Early Embryonic Lethality and Enhanced Apoptosis in the TRAF Interacting Protein TRIP Deficiency Mice

KANG, Misun,PARK, Soonju,CHOI, Seung-A,PARK, Ei-Soon,KIM, Jin-Man,JEONG, Yongsu,CHOE, Joonho,RHO, Jaerang 충남대학교 형질전환복제돼지연구센터 2007 논문집 Vol. No.10

Increased expression of connexin43 on the aortic valve in the hypercholesterolemic rabbit model.

Wang, Young Pil,Choe, Misun,Choi, Si Young,Jin, Ung,Kim, Chi Kyung,Seo, Eun Joo,Cho, Il Jin,Park, Chan Beom Taylor Francis 2009 Journal of investigative surgery Vol.22 No.2

<P>BACKGROUND: Aortic valve sclerosis is associated with increased risk of cardiovascular death and myocardial infarction. However, the relevance of connexin43 in aortic valve sclerosis remains unclear. We hypothesized that the mechanism regulating aortic valve sclerosis is associated with the alteration of cell-to-cell communication. METHODS: Twenty male New Zealand rabbits were divided into two groups. Group 1 (n = 10) were fed a normal chow diet, while those in group 2 (n = 10) received a diet containing 1% cholesterol for 12 weeks. After utanizing the animals, the aortic valves were excised for analysis. RESULTS: Myofibroblasts and macrophages were more highly expressed in the cholesterol diet group. Osteopontin and connexin43 were found to concentrate within the endothelial layer on the aortic side of the valve leaflets in the cholesterol diet group. A real-time polymerase chain reaction revealed increased connexin43 and osteopontin mRNA levels in the hypercholesterolemic aortic valves. CONCLUSIONS: The present study demonstrates that hypercholesterolemia increases the expression of connexin43 in the rabbit aortic valve. The results suggest that alterations in gap junctional intercellular communication via connexin43 gap junctions may play a role in the development of aortic valve sclerosis.</P>

Intensive Nutrition Management in a Patient with Short Bowel Syndrome Who Underwent Bariatric Surgery

( Meera Kweon ),( Dal Lae Ju ),( Misun Park ),( Jihyeong Choe ),( Yun-suhk Suh ),( Eun-mi Seol ),( Hyuk-joon Lee ) 한국임상영양학회 2017 Clinical Nutrition Research Vol.6 No.3

Many individuals with short bowel syndrome (SBS) require long-term parenteral nutrition (PN) to maintain adequate nutritional status. Herein, we report a successful intestinal adaptation of a patient with SBS through 13 times intensive nutritional support team (NST) managements. A thirty-five-year-old woman who could not eat due to intestinal discontinuity visited Seoul National University Hospital for reconstruction of the bowel. She received laparoscopic Roux-en-Y gastric bypass (RYGB) due to morbid obesity in Jan 2013 at a certain hospital and successfully reduced her weight from 110 kg to 68 kg. However, after a delivery of the second baby by cesarean section in Jul 2016, most of small bowel was herniated through Peterson`s defect, and emergent massive small bowel resection was performed. Thereafter, she visited our hospital for the purpose of intestinal reconstruction. In Sep 2016, she received side-to-side gastrogastrostomy and revision of double barrel enterostomy. The remaining small bowel included whole duodenum, 30 cm of proximal jejunum, and 10 cm of terminal ileum. Pylorus and ileocecal valves were intact. The patient given only PN after surgery was provided rice-based soft fluid diet after 10 day of operation. Through intensive nutritional management care, she could start solid meals, and finally stop the PN and eat only orally at 45 days postoperatively. Three nutritional interventions were conducted over 2 months after the patient was discharged. She did not require PN during this period, and maintained her weight within the normal weight range. Similar interventions could be used for other patients with malabsorption problems similar to SBS.

