https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/4 Sun, 05 Apr 2026 06:32:28 GMT 2026-04-05T06:32:28Z https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/79436 Title: Therapeutic reprogramming of circulating myeloid cells via signal regulatory protein a extracellular vesicles in acute kidney injury Authors: Shin, Dong-U; Jo, Min Kyoung; Kwon, Minjeong; Jeong, Yewon; Cho, Bogyeong; Kim, Seong A.; Choi, Ga-Eun; Kim, Seohyun; Song, Seok Ho; Joo, Hyemin; KIM, Hyun Jung; Lee, Jung Pyo; Lee, Jeonghwan; Kim, In-San; Nam, Gi Hoon Abstract: Introduction: Acute kidney injury (AKI) presents significant clinical challenges, with high mortality and progression risk to chronic kidney disease. Mechanisms remain incompletely understood and disease-specific therapies are lacking. Recent evidence highlights the pivotal role of infiltrating myeloid cells in perpetuating kidney inflammation. CD47, a key cell surface immune checkpoint protein, is upregulated in inflammation and regulates myeloid cell infiltration, making it an attractive therapeutic target. Methods: Single-cell RNA sequencing and CD47 protein staining were used to identify CD47 expressions in human AKI specimens and two mouse models (cis-platin and bilateral ischemia/reperfusion). To therapeutically exploit this, we engineered extracellular vesicles (EVs) from human bone marrow mesenchymal stem cells to express a high-affinity signal regulatory protein a (SIRP alpha) variant (SIRP-EVs), the ligand for CD47. The efficacy of SIRP-EVs was evaluated in murine AKI models. Results: CD47 expression was significantly elevated in myeloid populations, particularly macrophages, in both human AKI tissues and mouse models. A single systemic administration of SIRP-EVs in murine AKI models exhibited therapeutic effects, including improved kidney function markers, reduced pro-inflammatory cytokine production, and ameliorated kidney histopathology. Mechanistically, SIRP-EVs preferentially localize to circulating myeloid cells, modulate CD47 expression, and subsequently inhibit their migration into injured kidney tissue. Moreover, single cell transcriptomics revealed that SIRP-EV treatment reprograms circulating macrophages toward pro-resolving phenotypes, characterized by upregulation of genes associated with tissue repair. Conclusions: Targeting CD47 on circulating myeloid cells with SIRP-EVs provides a systemic, blood-focused immunomodulatory strategy that precedes tissue infiltration, contrasting with conventional tissue-centric approaches. Our findings support SIRP-EVs as a promising therapeutic option for AKI and potentially other inflammation-driven diseases through selective modulation and reprogramming of peripheral myeloid cells. Sun, 01 Mar 2026 00:00:00 GMT https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/79436 2026-03-01T00:00:00Z https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78750 Title: NDST3-Induced Epigenetic Reprogramming Reverses Neurodegeneration in Parkinson's Disease Authors: Chang, Yujung; Na, Yongwoo; Im, Hyeonjoo; Yang, Garam; Yang, Seungseon; Shim, Hyun-soo; Kim, Chunggoo; Kim, Gyeung Yun; Park, Hyeok-ju; Kim, Hee-young; Lee, Seungeun; Lee, Wonwoong; Ha, Yoon; Park, Sungho; Kim, Jieun; Cho, Won-young; Sun, Woong; Kim, Jong Seo; Yoo, Junsang Abstract: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons (DN) in the substantia nigra and disruption of cellular maintenance. Here, we demonstrate that NDST3-mediated epigenetic reprogramming halts neuronal degeneration and restores motor function in an animal model of PD. Following NDST3 administration, the DN and its associated circuits in the substantia nigra and striatum showed marked revitalization, accompanied by a considerable alleviation of PD-like motor deficits. Integrative single-cell and spatial RNA sequencing with CUT&RUN revealed that NDST3-driven reactivation of pathways is linked to neuronal survival, synaptic integrity, and steering of compromised cells toward a resilient phenotype. By recalibrating the epigenetic landscape, NDST3 promotes cellular maintenance and functional recovery in key motor circuits. These findings highlight NDST3's therapeutic potential as an epigenetic modulator of PD. These findings provide insights into the mechanisms underlying neuronal revitalization and highlight the potential of NDST3 as a novel agent for restoring brain function in neurodegenerative conditions. © 2025 Stand up Therapeutics and The Author(s). Advanced Science published by Wiley-VCH GmbH. Sun, 