluated differentiation, invasion, and immunophenotype in naive and IOP-labeled MSCs. We evaluated phantoms containing varying numbers of IOP-labeled MSCs (9 x 103-1.5 x 105 cells) using R2-, R2*-, and R1-weighted MRI, and generated corresponding relaxation rate maps to assess concentration dependent contrast and detection sensitivity. Iron content was comparable between IOP-labeled and dual-labeled MSCs (9.2 {+/-} 2.6 and 11.6 {+/-} 1.4 pg/cell, respectively), with >91% viability across all groups. IOP-labeled MSCs retained invasion and differentiation potential. At the highest labeled-cell concentration, R2*, R2, and R1 increased approximately 4, 2.5, and 1.5 fold, respectively, relative to the agarose control. The estimated detection limits were approximately 2 x 103 cells for R2* and 6 x 103 cells for R2 and R1. These findings demonstrate that dual labeling of MSCs with IOPs and oncolytic virus preserves key cellular characteristics while providing MRI-detectable contrast, supporting further investigation of this approach for image-guided tracking of cell-based cancer therapies.

bioengineering↗

bioRxiv2025

Senescent astrocytic deposits drive cognitive decline by disrupting tripartite synapse in the aging brain

Brain aging involves synapse decline, with astrocytes playing a key role in synapse homeostasis. However, the impact of astrocyte senescence on synaptic dysfunction and cognitive decline remains unclear. Here, we identified a hallmark of aging astrocytes--Senescent Astrocytic Deposits (SAD) observed at aged rodents, macaques, and human hippocampal astrocytic processes --that is associated with tripartite synapse dysfunction and memory decline. Laser capture microdissection-coupled mass spectrometry (LCM-MS), spatial transcriptome analysis and 3D electron microscopy revealed that SAD are abnormal protein deposits at the processes of ApoE-high expression astrocyte subtype and associated with dysfunctional tripartite synapses. Using a transgenic mouse (Nrbf2 knockout) with accelerated SAD formation as a tool for genetic manipulation, we clearly demonstrated that age-dependent defect of phagocytosis at maturation stage in astrocytic drives SAD accumulation, synaptic injury and cognitive deficits. Collectively, our findings establish SAD as a mechanistic link between astrocyte senescence and synaptic damage, underscoring the critical role of astrocytic phagocytic function in preserving synaptic homeostasis and cognitive function during aging. Significance StatementThis study reveals that impaired phagocytic maturation in senescent astrocytes leads to formation of SAD and impaired synaptic plasticity, identifying hippocampal astrocyte senescence as a key contributor to age-related cognitive decline.

neuroscience↗

bioRxiv2022

Plant-on-Chip: core morphogenesis processes in the tiny plant Wolffia australiana

A plant can be thought of as a colony comprising numerous growth buds, each developing to its own rhythm. Such lack of synchrony impedes efforts to describe core principles of plant morphogenesis, dissect the underlying mechanisms, and identify regulators. Here, we use the tiniest known angiosperm to overcome this challenge and provide an ideal model system for plant morphogenesis. We present a detailed morphological description of the monocot Wolffia australiana, as well as high-quality genome information. Further, we developed the Plant-on-Chip culture system and demonstrate the application of advanced technologies such as snRNA-seq, protein structure prediction, and gene editing. We provide proof-of-concept examples that illustrate how W. australiana can open a new horizon for deciphering the core regulatory mechanisms of plant morphogenesis. SignificanceWhat is the core morphogenetic process in angiosperms, a plant like a tree indeterminately growing, or a bud sequentially generating limited types of organs? Wolffia australiana, one of the smallest angiosperms in the world may help to make a distinction. Wolffia plantlet constitutes of only three organs that are indispensable to complete life cycle: one leaf, one stamen and one gynoecium. Before the growth tip is induced to flower, it keeps branching from the leaf axil and the branches separate from the main plantlet. Here we present a high-quality genome of W. australiana, detailed morphological description, a Plant-on-Chip cultural system, and some principle-proof experiments, demonstrating that W. australiana is a promising model system for deciphering core developmental program in angiosperms.

plant biology↗

bioRxiv2022

Cellular Mechanisms Underlying Central Sensitization in a Mouse Model of Chronic Muscle Pain

Chronic pain disorders are often associated with psychiatric symptoms. The central nucleus of the amygdala (CeA) has emerged as an integrative hub for nociceptive and affective components during the development of central pain. Although the exact cause for this process remains unknown, prior adverse injuries are precipitating factors and thought to transform nociceptors into a primed state for chronic pain. However, the cellular basis underlying the primed state and the subsequent pain chronification remains unknown. Here, we investigated cellular and synaptic alterations of the CeA in a mouse model of chronic muscle pain. In these mice, local infusion of pregabalin, a clinically approved drug for fibromyalgia and other chronic pain disorders, into the CeA or selective inactivation of somatostatin-expressing CeA (CeA-SST) neurons during the priming phase prevented pain chronification. Further, electrophysiological recording revealed that CeA-SST neurons received increased excitatory transmission and showed enhanced excitability in chronic pain states. In line with the possible role of CeA-SST neurons in central sensitization, chemogenetic inactivation of CeA-SST neurons or pharmacological suppression of nociceptive afferents from the brainstem to CeA-SST neurons by pregabalin after the development of chronic muscle pain alleviated pain and negative emotions.

neuroscience↗