https://scholarworks.unist.ac.kr/handle/201301/2 2026-04-08T20:40:31Z https://scholarworks.unist.ac.kr/handle/201301/91274 Title: Antiplatelet activity of a Korean red ginseng–derived saponin fraction and its inhibition of influenza A virus–induced thrombosis Author(s): Lee, Ga Hee; Oh, Jueun; Lee, Jin Pyo; Heo, Na Yoon; Lee, SangJoon; Lee, Dong-Ha Abstract: Background: Platelets play a central role in thrombus formation, which is a major cause of morbidity and mortality worldwide. Viral infections have been reported to further promote thrombus formation, posing a critical risk in unpredictable pandemic situations. Therefore, we evaluated whether a Korean red ginseng–derived saponin fraction could serve as a safe and effective antithrombotic agent by assessing its inhibitory effects. Methods: Human platelets were examined using an aggregometer, flow cytometry, fluorescence assays, ELISA kits, and western blotting to assess cGMP, intracellular Ca2+ levels, fibrinogen binding, granule secretion (ATP and serotonin), and phosphorylation of IP3R, VASP, MAPKs, PI3K/Akt, and cPLA2. Thrombin-induced clot retraction was quantified. The in vivo effects were further evaluated in influenza A virus (IAV)-infected mice using a FeCl3-induced carotid artery thrombosis model, where thrombus formation and blood flow were monitored. Results: The saponin fraction markedly inhibited platelet aggregation, enhanced cGMP production, and increased phosphorylation of IP3R and VASP Ser239. Conversely, it suppressed phosphorylation of MAPKs (JNK and p38), PI3K/Akt, and cPLA2, thereby blocking downstream signaling pathways. In vivo, IAV infection accelerated thrombus formation and reduced blood flow, whereas administration of the saponin fraction significantly attenuated these pathological changes. Conclusion: The saponin fraction effectively suppressed platelet activation in vitro and thrombus formation in vivo, even under virus-induced prothrombotic conditions. These findings suggest that the saponin fraction has potential as a safe and effective natural antithrombotic agent. 2025-12-31T15:00:00Z https://scholarworks.unist.ac.kr/handle/201301/91250 Title: Fucoxanthin Extracted from the Microalgae Phaeodactylum tricornutum Ameliorates Alzheimer's Pathologies with the Reduction of Aβ-Induced NLRP3 Inflammasome Activation in APP/PS1 Mice Author(s): Ahn Na-Hyun; Hong Sung-Chul; Hong Chi Rac; Lee Eun Ha; Lee Joo-Hee; Choi Su-Bin; Jung Jaewoon; Kim Yebeen; Kim, Jung-Seok; Park Keunwan; Kim Yun Kyung; Kim Youngsoo; Yang Seung-Hoon Abstract: Alzheimer's disease (AD) is a progressive neurodegenerative disorder, one of the most common types of dementia, accompanying severe learning and memory dysfunctions. In AD brains, the misfolded aggregation and deposits of amyloid-beta (A beta) and tau are frequently observed before the cognitive symptom onset; thus, trials for alleviation of these lesions are considered commensurate strategies with AD treatment. Additionally, increasing evidence suggests that misfolded and aggregated proteins induce the activation of microglia and astrocytes by the release of the inflammatory mediators via the activation of the inflammatory signaling cascade, which consequently contributes to AD pathogenesis. Here, we investigated the therapeutic potential of fucoxanthin, a compound derived from the microalgae Phaeodactylum tricornutum, in mitigating AD pathologies. Fucoxanthin was shown to inhibit the aggregation of A beta and tau, converting their aggregates to monomeric forms. In the brain of APP/PS1 transgenic mice, fucoxanthin administration significantly reduced the levels of A beta plaques and hyperphosphorylated tau and further ameliorated cognitive impairments by inhibiting the activation of microglia and astrocytes. Notably, fucoxanthin effectively regulated A beta-induced NLRP3 inflammasome activation in astrocytes, reducing neuroinflammation associated with AD. Thus, our findings showing the multifaceted therapeutic mode of action of fucoxanthin against AD provide that fucoxanthin would have promising roles in the strategies of AD treatment. 2025-12-31T15:00:00Z https://scholarworks.unist.ac.kr/handle/201301/91165 Title: TonEBP regulates ESR1 transcription and ER-dependent proliferation in ER-positive breast cancer Author(s): Kang, Hyun Je; Song, Hana; Park, Hyun; Park, Hye-Kyung; Shin, Go Woon; Son, Keoung Sun; Jeong, Yeseul; Ko, Seung Mi; Nam, Dougu; Kwon, Hyug Moo; Choi, Soo Youn Abstract: Estrogen receptor alpha (ER alpha), encoded by ESR1, is a central determinant of luminal breast cancer growth, yet the mechanisms sustaining basal ESR1 transcription remain incompletely defined. Here we identify tonicity-responsive enhancer-binding protein (TonEBP) as a promoter-associated regulator of ESR1 transcription and ER-dependent proliferation in ER-positive breast cancer. Elevated TonEBP expression correlated with adverse clinical outcomes across independent patient cohorts. In ER-positive cells, TonEBP depletion impaired proliferation, induced G1-phase accumulation, and attenuated ER signaling. A functional TonEBP-binding motif (TonE) was identified within the proximal ESR1 promoter; its mutation reduced promoter activity, and chromatin immunoprecipitation confirmed TonEBP enrichment at the endogenous locus. Consistently, TonEBP knockdown decreased ESR1 expression, ER alpha abundance, and estrogen response element-dependent transcription, while enhancing sensitivity to tamoxifen and doxorubicin. These findings support a model in which TonEBP sustains ER alpha expression through promoter-level regulation of ESR1, linking stress-responsive transcriptional control to hormone-dependent growth in luminal breast cancer. 2026-03-31T15:00:00Z https://scholarworks.unist.ac.kr/handle/201301/90788 Title: Distinct modes of dopamine modulation on striatopallidal synaptic transmission Author(s): Lee, Youngeun Lina; Reva, Maria; Kim, Ki Jung; Kim, Hyun-Jin; Kim, Yemin; Cho, Eunjeong; Jeong, Minseok; Kwak, Youngjong; Myung, Kyungjae; Li, Yulong; Lee, Seung Eun; Jang, Dong Pyo; Lee, C. Justin; Lüscher, Christian; Kim, Jae-Ick Abstract: Dopamine affects voluntary movement by modulating basal ganglia function. However, the contribution of dopamine on striatopallidal synapses, an initial hub in the indirect pathway connecting the striatum to the GPe, remains poorly understood because of the sparse dopaminergic innervation. Here, we combine optogenetic projection targeting, whole cell patch clamp recordings in acute brain slices from mice, and computational modeling to overcome this limitation. We show that dopamine activates D2 receptors (D2Rs) and D4 receptors (D4Rs) differentially in distinct GPe subregions. In a pinwheel-like fashion, dorsolateral and ventromedial GPe expresses high levels of D2Rs, which exert presynaptic inhibition, while in dorsomedial and ventrolateral GPe D4Rs cause postsynaptic inhibition. Dopamine depletion by 6-OHDA reshapes the region-specific effect of dopamine, shifting it in the opposite direction and contributing to hypokinesia. These findings reveal the mechanism by which the different modality information conveyed spatially through the indirect pathway is differentially modulated by dopamine at striatopallidal synapses. 2026-02-28T15:00:00Z