https://scholar.dgist.ac.kr/handle/20.500.11750/1118 2026-04-04T14:49:52Z https://scholar.dgist.ac.kr/handle/20.500.11750/10055 Title: Glutamate decarboxylase 67 contributes to compensatory insulin secretion in aged pancreatic islets Author(s): Cho, Jung Hoon; Lee, Kyeong-Min; Lee, Yun-Il; Nam, Hong Gil; Jeon, Won Bae Abstract: Pancreatic islets play an essential role in regulating blood glucose levels. Age-dependent development of glucose intolerance and insulin resistance results in hyperglycemia, which in turn stimulates insulin synthesis and secretion from aged islets, to fulfill the increased demand for insulin. However, the mechanism underlying enhanced insulin secretion remains unknown. Glutamic acid decarboxylase 67 (GAD67) catalyzes the conversion of glutamate into γ-aminobutyric acid (GABA) and CO 2 . Both glutamate and GABA can affect islet function. Here, we investigated the role of GAD67 in insulin secretion in young (3 month old) and aged (24 month old) C57BL/6J male mice. Unlike young mice, aged mice displayed glucose-intolerance and insulin-resistance. However, aged mice secreted more insulin and showed lower fed blood glucose levels than young mice. GAD67 levels in primary islets increased with aging and in response to high glucose levels. Inhibition of GAD67 activity using a potent inhibitor of GAD, 3-mercaptopropionic acid, abrogated glucose-stimulated insulin secretion from a pancreatic β-cell line and from young and aged islets. Collectively, our results suggest that blood glucose levels regulate GAD67 expression, which contributes to β-cell responses to impaired glucose homeostasis caused by advanced aging. © 2019, © 2019 The Author(s). Published with license by Taylor & Francis Group, LLC. 2019-02-28T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/9506 Title: Orientation-dependent optical characterization of atomically thin transition metal ditellurides Author(s): Hoang, Anh Tuan; Shinde, Sachin M.; Katiyar, Ajit K.; Dhakal, Krishna P.; Chen, Xiang; Kim, Hyunmin; Lee, Suk Woo; Lee, Zonghoon; Ahn, Jong-Hyun Abstract: Molybdenum ditellurides (MoTe2) have recently attracted attention owing to their excellent structurally tunable nature between 1T′(metallic)- and 2H(semiconducting)-phases; thus, the controllable fabrication and critical identification of MoTe2 are highly desired. Here, we semi-controllably synthesized 1T′- and 2H-MoTe2 crystals using the atmospheric pressure chemical vapor deposition (APCVD) technique and studied their grain-orientation dependency using polarization-sensitive optical microscopy, Raman scattering, and second-harmonic generation (SHG) microspectroscopy. The polycrystalline 1T′-MoTe2 phase with quasi-1D Mo-Mo zigzag chains showed anisotropic optical absorption, leading to a clear visualization of the lattice domains. On the other hand, 2H-MoTe2 lattice grains did not exhibit any discernible difference under polarized light illumination. The combined aforementioned microscopy techniques could be used as an easy-to-access and non-destructive tool for a quick and solid identification of intended lattice orientation development in industry-scale MoTe2 crystal manufacturing. © 2018 The Royal Society of Chemistry. 2018-11-30T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/9348 Title: Effect of young exosomes injected in aged mice Author(s): Lee, Bo-Ram; Kim, Jung-Hee; Choi, Eun-Sook; Cho, Jung-Hoon; Kim, Eunjoo Abstract: Introduction: Exosomes, nano-sized extracellular vesicles, are known to circulate through the blood stream to transfer molecular signals from tissue to tissue. Methods: To determine whether exosomes affect aging in animals, we primarily identified the changes in exosomal miRNA contents during the aging process. In exosomes from 12-month-old mice, mmu-miR-126-5p and mmu-miR-466c-5p levels were decreased and mmu-miR-184-3p and mmu-miR-200b-5p levels were increased significantly compared with those of 3-month-old mice. Their levels in exosomes were partially correlated with those in tissues: levels of only mmu-miR-126-5p and mmu-miR-466c-5p in lungs and/or liver were decreased, but those of mmu-miR-184-3p and mmu-miR-200b-5p in tissues did not coincide with those of exosomes. Results and discussion: In the aged tissues injected with young exosomes isolated from serum, mmu-miR-126b-5p levels were reversed in the lungs and liver. Expression changes in aging-associated molecules in young exosome-injected mice were obvious: p16(Ink4A), MTOR, and IGF1R were significantly downregulated in the lungs and/or liver of old mice. In addition, telomerase-related genes such as Men1, Mre11a, Tep1, Terf2, Tert, and Tnks were significantly upregulated in the liver of old mice after injection of young exosomes. Conclusion: These results indicate that exosomes from young mice could reverse the expression pattern of aging-associated molecules in aged mice. Eventually, exosomes may be used as a novel approach for the treatment and diagnosis of aging animals. 2018-08-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/6508 Title: Inhibitory effect of luteolin on osteoclast differentiation and function Author(s): Lee, Ji-Won; Ahn, Jae-Yong; Hasegawa, Shin-ichi; Cha, Byung-Yoon; Yonezawa, Takayuki; Nagai, Kazuo; Seo, Hwa-Jeong; Jeon, Won Bae; Woo, Je-Tae Abstract: Osteoclasts are multinucleated cells that play a crucial role in bone resorption, and are formed by the fusion of mononuclear osteoclasts derived from osteoclast precursors of the macrophage lineage. Compounds that specifically target functional osteoclasts would be ideal candidates for anti-resorptive agents for clinical applications. In the present study, we investigated the effects of luteolin, a flavonoid, on the regulation of receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis, functions and signaling pathway. Addition of luteolin to a coculture system of mouse bone marrow cells and ST2 cells in the presence of 10-8 M 1α,25(OH)2D3 caused significant inhibition of osteoclastogenesis. Luteolin had no effects on the 1α,25(OH) 2D3-induced expressions of RANKL, osteoprotegerin and macrophage colony-stimulating factor mRNAs. Next, we examined the direct effects of luteolin on osteoclast precursors using bone marrow macrophages and RAW264.7 cells. Luteolin completely inhibited RANKL-induced osteoclast formation. Moreover, luteolin inhibited the bone resorption by mature osteoclasts accompanied by the disruption of their actin rings, and these effects were reversely induced by the disruption of the actin rings in mature osteoclasts. Finally, we found that luteolin inhibited RANKL-induced osteoclastogenesis through the suppression of ATF2, downstream of p38 MAPK and nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) expression, respectively. Taken together, the present results indicate that naturally occurring luteolin has inhibitory activities toward both osteoclast differentiation and functions through inhibition of RANKL-induced signaling pathway as well as actin ring disruption, respectively. © 2010 Springer Science+Business Media B.V. 2009-11-30T15:00:00Z