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Kang, Miso,Oh, Nam Su,Kim, Minjoo,Ahn, Hyeon Yeong,Yoo, Hye Jin,Sun, Minghan,Kang, Shin-Ho,Yang, Hye Jeong,Kwon, Dae Young,Lee, Jong Ho The Royal Society of Chemistry 2017 Food & Function Vol.8 No.4
<P><I>Objective</I>: The objective of this study was to investigate the impact of supplementation with fermented Maillard-reactive whey protein (F-MRP) on natural killer (NK) cell activity, circulating cytokines, and serum protein levels.<I>Methods</I>: A randomized, double-blind, placebo-controlled study was conducted on a sample of 80 participants without diabetes or obesity. Over an 8-week study period, the F-MRP group consumed 6 g of powder containing 4.2 g of F-MRP each day, whereas the placebo group consumed the same amount of maltodextrin. For each participant, NK cell activity was evaluated based on the ratio of effector cells (E; peripheral blood mononuclear cells, PBMCs) to target cells (T; K562 cells) at E : T ratios of 10 : 1, 5 : 1, 2.5 : 1, and 1.25 : 1.<I>Results</I>: Body mass index (BMI) and NK cell activity under all assay conditions were significantly increased in the F-MRP group at the 8-week follow-up visit compared with the values at the baseline, whereas the placebo group showed significant reductions in NK cell activity (at an E : T ratio of 5 : 1), serum albumin, and pre-albumin at the 8-week follow-up visit compared with the values at the baseline. When comparing the changes between the placebo and F-MRP groups, the increases in NK cell activity under all assay conditions and serum interleukin (IL)-12 in the F-MRP group were greater than those in the placebo group after adjusting for baseline values. There were also significant differences in pre-albumin and insulin-like growth factor (IGF)-1 between the two groups; the change in (Δ) IL-12 was positively correlated with both Δpre-albumin (<I>r</I>= 0.435,<I>P</I>= 0.006) and ΔNK cell activity at an E : T ratio of 10 : 1 (<I>r</I>= 0.571,<I>P</I>< 0.001) in the F-MRP group.<I>Conclusion</I>: Daily consumption of F-MRP enhanced NK cell function, which was positively associated with ΔIL-12. Moreover, ΔIL-12 was positively correlated with Δpre-albumin.</P>
Choi, Daheui,Lee, Hwankyu,Kim, Hyun-Bum,Yang, Miso,Heo, Jiwoong,Won, Younsun,Jang, Seung Soon,Park, Jong Kuk,Son, Youngsook,Oh, Tong In,Lee, EunAh,Hong, Jinkee American Chemical Society 2017 Chemistry of materials Vol.29 No.5
<P>Intravenous administration of mesenchymal stem cells (MSCs) has served as a clinical intervention for inflammatory diseases. Once entered to blood circulation, MSCs are exposed to a harsh environment which sharply decreases cell viability due to the fact that injected cells, being susceptible to shear stress, are subjected to the high velocities of the bloodstream and lack of proper mechanical support that keeping them in an attachment -deprived state. Here, we coated the nanofilm onto viable MSCs by depositing poly-L -lysineand hyaluronic acid molecules along with arginine-glycine-aspartic acid (RGD peptide) as building blocks to protect cells from shear stress and stabilize them in a single cell, suspension state. In this article, we found that nanofilmcoated cells showed significantly increased cell survival in vitro and in vivo, which was also supported by the activation of survival-related protein, Akt. The coated nanofilm did not interfere with the sternness of MSCs which was determined based on the colony forming unit -fibroblast (CPU-F) assay and in vitro differentiation potential. Because of the characteristics of films showing light molecular deposition density, flexibility, and looseness, application of nanofilms did not block cell migration. When the cells were administrated intravenously, the nanofilm coated MSCs not only prolonged blood circulation lifetime but also showed increased stem cell recruitment to injured tissues in the muscle injury in vivo model, due to prolonged survival. Surface modification of MSCs using nanofilms successfully modulated cell activity enabling them to survive the anoikis-inducing state, and this can provide a valuable tool to potentiate the efficacy of MSCs for in vivo cell therapy.</P>
Hwang, Jun-Ha,Han, Uiyoung,Yang, Miso,Choi, Yonghyun,Choi, Jonghoon,Lee, Jong-Min,Jung, Han-Sung,Hong, Jinkee,Hong, Jeong-Ho Elsevier 2019 ACTA BIOMATERIALIA Vol.86 No.-