MicroRNA-26a/-26b-COX-2-MIP-2 Loop Regulates Allergic Inflammation and Allergic Inflammation-promoted Enhanced Tumorigenic and Metastatic Potential of Cancer Cells

Kwon, Yoojung,Kim, Youngmi,Eom, Sangkyung,Kim, Misun,Park, Deokbum,Kim, Hyuna,Noh, Kyeonga,Lee, Hansoo,Lee, Yun Sil,Choe, Jongseon,Kim, Young Myeong,Jeoung, Dooil American Society for Biochemistry and Molecular Bi 2015 The Journal of biological chemistry Vol.290 No.22

<P>Cyclooxgenase-2 (COX-2) knock-out mouse experiments showed that COX-2 was necessary for <I>in vivo</I> allergic inflammation, such as passive cutaneous anaphylaxis, passive systemic anaphylaxis, and triphasic cutaneous allergic reaction. TargetScan analysis predicted COX-2 as a target of miR-26a and miR-26b. miR-26a/-26b decreased luciferase activity associated with COX-2–3′-UTR. miR-26a/-26b exerted negative effects on the features of <I>in vitro</I> and <I>in vivo</I> allergic inflammation by targeting COX-2. ChIP assays showed the binding of HDAC3 and SNAIL, but not COX-2, to the promoter sequences of miR-26a and miR-26b. Cytokine array analysis showed that the induction of chemokines, such as MIP-2, in the mouse passive systemic anaphylaxis model occurred in a COX-2-dependent manner. ChIP assays showed the binding of HDAC3 and COX-2 to the promoter sequences of MIP-2. <I>In vitro</I> and <I>in vivo</I> allergic inflammation was accompanied by the increased expression of MIP-2. miR-26a/-26b negatively regulated the expression of MIP-2. Allergic inflammation enhanced the tumorigenic and metastatic potential of cancer cells and induced positive feedback involving cancer cells and stromal cells, such as mast cells, macrophages, and endothelial cells. miR-26a mimic and miR-26b mimic negatively regulated the positive feedback between cancer cells and stromal cells and the positive feedback among stromal cells. miR-26a/-26b negatively regulated the enhanced tumorigenic potential by allergic inflammation. COX-2 was necessary for the enhanced metastatic potential of cancer cells by allergic inflammation. Taken together, our results indicate that the miR26a/-26b-COX-2-MIP-2 loop regulates allergic inflammation and the feedback relationship between allergic inflammation and the enhanced tumorigenic and metastatic potential.</P>

Transglutaminase II/MicroRNA-218/-181a Loop Regulates Positive Feedback Relationship between Allergic Inflammation and Tumor Metastasis

Eom, Sangkyung,Kim, Youngmi,Kim, Misun,Park, Deokbum,Lee, Hansoo,Lee, Yun Sil,Choe, Jongseon,Kim, Young Myeong,Jeoung, Dooil American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.43

<P>The molecular mechanism of transglutaminase II (TGaseII)-mediated allergic inflammation remains largely unknown. TGaseII, induced by antigen stimulation, showed an interaction and co-localization with FcϵRI. TGaseII was necessary for <I>in vivo</I> allergic inflammation, such as triphasic cutaneous reaction, passive cutaneous anaphylaxis, and passive systemic anaphylaxis. TGaseII was necessary for the enhanced metastatic potential of B16F1 melanoma cells by passive systemic anaphylaxis. TGaseII was shown to be a secreted protein. Recombinant TGaseII protein increased the histamine release and β-hexosaminidase activity, and enhanced the metastatic potential of B16F1 mouse melanoma cells. Recombinant TGaseII protein induced the activation of EGF receptor and an interaction between EGF receptor and FcϵRI. Recombinant TGaseII protein displayed angiogenic potential accompanied by allergic inflammation. R2 peptide, an inhibitor of TGaseII, exerted negative effects on <I>in vitro</I> and <I>in vivo</I> allergic inflammation by regulating the expression of TGaseII and FcϵRI signaling. MicroRNA (miR)-218 and miR-181a, decreased during allergic inflammation, were predicted as negative regulators of TGaseII by microRNA array and TargetScan analysis. miR-218 and miR-181a formed a negative feedback loop with TGaseII and regulated the <I>in vitro</I> and <I>in vivo</I> allergic inflammation. TGaseII was necessary for the interaction between mast cells and macrophages during allergic inflammation. Mast cells and macrophages, activated during allergic inflammation, were responsible for the enhanced metastatic potential of tumor cells that are accompanied by allergic inflammation. In conclusion, the TGaseII/miR-218/-181a feedback loop can be employed for the development of anti-allergy therapeutics.</P>

