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- 저자 : Jooyeon Jhun (검색결과 13 건)
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Jhun JooYeon,우진석,Kwon Ji Ye,Na Hyun Sik,Cho Keun-Hyung,김선애,Kim Seok Jung,문수진,Park Sung-Hwan,조미라 대한면역학회 2022 Immune Network Vol.22 No.4
Osteoarthritis (OA) is the most common form of arthritis associated with ageing. Vitamin D has diverse biological effect on bone and cartilage, and observational studies have suggested it potential benefit in OA progression and inflammation process. However, the effect of vitamin D on OA is still contradictory. Here, we investigated the therapeutic potential of vitamin D in OA. Six-week-old male Wistar rats were injected with monosodium iodoacetate (MIA) to induce OA. Pain severity, cartilage destruction, and inflammation were measured in MIA-induced OA rats. Autophagy activity and mitochondrial function were also measured. Vitamin-D (1,25(OH)2D3) and celecoxib were used to treat MIA-induced OA rats and OA chondrocytes. Oral supplementation of vitamin D resulted in significant attenuations in OA pain, inflammation, and cartilage destruction. Interestingly, the expressions of MMP-13, IL-1β, and MCP-1 in synovial tissues were remarkably attenuated by vitamin D treatment, suggesting its potential to attenuate synovitis in OA. Vitamin D treatment in OA chondrocytes resulted in autophagy induction in human OA chondrocytes and increased expression of TFEB, but not LC3B, caspase-1 and -3, in inflamed synovium. Vitamin D and celecoxib showed a synergistic effect on antinociceptive and chondroprotective properties in vivo. Vitamin D showed the chondroprotective and antinociceptive property in OA rats. Autophagy induction by vitamin D treatment may be a promising treatment strategy in OA patients especially presenting vitamin D deficiency. Autophagy promoting strategy may attenuate OA progression through protecting cells from damage and inflammatory cell death.
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JooYeon Jhun,Keun hyung Cho,Seung Yoon Lee,Jiyoung Kim,Jun-Ki Min,Mi-La Cho 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Small heterodimer partner interacting leucine zipper protein (SMILE) is a member of the bZIP family of proteins and an orphan nuclear receptor. However, there is little known about its influence on osteoarthritis. The purpose of this study is to investigate whether the effect of SMILE on Monosodium-Iodoacetate-Induced arthritis in SMILE Tg. In MIAinjected SMILE Tg mice, nociceptive properties, degree of cartilage damage, and the level of inflammatory factors in articular cartilage were increased compared to MIA-injected wild-type mice. Interestingly, SMILE over expression reduced nociceptive properties and cartilage destruction, as well as inflammation related factors in MIA injected SMILE tg mice compared to MIA-injected wild-type mice. SMILE over expression suppressed he expression of metalloproteinase-3, nitrotyrosine, IL-1b and IL-6 increased in OA joints. Also, the protein levels of mTOR inhibition and AMPK upregulation by SMILE. Taken together, our study demonstrates that SMILE is a potential therapeutic agent for osteoarthritis.