<P><B>Abstract</B></P> <P>In regenerative medicine, the generation of therapeutic stem cells and tissue engineering are important for replacing damaged tissues. Numerous studies have attempted to produce cellular components that mimic the native tissue for gaining optimal function. Particularly, the extracellular matrix (ECM) composition plays an important role in cellular functions including determining the fates of mesenchymal stem cells (MSCs). Here, we evaluated the osteogenic effects of a nanofilm in which oppositely charged polyelectrolytes were alternately adsorbed onto the cell surface to create an artificial ECM environment for single MSCs. Interestingly, nanofilm composed of collagen (Col) and alginate (AA) showed relatively high stiffness and MSCs coated with the Col/AA nanofilm showed increased osteogenic differentiation efficiency compared to other nanofilm-coated MSCs. Further analysis revealed that the Col/AA nanofilm coating stimulated osteogenesis by activating transcriptional coactivators with the PDZ binding motif through extracellular signal-related kinase and p38 MAPK signaling. This nano-sized cellular coating will facilitate the development of nanotechnology for controlling cellular functions and advance stem cell-based clinical applications for regenerative medicine.</P> <P><B>State of Significance</B></P> <P>In this study, we developed an artificial cellular nano-environment formed by multilayer nanofilms. We demonstrated that the nanofilms introduced to mesenchymal stem cells (MSCs) stimulate osteogenic differentiation by regulating intracellular signaling. Among the various nanofilm combinations, the induction of osteogenic gene transcription in collagen (Col) and alginate (AA) film-coated MSCs was the most pronounced compared to that on other nanofilms. A minimum number of Col/AA nanofilm bilayers (n = 2) was required for effective induction of MSC osteogenic differentiation. In addition, we observed the correlation between the promoting effect of osteogenic differentiation and stiffness of the nanofilm. Our results may be useful for developing a cell coating model system widely applicable in bioengineering and regenerative medicine.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Kim, Ki-Hye,Kim, Tae-Sung,Lee, Joy G.,Park, Jeong-Kyu,Yang, Miso,Kim, Jin-Man,Jo, Eun-Kyeong,Yuk, Jae-Min The Korean Association of Immunobiologists 2014 Immune Network Vol.14 No.6
Mycobacterium scrofulaceum is an environmental and slow-growing atypical mycobacterium. Emerging evidence suggests that M. scrofulaceum infection is associated with cervical lymphadenitis in children and pulmonary or systemic infections in immunocompromised adults. However, the nature of host innate immune responses to M. scrofulaceum remains unclear. In this study, we examined the innate immune responses in murine bone marrow-derived macrophages (BMDMs) infected with different M. scrofulaceum strains including ATCC type strains and two clinically isolated strains (rough and smooth types). All three strains resulted in the production of proinflammatory cytokines in BMDMs mediated through toll-like receptor-2 and the adaptor MyD88. Activation of MAPKs (extracellular signal-regulated kinase 1/2, and p38, and c-Jun N-terminal kinase) and nuclear receptor (NF)-${\kappa}B$ together with intracellular reactive oxygen species generation were required for the expression of proinflammatory cytokines in BMDMs. In addition, the rough morphotypes of M. scrofulaceum clinical strains induced higher levels of proinflammatory cytokines, MAPK and NF-${\kappa}B$ activation, and ROS production than other strains. When mice were infected with different M. scrofulaceum strains, those infected with the rough strain showed the greatest hepatosplenomegaly, granulomatous lesions, and immune cell infiltration in the lungs. Notably, the bacterial load was higher in mice infected with rough colonies than in mice infected with ATCC or smooth strains. Collectively, these data indicate that rough M. scrofulaceum induces higher inflammatory responses and virulence than ATCC or smooth strains.
Heo Haejeong,Kim Jong-Hwan,Lim Hyun Jung,Kim Jeong-Hwan,Kim Miso,Koh Jaemoon,Im Joo-Young,Kim Bo-Kyung,Won Misun,Park Ji-Hwan,Shin Yang-Ji,윤미란,Cho Byoung Chul,Kim Yong Sung,Kim Seon-Young,김미랑 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Acquired resistance to inhibitors of anaplastic lymphoma kinase (ALK) is a major clinical challenge for ALK fusion-positive non-small-cell lung cancer (NSCLC). In the absence of secondary ALK mutations, epigenetic reprogramming is one of the main mechanisms of drug resistance, as it leads to phenotype switching that occurs during the epithelial-to-mesenchymal transition (EMT). Although drug-induced epigenetic reprogramming is believed to alter the sensitivity of cancer cells to anticancer treatments, there is still much to learn about overcoming drug resistance. In this study, we used an in vitro model of ceritinib-resistant NSCLC and employed genome-wide DNA methylation analysis in combination with single-cell (sc) RNA-seq to identify cytidine deaminase (CDA), a pyrimidine salvage pathway enzyme, as a candidate drug target. CDA was hypomethylated and upregulated in ceritinib-resistant cells. CDA-overexpressing cells were rarely but definitively detected in the naïve cell population by scRNA-seq, and their abundance was increased in the acquired-resistance population. Knockdown of CDA had antiproliferative effects on resistant cells and reversed the EMT phenotype. Treatment with epigenome-related nucleosides such as 5-formyl-2′-deoxycytidine selectively ablated CDA-overexpressing resistant cells via accumulation of DNA damage. Collectively, our data suggest that targeting CDA metabolism using epigenome-related nucleosides represents a potential new therapeutic strategy for overcoming ALK inhibitor resistance in NSCLC.