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Your search keyword '"Jung, Myeong Hee"' showing total 39 results
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39 results on '"Jung, Myeong Hee"'

4. Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction

Author

Park, Jeong Rang, primary, Ahn, Jong Hwa, additional, Jung, Myeong Hee, additional, Kim, Jin Hyun, additional, Kang, Min Gyu, additional, Kim, Kye Hwan, additional, Jang, Jeong Yoon, additional, Park, Hyun Woong, additional, Koh, Jin-Sin, additional, Hwang, Seok-Jae, additional, Park, Yongwhi, additional, Jeong, Young-Hoon, additional, Kwak, Choong Hwan, additional, and Hwang, Jin-Yong, additional

Published
2022
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6. Supplementary_figure_1 – Supplemental material for The protective effect of human adiposederived mesenchymal stem cells on cisplatin-induced nephrotoxicity is dependent on their level of expression of heme oxygenase-1

Author

Cho, Hyun Seop, Jang, Ha Nee, Jung, Myeong Hee, Jang, Si Jung, Jeong, Sang-Ho, Lee, Tae Won, Eunjin Bae, Se-Ho Chang, Park, Dong Jun, and Kim, Jin Hyun

Subjects
110203 Respiratory Diseases, 70706 Veterinary Medicine, FOS: Clinical medicine, FOS: Veterinary sciences, Cell Biology, FOS: Health sciences, Biochemistry, FOS: Biological sciences, Medicine, 110309 Infectious Diseases, 111702 Aged Health Care, 111403 Paediatrics, 111599 Pharmacology and Pharmaceutical Sciences not elsewhere classified, 69999 Biological Sciences not elsewhere classified
Abstract

Supplemental material, Supplementary_figure_1 for The protective effect of human adiposederived mesenchymal stem cells on cisplatin-induced nephrotoxicity is dependent on their level of expression of heme oxygenase-1 by Hyun Seop Cho, Ha Nee Jang, Myeong Hee Jung, Si Jung Jang, Sang-Ho Jeong, Tae Won Lee, Eunjin Bae, Se-Ho Chang, Dong Jun Park and Jin Hyun Kim in European Journal of Inflammation

Published
2020
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14. Therapeutic Effects of Intranasal Tofacitinib on Chronic Rhinosinusitis with Nasal Polyps in Mice.

Author

Joo, Yeon‐Hee, Cho, Hyun‐Jin, Jeon, Yung Jin, Kim, Jin Hyun, Jung, Myeong Hee, Jeon, Sea‐Yuong, Suh, Young Sun, Park, Jung Je, and Kim, Sang‐Wook

Abstract

Objectives: The Janus kinase/signal transducer and activator of transcription (JAK–STAT) pathway play a key role in immune modulation, especially in the polarization of T helper cells. JAK inhibitors reduce inflammation by inhibiting the phosphorylation of STAT. We investigated whether a JAK inhibitor, tofacitinib, can reduce inflammation in a mouse model of chronic rhinosinusitis with nasal polyps (CRSwNP). Methods: An eosinophilic CRSwNP model was induced using 4‐week‐old BALB/c mice. The therapeutic effects of topical tofacitinib were compared with the effects of triamcinolone acetonide (TAC). Polyp formation and eosinophilic infiltration were assessed by histology. Levels of phosphorylated STAT (pSTAT), eosinophil cationic protein, and eotaxin were measured by immunohistochemistry. Gene expression levels of GATA‐3 was measured using quantitative PCR. The production of cytokines in sinonasal tissues, including interleukin IL‐4, IL‐5, IL‐12, and interferon‐γ, were measured using enzyme‐linked immunosorbent assays (ELISA). Results: Topical tofacitinib administration significantly reduced the number of polyp‐like lesions and the degree of eosinophilic infiltration, with an efficacy comparable with that of systemic TAC administration. Similarly, the levels of pSTAT6, eosinophil cationic protein, and eotaxin decreased with tofacitinib treatment. Tofacitinib decreased the gene expression level of GATA‐3. Lastly, tofacitinib significantly decreased IL‐4 and IL‐5 production to a similar extent as that by systemic or topical TAC administration. Tofacitinib, but not TAC, significantly increased the production of interferon‐γ. Conclusion: Topical tofacitinib administration may be an effective treatment for eosinophilic CRSwNP by inhibiting phosphorylation of STATs. Level of Evidence: N/A. Laryngoscope, 131:E1400–E1407, 2021 [ABSTRACT FROM AUTHOR]

Published
2021
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29. Effects of Peroxisome Proliferator-Activated Receptor-δ Agonist on Cardiac Healing after Myocardial Infarction

Author

Park, Jeong Rang, primary, Ahn, Jong Hwa, additional, Jung, Myeong Hee, additional, Koh, Jin-Sin, additional, Park, Yongwhi, additional, Hwang, Seok-Jae, additional, Jeong, Young-Hoon, additional, Kwak, Choong Hwan, additional, Lee, Young Soo, additional, Seo, Han Geuk, additional, Kim, Jin Hyun, additional, and Hwang, Jin-Yong, additional