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Jiyoung Kim,JooYeon Jhun,Jin Seok Woo,Seung Hoon Lee,Jeong-Hee Jeong,KyungAh Jung,Wonhee Hur,Seon-Yeong Lee,Jae Yoon Ryu,Young-Mee Moon,Yoon Ju Jung,Kyo Young Song,Kiyuk Chang,Seung Kew Yoon,Sung-Hwan 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Obesity, a condition characterized by excessive accumulation of body fat, is a metabolic disorder related to an increased risk of chronic inflammation. Obesity is mediated by signal transducer and activator of transcription (STAT) 3, which is regulated by genes associated with retinoid interferon-induced mortality (GRIM) 19, a protein ubiquitously expressed in various human tissues. In this study, we investigated the role of GRIM19 in diet-induced obese C57BL/6 mice via intra venous or intramuscular administration of a plasmid encoding GRIM19. Splenocytes from wild-type and GRIM19-overexpressing mice were compared using enzyme-linked immunoassay, real-time polymerase chain reaction, Western blotting, flow cytometry, and histological analyses. GRIM19 attenuated the progression of obesity by regulating STAT3 activity and enhancing brown adipose tissue (BAT) differentiation. GRIM19 regulated the differentiation of mouse-derived 3T3-L1 preadipocytes into adipocytes, while modulating gene expression in white adipose tissue (WAT) and BAT. GRIM19 overexpression reduced diet-induced obesity and enhanced glucose and lipid metabolism in the liver. Moreover, GRIM19 overexpression reduced WAT differentiation and induced BAT differentiation in obese mice. GRIM19-transgenic mice exhibited reduced mitochondrial superoxide levels and a reciprocal balance between Th17 and Treg cells. These results suggest that GRIM19 attenuates the progression of obesity by controlling adipocyte differentiation.
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IL-17 axis accelerates the inflammatory progression of obese in mice via TBK1 and IKBKE pathway
Lee, Seung Hoon,Jhun, JooYeon,Byun, Jae-Kyung,Kim, Eun-Kyung,Jung, KyoungAh,Lee, Ji Eun,Choi, Jong Young,Park, Sung-Hwan,Cho, Mi-La Elsevier 2017 Immunology letters Vol.184 No.-
<P><B>Abstract</B></P> <P>Obesity mediates immune inflammatory response and induces IL-17 expression. Adipgenesis can be regulated by IL-17 and it causes TBK1 activation. The inhibition of TBK1 and the inhibition of I IKBKE reduces inflammatory response and improves obesity. It is hypothesized that IL-17 deficiency inhibits obesity progression and inflammation. 3T3-L1 preadipocytes were differentiated in vitro and treated with IL-17. RAW264.7 cells and differentiated 3T3-L1 were pretreated with TBK1 inhibitor and then stimulated with IL-17. Wild-type and IL-17 knock out mice were fed with high-fat diet. IL-17 inhibits adipocyte differentiation from mouse-derived 3T3-L1 preadipocytes and reduces mRNA expression of proadipogenic transcription factors and adipokines in adipocyte cells. IL-17 also showed up-regulation of mRNA levels of inflammatory cytokines in RAW cells. The inhibitor of TBK1 and IKBKE attenuates the effect of IL-17. Loss of IL-17 deficiency improves diet-induced obesity, fatty liver, glucose and lipid metabolism in mice. The expression of TBK1 and IKBKE decreased in the spleen and liver of IL-17 deficiency mice. Moreover, the inflammatory response within the visceral adipose tissue and Th1 cells were inhibited, however, M2 macrophage and Th2 cells increased in IL-17 deficiency mice. IL-17 inhibits adipogenesis where a lack of IL-17 ameliorates glucose metabolism. As well, the inhibition of TBK1 reduces inflammation induced by IL-17. Therefore, IL-17 may be involved in the development of obesity and metabolic dysfunction in a TBK1-dependent manner.</P> <P><B>Highlights</B></P> <P> <UL> <LI> IL-17 induced TBK1-mediates immune inflammatory response in adipocytes and downregulated adipocyte differentiation. </LI> <LI> Loss of IL-17 reduced inflammation and improved fatty liver in obesity animal model. </LI> <LI> The inhibition of TBK1 could decrease inflammatory response in RAW 264.7 cells. </LI> </UL> </P>