Inhibition of Cathepsin S Induces Mitochondrial ROS That Sensitizes TRAIL-Mediated Apoptosis Through p53-Mediated Downregulation of Bcl-2 and c-FLIP

Seo, Bo Ram,Min, Kyoung-jin,Woo, Seon Min,Choe, Misun,Choi, Kyeong Sook,Lee, Young-Kyung,Yoon, Gyesoon,Kwon, Taeg Kyu Mary Ann Liebert, Inc. Publishers 2017 ANTIOXIDANTS AND REDOX SIGNALING Vol. No.

<P>Conclusion: Our results indicated that inhibition of cathepsin S stimulates TRAIL-induced apoptosis through downregulation of Bcl-2 and Cbl-mediated c-FLIP by ROS-mediated p53 expression.</P>

Long-term prognosis of BK virus-associated nephropathy in kidney transplant recipients

( Woo Yeong Park ),( Seong Sik Kang ),( Kyubok Jin ),( Sung Bae Park ),( Misun Choe ),( Seungyeup Han ) 대한신장학회 2018 Kidney Research and Clinical Practice Vol.37 No.2

Background: The long-term prognosis of BK virus-associated nephropathy (BKVAN) in kidney transplant recipients (KTRs) is uncertain. We evaluated the long-term prognosis in KTRs with BKVAN and the clinical significance of BKVAN on post-transplant clinical outcome. Methods: We retrospectively analyzed the medical records of 582 patients who underwent kidney transplant (KT) between 2001 and 2014. We divided the patients into a BKVAN group (15 patients) diagnosed by allograft biopsy and a control group (356 patients). Results: The incidence of BKVAN was 4.0%, and the mean follow-up duration was 93.1 ± 52.3 months. Median time from KT to BKVAN diagnosis was 5.9 months (interquartile range [IQR], 4.4-8.7). In the BKVAN group, 9 (60.0%) KTRs with combined acute rejection progressed to graft failure, and the median time from BKVAN diagnosis to graft failure was 36.2 months (IQR, 9.7-65.5). Death-censored graft survival rate and patient survival rate in the BKVAN group were significantly lower than those in the control group. BKVAN and rejection were independent risk factors for graft failure. In the subgroup analysis, death-censored graft survival rate of KTRs with BKVAN with acute rejection was significantly worst in comparison with similar patients without BKVAN regardless of acute rejection (P < 0.001). Conclusion: The long-term prognosis of BKVAN with acute rejection was very poor because of graft failure caused by inadequate treatment for acute rejection considering BKVAN. Therefore, we should carefully monitor the allograft status of KTRs through regular surveillance tests after treatment for BKVAN with acute rejection.

Acute interstitial nephritis with acute kidney injury after COVID-19 vaccination: a case report

Lim Jimin,Paek Jin Hyuk,Shin Hyeong Chan,Park Woo Yeong,Jin Kyubok,Choe Misun,Han Seungyeup,Kim Yaerim 대한백신학회 2024 Clinical and Experimental Vaccine Research Vol.13 No.1

In the context of the massive spread of coronavirus disease 2019 (COVID-19), the development of a COVID-19 vaccine is urgently needed. The Pfizer-BioNTech COVID-19 vaccine has been widely applied across global populations. Herein, we report a case of acute interstitial nephritis with acute kidney injury in a young healthy subject after administration of the COVID-19 vaccine. A 20-year-old man was admitted with abdominal discomfort and nausea. He had received the Pfizer-BioNTech COVID-19 vaccine 6 days before. At 9 days after vaccination, his kidney function was decreased, with serum creatinine levels of 1.8 mg/dL. Even with supportive care with hydration, his kidney function worsened, and he underwent a kidney biopsy. The pathology findings revealed diffuse interstitial infiltration of inflammatory cells, predominantly comprising lymphocytes, with preservation of the glomerulus. No abnormal findings were noted by immunofluorescence or electron microscopy. Based on a diagnosis of drug-related acute interstitial nephritis, we treated the patient with high-dose prednisolone. After administration of prednisolone, kidney function slowly improved. A close linkage between COVID-19 vaccination and acute interstitial nephritis should be considered in the clinic, despite the low incidence.