Published
2016
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36. Glutamine attenuates tubular cell apoptosis in acute kidney injury via inhibition of the c-Jun N-terminal kinase phosphorylation of 14-3-3*

Author

Kim, Yoon Sook, primary, Jung, Myeong Hee, additional, Choi, Mee Young, additional, Kim, Young Hee, additional, Sheverdin, Vadim, additional, Kim, Jin Hyun, additional, Ha, Hye Jeong, additional, Park, Dong Jun, additional, Kang, Sang Soo, additional, Cho, Gyeong Jae, additional, Choi, Wan Sung, additional, and Chang, Se-Ho, additional

Published
2009
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38. Periostin may play a protective role in the development of eosinophilic chronic rhinosinusitis with nasal polyps in a mouse model.

Author

Kim, Sang‐Wook, Kim, Jin Hyun, Jung, Myeong Hee, Hur, Dong Gu, Lee, Hong‐Kyoung, Jeon, Sea‐Yuong, and Kim, Dae Woo

Abstract

Objectives/Hypothesis Several genes have been reported to be upregulated in human nasal polyps in previous genetic analyses. Among these genes, periostin is known to be overexpressed in nasal polyps obtained from aspirin-sensitive patients. Using periostin-null mice, we investigated the role of periostin in a murine model of eosinophilic rhinosinusitis with nasal polyps. Study Design Animal study. Methods Eosinophilic rhinosinusitis was induced in both periostin-null and wild-type mice according to previously established protocols. In brief, ovalbumin (OVA) was used for sensitization and prolonged intranasal stimulation. Staphylococcus aureus enterotoxin B was applied intranasally to develop polyplike lesions. To examine the inflammation and mucosal lesions, hematoxylin and eosin, Sirius red, and Giemsa staining were performed. Results There was no definite difference in the maximal mucosal thickness between periostin-null and wild-type mice. In contrast, some parameters of inflammation, including the number of polyplike lesions and mast cells, were aggravated in the periostin-null mice compared to wild type. Eosinophilic infiltration was aggravated in the OVA-stimulated periostin-null mice, compared to OVA-stimulated wild-type mice, whereas there was no apparent difference between wild-type and periostin-null mice challenged with additional S aureus enterotoxin B. Conclusions The loss of periostin appears to enhance polyplike lesion formation and mast cell infiltration in a mouse model of eosinophilic rhinosinusitis with nasal polyps. [ABSTRACT FROM AUTHOR]

Published
2013
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39. Human adipose tissue-derived mesenchymal stem cells protect kidneys from cisplatin nephrotoxicity in rats.

Author

Kim JH, Park DJ, Yun JC, Jung MH, Yeo HD, Kim HJ, Kim DW, Yang JI, Lee GW, Jeong SH, Roh GS, and Chang SH

Subjects
Acute Kidney Injury pathology, Animals, Apoptosis physiology, Cells, Cultured, Extracellular Signal-Regulated MAP Kinases metabolism, Humans, In Vitro Techniques, Kidney metabolism, MAP Kinase Kinase 4 metabolism, Male, Models, Animal, Phenotype, Rats, Sprague-Dawley, Signal Transduction, Tumor Suppressor Protein p53 metabolism, Acute Kidney Injury chemically induced, Acute Kidney Injury prevention & control, Adipose Tissue cytology, Cisplatin adverse effects, Kidney pathology, Mesenchymal Stem Cell Transplantation, Mesenchymal Stem Cells cytology
Abstract

Cisplatin has multiple cellular targets and modes of action that lead to nephrotoxicity. This suggests novel therapies that act at multiple cisplatin target sites may be effective. We tested whether human adipose tissue-derived mesenchymal stem cells (Ad-MSCs) can affect multiple target sites and protect against cisplatin-induced kidney damage. Rats were divided into four groups: control, infused with Ad-MSCs, injected with cisplatin, and cisplatin followed by infusion of Ad-MSCs. Animal survival and renal function were decreased and histological damage was increased in cisplatin-treated rats at day 3. Infusion of Ad-MSCs ameliorated renal dysfunction and tissue injury caused by cisplatin, leading to increased survival. Apoptotic cell death in the kidney was significantly reduced by infusion of Ad-MSCs. Activation of p53, JNK, and ERK and the expression of inflammation-related molecules were also decreased in the kidney that received Ad-MSCs. Very few Ad-MSCs were detected in the kidney. Conditioned medium from cultured Ad-MSCs had renal-protective functions in vivo and in vitro. Renal dysfunction and tissue damage caused by cisplatin were significantly reduced in rats treated with Ad-MSCs-conditioned medium. The viability of cultured renal proximal tubular cells exposed to cisplatin was also improved by coculture with Ad-MSCs or with conditioned medium. Release of proinflammatory mediators induced by cisplatin was inhibited in coculture with Ad-MSCs. Our results show that human Ad-MSCs exert a paracrine-protective effect on cisplatin nephrotoxicity at multiple target sites and suggest that human Ad-MSCs might be a new therapeutic approach for patients with acute kidney injury.

Published
2012
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