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Lee, Seung Hoon,Kwon, Ji Ye,Jhun, JooYeon,Jung, KyungAh,Park, Sung-Hwan,Yang, Chul Woo,Cho, YongSin,Kim, Seok Jung,Cho, Mi-La Elsevier Science 2018 IMMUNOLOGY LETTERS Vol.203 No.-
<P><B>Abstract</B></P> <P>Osteoarthritis (OA) is a chronic and degenerative disease that causes pain, cartilage deformation, and joint inflammation. <I>Lactobacillus</I> species have been used as dietary supplements to induce the production of antimicrobial and anti-inflammatory factors. The goal of this study was to determine whether <I>Lactobacillus acidophilus</I> ameliorates monosodium iodoacetate-induced OA. <I>L. acidophilus</I> showed anti-nociceptive properties and protected against cartilage destruction. It also downregulated the levels of proinflammatory cytokines and increased the levels of anti-inflammatory cytokines in the joints of OA rats. <I>L. acidophilus</I> additionally restored the balance between anabolic and catabolic factors in chondrocytes from OA patients. These results suggest that <I>L. acidophilus</I> can alleviate OA-associated pain and delay the progression of the disease by inhibiting proinflammatory cytokine production and reducing cartilage damage.</P> <P><B>Highlights</B></P> <P> <UL> <LI> <I>L. acidophilus</I> improves MIA-induced OA development through downregulation of pain severity and cartilage damage. </LI> <LI> <I>L. acidophilus</I> decreases the expression of proinflammatory cytokines but promotes anti-inflammatory cyotokines production in joint. </LI> <LI> <I>L. acidophilus</I> regulates a reciprocal balance between anabolic and catabolic factors in OA chondrocytes. </LI> </UL> </P>
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Keun hyung Cho,Hyun-Sik Na,JooYeon Jhun,Jiyoung Kim,Seung Yoon Lee,Jeong soo Lee,In Gyu Um,Seok Jung Kim,Mi-La Cho 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Osteoarthritis (OA) is a disease that reduces quality of life due to pain caused by persistent joint destruction. In addition, as a representative chronic disease, it causes inflammation and affects immunity, and it is one of the diseases that is difficult to cure, so treatment and improvement methods are urgently needed. In a previous study, we published that LA-1 improves osteoarthritis and has cartilage protection by controlling inflammation. However, it was not known how LA-1 improves osteoarthritis in the body. So in this study, it was confirmed that the administration of LA-1 to the MIA-induced OA rat model reduces the pain threshold, protects cartilage, and regulates inflammation markers in the articular synovium. Additionally, collecting and analyzing the feces of the disease model, it affected the gastrointestinal system and improved the environment of the microbiome. Interestingly, by providing LA-1, it was confirmed that the diversity and abundance of microbiome in the intestine were changed, and that the bacteria that produced SCFAs increased. In addition, daily supply of butyrate, one of the SCFAs produced by certain bacteria, triggers autophagy activation and tends to decrease necroptosis. This suggests that systemic immunity as well as OA is regulated according to changes in the intestinal microbial community, and that activation of autophagy can indirectly reduce abnormal cell death. In addition, assuming that osteoarthritis is a chronic degenerative disease, cell analysis was performed using splenocyte and blood assuming that the immune system is deteriorated. As a result, both splenocytes and PBMCs confirmed that regulatory T cells increased and Th17 cells decreased. In summary, providing LA-1 leads to increased production of SCFAs by altering the microbes in the intestine. Accordingly, it is possible to suppress the progression of OA and control pain due to OA, and improve an abnormal joint environment by controlling autophagy and necroptosis.
