Jae-A Han, Jungeun An, and Myunggon KoMol. Cells 2015; 38(11): 925-935 https://doi.org/10.14348/molcells.2015.0294
Abstract : DNA methylation is a well-characterized epigenetic modification that plays central roles in mammalian development, genomic imprinting, X-chromosome inactivation and silencing of retrotransposon elements. Aberrant DNA methylation pattern is a characteristic feature of cancers and associated with abnormal expression of oncogenes, tumor suppressor genes or repair genes. Ten-eleven-translocation (TET) proteins are recently characterized dioxygenases that catalyze progressive oxidation of 5-methylcytosine to produce 5-hydroxymethylcytosine and further oxidized derivatives. These oxidized methylcytosines not only potentiate DNA demethylation but also behave as independent epigenetic modifications
Sang-Ho Song, and George J. AugustineMol. Cells 2015; 38(11): 936-940 https://doi.org/10.14348/molcells.2015.0233
Abstract : Synapsins were the first presynaptic proteins identified and have served as the flagship of the presynaptic protein field. Here we review recent studies demonstrating that different members of the synapsin family play different roles at presynaptic terminals employing different types of synaptic vesicles. The structural underpinnings for these functions are just beginning to be understood and should provide a focus for future efforts.
Aiguo Li, Libin Yang, Xiaolin Geng, Xingmei Peng, Tan Lu, Yanjun Deng, and Yuzheng DongMol. Cells 2015; 38(11): 941-949 https://doi.org/10.14348/molcells.2015.2353
Abstract : Rheumatoid arthritis is a chronic inflammatory disease that leads to bone and cartilage erosion. The inhibition of osteoblast differentiation by the inflammatory factor TNF-α is critical for the pathogenesis of rheumatoid arthritis. To modulate TNF-α mediated inhibition of osteoblast differentiation is required to improve therapeutic efficacy of rheumatoid arthritis. Here, we explored the potential role of rocaglamide-A, a component of
Sang-Je Park, Young-Hyun Kim, Sang-Rae Lee, Se-Hee Choe, Myung-Jin Kim, Sun-Uk Kim, Ji-Su Kim, Bo-Woong Sim, Bong-Seok Song, Kang-Jin Jeong, Yeung-Bae Jin, Youngjeon Lee, Young-Ho Park, Young Il Park, Jae-Won Huh, and Kyu-Tae ChangMol. Cells 2015; 38(11): 950-958 https://doi.org/10.14348/molcells.2015.0121
Shan Wang, Ting Wang, Tao Wang, and Lintao JiaMol. Cells 2015; 38(11): 959-965 https://doi.org/10.14348/molcells.2015.0137
Abstract : Inducible and reversible gene silencing in desired types of cells is instrumental for deciphering gene functions using cultured cells or
Ji-Young Lim, Da-Bin Ryu, Sung-Eun Lee, Gyeongsin Park, Eun Young Choi, and Chang-Ki MinMol. Cells 2015; 38(11): 966-974 https://doi.org/10.14348/molcells.2015.0158
Abstract : Despite the presence of toll like receptor (TLR) expression in conventional TCRαβ T cells, the direct role of TLR signaling via myeloid differentiation factor 88 (MyD88) within T lymphocytes on graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) effect after allogeneic stem cell transplantation (allo-SCT) remains unknown. In the allo-SCT model of C57BL/6 (H-2b) → B6D2F1 (H-2b/d), recipients received transplants of wild type (WT) T-cell-depleted (TCD) bone marrow (BM) and splenic T cells from either WT or MyD88 deficient (MyD88KO) donors. Host-type (H-2d) P815 mastocytoma or L1210 leukemia cells were injected either subcutaneously or intravenously to generate a GVHD/GVL model. Allogeneic recipients of MyD88KO T cells demonstrated a greater tumor growth without attenuation of GVHD severity. Moreover, GVHD-induced GVL effect, caused by increasing the conditioning intensity was also not observed in the recipients of MyD88KO T cells.
