https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/111692 2026-04-04T21:06:32Z 2026-04-04T21:06:32Z Jeong, Haengdueng Lee, Buhyun Cho, Soo Young Lee, Yura Kim, Jiseon Hur, Sumin Cho, Kyungrae Kim, Kwang H. Kim, Sung-Hee Nam, Ki Taek https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/122075 2026-01-09T07:04:28Z 2025-02-01T00:00:00Z

Title: Microbiota-derived short-chain fatty acids determine stem cell characteristics of gastric chief cells Authors: Jeong, Haengdueng; Lee, Buhyun; Cho, Soo Young; Lee, Yura; Kim, Jiseon; Hur, Sumin; Cho, Kyungrae; Kim, Kwang H.; Kim, Sung-Hee; Nam, Ki Taek Abstract: The gastric mucosa is a highly dynamic tissue that undergoes constant self-renewal through stem cell differentiation. Chief cells maintain a quiescent state in homeostasis but are responsible for regeneration after injury. Although the role of microbiome-host interactions in the intestine is well studied, less is known about these interactions in the stomach. Using the mouse organoid and germ-free mouse models, we show that microbiota-derived short-chain fatty acids (SCFAs) suppress the proliferation of chief cells in mice. This effect is mediated by activation of G-protein-coupled receptor 43. Most importantly, through metabolomics and transplantation studies, we show butyrate-producing Lactobacillus intestinalis modulates the proliferation of chief cells in mice. Our findings identify a mechanism by which the microbiota regulates the cell characteristics of chief cells, providing insight into the complex interplay between the host and its microbial environment and the mechanisms underlying gastric homeostasis, with potential therapeutic implications for gastric diseases. © 2024 Elsevier Inc.

2025-02-01T00:00:00Z Mun, Seok-Jun Cho, Euni Gil, Woo Jin Kim, Seong Jae Kim, Hyo Keun Ham, Yu Seong Yang, Chul-Su https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/122002 2025-01-16T07:00:19Z 2024-12-01T00:00:00Z

Title: Dual alarmin-receptor-specific targeting peptide systems for treatment of sepsis Authors: Mun, Seok-Jun; Cho, Euni; Gil, Woo Jin; Kim, Seong Jae; Kim, Hyo Keun; Ham, Yu Seong; Yang, Chul-Su Abstract: The pathophysiology of sepsis is characterized by a systemic inflammatory response to infection; however, the cytokine blockade that targets a specific early inflammatory mediator, such as tumor necrosis factor, has shown disappointing results in clinical trials. During sepsis, excessive endotoxins are internalized into the cytoplasm of immune cells, resulting in dysregulated pyroptotic cell death, which induces the leakage of late mediator alarmins such as HMGB1 and PTX3. As late mediators of lethal sepsis, overwhelming amounts of alarmins bind to high-affinity TLR4/MD2 and low-affinity RAGE receptors, thereby amplifying inflammation during early-stage sepsis. In this study, we developed a novel alarmin/receptor-targeting system using a TLR4/MD2/RAGE-blocking peptide (TMR peptide) derived from the HMGB1/PTX3-receptors interacting motifs. The TMR peptide successfully attenuated HMGB1/PTX3- and LPS-mediated inflammatory cytokine production by impairing its interactions with TLR4 and RAGE. Moreover, we developed TMR peptide-conjugated liposomes (TMR-Lipo) to improve the peptide pharmacokinetics. In combination therapy, moderately antibiotic-loaded TMR-Lipo demonstrated a significant therapeutic effect in a mouse model of cecal ligation- and puncture-induced sepsis. The identification of these peptides will pave the way for the development of novel pharmacological tools for sepsis therapy. © 2024 The Authors

2024-12-01T00:00:00Z Kim, Sasuk Lim, Juhee Bang, Yeojin Moon, Jisook Kwon, Min-Soo Hong, Jin Tae Jeon, Jeha Seo, Hyemyung Choi, Hyun Jin https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/121892 2025-01-31T04:30:18Z 2024-12-01T00:00:00Z

Title: Editorial Expression of Concern: Alpha-Synuclein Suppresses Retinoic Acid-Induced Neuronal Differentiation by Targeting the Glycogen Synthase Kinase-3β/β-Catenin Signaling Pathway Authors: Kim, Sasuk; Lim, Juhee; Bang, Yeojin; Moon, Jisook; Kwon, Min-Soo; Hong, Jin Tae; Jeon, Jeha; Seo, Hyemyung; Choi, Hyun Jin Abstract: [No abstract available]

2024-12-01T00:00:00Z Yoon, Chanjin Keun,Kim, Hyo Ham, Yu Seong Gil, Woo Jin Mun, Seok-Jun Cho, Euni Yuk, Jae-Min Yang, Chul-Su https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/120774 2024-11-26T00:00:21Z 2024-10-01T00:00:00Z

Title: Toxoplasma gondii macrophage migration inhibitory factor shows anti- Mycobacterium tuberculosis potential via AZIN1/STAT1 interaction Authors: Yoon, Chanjin; Keun,Kim, Hyo; Ham, Yu Seong; Gil, Woo Jin; Mun, Seok-Jun; Cho, Euni; Yuk, Jae-Min; Yang, Chul-Su Abstract: Mycobacterium tuberculosis (MTB) is a pathogenic bacterium, belonging to the family Mycobacteriaceae, that causes tuberculosis (TB). Toxoplasma gondii macrophage migration inhibitory factor (TgMIF), a protein homolog of macrophage migration inhibitory factor, has been explored for its potential to modulate immune responses during MTB infections. We observed that TgMIF that interacts with CD74, antizyme inhibitor 1 (AZIN1), and signal transducer and activator of transcription 1 (STAT1) modulates endocytosis, restoration of mitochondrial function, and macrophage polarization, respectively. These interactions promote therapeutic efficacy in mice infected with MTB, thereby presenting a potential route to host-directed therapy development. Furthermore, TgMIF, in combination with first-line TB drugs, significantly inhibited drug-resistant MTB strains, including multidrug-resistant TB. These results demonstrate that TgMIF is potentially a multifaceted therapeutic agent against TB, acting through immune modulation, enhancement of mitochondrial function, and dependent on STAT1 and AZIN1 pathways.

2024-10-01T00:00:00Z