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Jeong Su Lee,Yun Hwan Kim,JooYeon Jhun,Hyun Sik Na,In Gyu Um,Jeong Won Choi,Jin Seok Woo,Seung Hyo Kim,Asode Ananthram Shetty,Seok Jung Kim,Mi-La Cho The Korean Association of Immunobiologists 2024 Immune Network Vol.24 No.3
Osteoarthritis (OA) involves cartilage degeneration, thereby causing inflammation and pain. Cardiovascular diseases, such as dyslipidemia, are risk factors for OA; however, the mechanism is unclear. We investigated the effect of dyslipidemia on the development of OA. Treatment of cartilage cells with low-density lipoprotein (LDL) enhanced abnormal autophagy but suppressed normal autophagy and reduced the activity of transcription factor EB (TFEB), which is important for the function of lysosomes. Treatment of LDL-exposed chondrocytes with rapamycin, which activates TFEB, restored normal autophagy. Also, LDL enhanced the inflammatory death of chondrocytes, an effect reversed by rapamycin. In an animal model of hyperlipidemia-associated OA, dyslipidemia accelerated the development of OA, an effect reversed by treatment with a statin, an anti-dyslipidemia drug, or rapamycin, which activates TFEB. Dyslipidemia reduced the autophagic flux and induced necroptosis in the cartilage tissue of patients with OA. The levels of triglycerides, LDL, and total cholesterol were increased in patients with OA compared to those without OA. The C-reactive protein level of patients with dyslipidemia was higher than that of those without dyslipidemia after total knee replacement arthroplasty. In conclusion, oxidized LDL, an important risk factor of dyslipidemia, inhibited the activity of TFEB and reduced the autophagic flux, thereby inducing necroptosis in chondrocytes.
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Jeonghyeon Moon,Seung Hoon Lee,Seon-yeong Lee,Jaeyoon Ryu,Jooyeon Jhun,JeongWon Choi,Gyoung Nyun Kim,노상호,박성환,조미라 대한면역학회 2020 Immune Network Vol.20 No.5
The protein encoded by the Gene Associated with Retinoid-Interferon-Induced Mortality-19 (GRIM-19) is located in the mitochondrial inner membrane and is homologous to the NADH dehydrogenase 1-alpha subcomplex subunit 13 of the electron transport chain. Multiple sclerosis (MS) is a demyelinating disease that damages the brain and spinal cord. Although both the cause and mechanism of MS progression remain unclear, it is accepted that an immune disorder is involved. We explored whether GRIM-19 ameliorated MS by increasing the levels of inflammatory cytokines and immune cells; we used a mouse model of experimental autoimmune encephalomyelitis (EAE) to this end. Six-to-eight-week-old male C57BL/6, IFNγ-knockout (KO), and GRIM-19 transgenic mice were used; EAE was induced in all strains. A GRIM-19 overexpression vector (GRIM19 OVN) was electrophoretically injected intravenously. The levels of Th1 and Th17 cells were measured via flow cytometry, immunofluorescence, and immunohistochemical analysis. IL-17A and IFNγ expression levels were assessed via ELISA and quantitative PCR. IL-17A expression decreased and IFNγ expression increased in EAE mice that received injections of the GRIM19 OVN. GRIM-19 transgenic mice expressed more IFNγ than did wild-type mice; this inhibited EAE development. However, the effect of GRIM-19 overexpression on the EAE of IFNγ-KO mice did not differ from that of the empty vector. GRIM-19 expression was therapeutic for EAE mice, elevating the IFNγ level. GRIM-19 regulated the Th17/Treg cell balance.
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Hyun Sik Na,Seon-young Lee,Hong Ki Min,Jooyeon Jhun,Jeong-Won Choi,Jeong Su Lee,In Gyu Um,Sung-Min Kim,Seung-Ki Kwok,Mi-La Cho,Sung-Hwan Park 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Background: Rheumatoid arthritis (RA) is a long-term autoimmune disorder that mostly affects the joints and leads to the destruction of cartilage. An RA model in non-human primates is especially useful because of their close phylogenetic relationship to humans in terms of cross-reactivity to compounds developed using modern drug technologies. Methods: We used a collagen-induced arthritis (CIA) model in Macaca fascicularis. CIA was induced by the immunization of chicken type II collagen. Swelling was measured as the longitudinal and transverse axes of 16 proximal interphalangeal joints. Results: A new system for visual evaluation was created, with a perfect score of 16. Individual behavioral analysis was also conducted. Serum was collected once a week after the first immunization. Blood chemistry and inflammatory cytokine parameters were higher in the CIA group than in the wild type group. Conclusion: In conclusion, we established CIA in M. fascicularis, and the results can be used for drug evaluation models
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