Ok Kyu Park, Jina Kwak, Yoo Jung Jung, Young Ho Kim, Hyun-Seok Hong, Byung Joon Hwang, Seung-Hae Kwon, and Yun KeeMol. Cells 2015; 38(11): 975-981 https://doi.org/10.14348/molcells.2015.0160
Abstract : Precise 3D spatial mapping of cells and their connections within living tissues is required to fully understand developmental processes and neural activities. Zebrafish embryos are relatively small and optically transparent, making them the vertebrate model of choice for live
Byung-Hak Kim, Mi Sun Choi, Hyun Gyu Lee, Song-Hee Lee, Kum Hee Noh, Sunho Kwon, Ae Jin Jeong, Haeri Lee, Eun Hee Yi, Jung Youl Park, Jintae Lee, Eun Young Joo, and Sang-Kyu YeMol. Cells 2015; 38(11): 982-990 https://doi.org/10.14348/molcells.2015.0169
Abstract : Exposure of the skin to ultraviolet radiation can cause skin damage with various pathological changes including inflammation. In the present study, we identified the skin-protective activity of 1,2,3,4,6-penta-O-galloyl-β-D-glucose (pentagalloyl glucose, PGG) in ultraviolet B (UVB) radiation-induced human dermal fibroblasts and mouse skin. PGG exhibited antioxidant activity with regard to intracellular reactive oxygen species (ROS) generation as well as ROS and reactive nitrogen species (RNS) scavenging. Furthermore, PGG exhibited anti-inflammatory activity, inhibiting the activation of nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling, resulting in inhibition of the expression of pro-inflammatory mediators. Topical application of PGG followed by chronic exposure to UVB radiation in the dorsal skin of hairless mice resulted in a significant decrease in the progression of inflammatory skin damages, leading to inhibited activation of NF-κB signaling and expression of pro-inflammatory mediators. The present study demonstrated that PGG protected from skin damage induced by UVB radiation, and thus, may be a potential candidate for the prevention of environmental stimuli-induced inflammatory skin damage.
Jinhyun Ryu, Nal Ae Yoon, Hyemin Seong, Joo Yeon Jeong, Seokmin Kang, Nammi Park, Jungil Choi, Dong Hoon Lee, Gu Seob Roh, Hyun Joon Kim, Gyeong Jae Cho, Wan Sung Choi, Jae-Yong Park, Jeong Woo Park, and Sang Soo KangMol. Cells 2015; 38(11): 991-997 https://doi.org/10.14348/molcells.2015.0197
Abstract : Tristetraprolin (TTP) is an AU-rich elements (AREs)-binding protein, which regulates the decay of AREs-containing mRNAs such as proto-oncogenes, anti-apoptotic genes and immune regulatory genes. Despite the low expression of TTP in various human cancers, the mechanism involving suppressed expression of TTP is not fully understood. Here, we demonstrate that Resveratrol (3,5,4′-trihydroxystilbene, Res), a naturally occurring compound, induces glioma cell apoptosis through activation of tristetraprolin (TTP). Res increased TTP expression in U87MG human glioma cells. Res-induced TTP destabilized the urokinase plasminogen activator and urokinase plasminogen activator receptor mRNAs by binding to the ARE regions containing the 3′ untranslated regions of their mRNAs. Furthermore, TTP induced by Res suppressed cell growth and induced apoptosis in the human glioma cells. Because of its regulation of TTP expression, these findings suggest that the bioactive dietary compound Res can be used as a novel anti-cancer agent for the treatment of human malignant gliomas.
Young-Sun Lee, Hyon-Seung Yi, Yang-Gun Suh, Jin-Seok Byun, Hyuk Soo Eun, So Yeon Kim, Wonhyo Seo, Jong-Min Jeong, Won-Mook Choi, Myung-Ho Kim, Ji Hoon Kim, Keun-Gyu Park, and Won-Il JeongMol. Cells 2015; 38(11): 998-1006 https://doi.org/10.14348/molcells.2015.0218
Abstract : Retinols are metabolized into retinoic acids by alcohol dehydrogenase (ADH) and retinaldehyde dehydrogenase (Raldh). However, their roles have yet to be clarified in hepatitis despite enriched retinols in hepatic stellate cells (HSCs). Therefore, we investigated the effects of retinols on Concanavalin A (Con A)-mediated hepatitis.Con A was injected into wild type (WT), Raldh1 knock-out (Raldh1?/?), CCL2?/? and CCR2?/? mice. For migration study of regulatory T cells (Tregs), we used