Survival and Prognosis of Patients with Pilocytic Astrocytoma: A Single-Center Study

( Jae Hui Park ),( Nani Jung ),( Seok Jin Kang ),( Heung Sik Kim ),( El Kim ),( Hee Jung Lee ),( Hye Ra Jung ),( Misun Choe ),( Ye Jee Shim ) 대한뇌종양학회·대한신경종양학회·대한소아뇌종양학회 2019 Brain Tumor Research and Treatment Vol.7 No.2

Background Pilocytic astrocytoma (PA) is a brain tumor that is relatively more common in children and young adults. Methods We retrospectively reviewed the medical records of patients with PA treated at a single center between 1988 and 2018. Results We included 31 subjects with PA. The median age at diagnosis was 13.4 years, and the median follow-up duration was 9.9 years. The total PA group had a 10-year disease-specific survival (DSS) rate of 92.6% [95% confidence interval (CI), 82.6-100] and 10-year progression-free survival (PFS) rate of 52.8% (95% CI, 32.0-73.6). In patients aged <20 years, tumors were more likely to be located in sites in which gross total tumor resection (GTR) was impossible. No statistically significant difference in 10-year DSS was found between the GTR (100%) and non-GTR (89.7%; 95% CI, 76.2-100; p=0.374) groups. However, a statistically significant difference in 10-year PFS was found between the GTR (100%) and non-GTR groups (30.7%; 95% CI, 8.6-52.8; p=0.012). In the non-GTR group, no statistically significant difference in 10-year DSS was found between the patients who received immediate additional chemotherapy and/or radiotherapy (Add-Tx group, 92.9%; 95% CI, 79.4-100) and the non-Add-Tx group (83.3%; 95% CI, 53.5-100; p=0.577). No statistically significant difference in 10- year PFS was found between the Add-Tx group (28.9%; 95% CI, 1.7-56.1) and non-Add-Tx group (33.3%; 95% CI, 0-70.9; p=0.706). Conclusion The PFS of the patients with PA in our study depended only on the degree of surgical excision associated with tumor location. This study is limited by its small number of patients and retrospective nature. A multicenter and prospective study is necessary to confirm these findings.

Anthocyanins From Black Soybean Seed Coat Enhance Wound Healing

Xu, Lianji,Choi, Tae Hyun,Kim, Sukwha,Kim, Sang-Hyon,Chang, Hyuk Won,Choe, Misun,Kwon, Sun Young,Hur, Ji An,Shin, Sung Chul,Chung, Jong Il,Kang, Dawon,Zhang, Duo by Lippincott Williams Wilkins 2013 Annals of plastic surgery Vol.71 No.4

ABSTRACT: Anthocyanins are known to have antioxidant and antiinflammatory effects. We hypothesized that anthocyanins would enhance wound healing in Sprague-Dawley rats. The purpose of this study was to evaluate our hypothesis and investigate the mechanism of wound healing enhancement. The cytoprotective effect of an immortalized epidermal keratinocyte cell line (HaCaT) and human neonatal dermal fibroblasts in response to various concentrations of anthocyanins was determined. Vascular endothelial growth factor (VEGF) and thrombospondin 1 (TSP1) of HaCaT were measured by Western blot analysis. Anthocyanins were applied to the wounds in rats, and the healing ratio was calculated. Tissue VEGF, TSP1, CD31, nuclear factor-&kgr;B, and phosphorylation of I&kgr;Bα were measured. The viability of the HaCaT cell line and human neonatal dermal fibroblasts increased under cytotoxicity by H2O2 in the anthocyanin-treated groups. The VEGF in the anthocyanin-treated groups increased, whereas TSP1 decreased. Wounds in the experimental groups healed faster, and VEGF and CD31 increased in the experimental groups, whereas TSP1 decreased. Anthocyanins inhibited the translocation of nuclear factor-&kgr;B (p65) from cytosol to nucleus and also prevented the phosphorylation of I&kgr;Bα. Anthocyanins enhance wound healing through a cytoprotective effect, enhancement of angiogenesis, and an antiinflammatory effect.