01 Mar 2026 00:00:00 GMT https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78750 2026-03-01T00:00:00Z https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/79305 Title: Analytical evaluation of intact human tissues using mid-frequency scanning acoustic microscopy at the mesoscopic scale Authors: Kim, Dasom; Koo, Jeongmo; Kim, Dai Hyun; Kim, Nam-Woon; Yu, Hyunung; Rhyu, Im Joo Abstract: Conventional histological examination requires irreversible sectioning, consuming tissue and precluding three-dimensional analysis. This limitation is particularly problematic for archival specimens and forensic investigations. Scanning acoustic microscopy (SAM) enables non-destructive tissue visualization through acoustic impedance contrast without sectioning or staining, offering a complementary approach to conventional histology. We investigated mid-frequency (50 MHz) SAM imaging of intact, formalin-fixed human tissue blocks representing diverse anatomical structures, including skull table, pineal gland, cerebellum, and scalp. SAM successfully delineated histologically meaningful microarchitectural features, including trilaminar skull organization with diploic channels; pineal calcifications (corpora arenacea); cerebellar cortical lamination with identifiable Purkinje cells; and stratified scalp architecture. Multifocal image integration and stereoscopic reconstruction enabled extended depth-of-field imaging and three-dimensional visualization of intact specimens. Corresponding hematoxylin-eosin and Masson's trichrome histology confirmed close structural agreement with SAM-derived contrasts. This non-destructive imaging approach preserves tissue integrity while generating digital datasets suitable for volumetric reconstruction and downstream computational analysis, supporting applications in anatomical education, tissue banking, pathology training, and biomedical research. Sun, 01 Feb 2026 00:00:00 GMT https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/79305 2026-02-01T00:00:00Z https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/77717 Title: Diesel exhaust particles attenuate skeletal muscle cell proliferation and induce skeletal muscle atrophy through activation of AMP-activated protein kinase Authors: Kang, Yeong Hoon; Lim, Hyun Joung; Park, Eunsook; Bang, Jihye; Han, Hee-Soo; Kim, Youngyoul; Kang, Min Ju; Uhm, Kyung-Ok; Kim, Hyeon Soo Abstract: BackgroundExtensive research has been conducted on the adverse effects of particulate matter on human health, primarily focusing on its impact on the respiratory and cardiovascular systems. However, there has been limited research on the effects of particulate matter on skeletal muscle at the cellular level.ObjectiveIn this study, we investigated the effects of diesel exhaust particles on skeletal muscle at the cellular level.MethodsC2C12 myoblasts were treated with 0, 1, 3, 10, 30, or 100 mu g/mL of SRM1650b diesel exhaust particles, and viability was measured using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The protein expression of key downstream molecules in the Akt signaling pathway was determined by western blotting. The relative expression of muscle-atrophy-related gene mRNA was analyzed using real-time PCR.ResultsIncubating C2C12 myotubes with diesel exhaust particles resulted in the activation of the AMP-activated protein kinase signaling pathway in a concentration- and time-dependent manner. Furthermore, the Akt/mTOR signaling pathway was inhibited in the presence of diesel exhaust particles, as evidenced by the decreased phosphorylation of Akt and downstream molecules such as mTOR, p70S6K1, and 4E-BP1. Additionally, diesel exhaust particles upregulated the expression of the muscle-atrophy-related genes MuRF-1 and MAFbx. Inhibition of AMP-activated protein kinase using compound C or AMPK alpha 2 small interfering RNA reversed the effects of diesel exhaust particles on Akt/mTOR signaling and atrophy-related gene expression.ConclusionsOur study provides valuable insights into the molecular mechanisms that underlie the harmful effects of diesel exhaust particles on skeletal muscle at the cellular level, emphasizing the significance of AMP-activated protein kinase signaling in muscle homeostasis. These findings may advance our understanding of the health risks associated with PM exposure and guide the development of preventive and therapeutic strategies. Sun, 01 Feb 2026 00:00:00 GMT https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/77717 2026-02-01T00:00:00Z