http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Han Ying-Hao,Mao Ying-Ying,Feng Yao-Yuan,Xiang Hong-Yi,Sun Hu-Nan,Jin Mei-Hua,Kwon Taeho 한국응용생명화학회 2022 Applied Biological Chemistry (Appl Biol Chem) Vol.65 No.3
In this study, we performed RNA sequencing of Prx II +/+ and Prx II −/− dermal mesenchymal stem cells (DMSCs) to identify differentially expressed genes (DEGs). To explore the role of Prx II in DMSCs, we performed Gene Ontology analysis of the DEGs. The results showed that the DEGs were mainly involved in the biological processes of cell migration, intercellular adhesion, and coordination of the regulation of stem cell homing. Through the construction of protein–protein interaction network, four hub genes Cd274 , Ccl5 , Il1b , and Stat1 involved in cell adhesion and cell homing were screened. Quantitative reverse transcription PCR analysis showed that Cd274 , Ccl5 , Il1b , and Stat1 were down regulated in Prx II −/− DMSCs. miRwalk and Starbase databases were further used to screen the upstream molecules miRNA and lncRNA regulating hub gene. Prx II was found to be involved in the regulation of stem cell homing via the Tctn2/miR-351/Stat1/Il1b axis. Thus, we demonstrated that Prx II is a key molecule in the regulation of the homing ability of DMSCs. Our results provide a theoretical foundation for improving the homing ability of DMSCs by targeting Prx II.
Han, Ying-Hao,Kwon, Jeong-Hoon,Yu, Dae-Yeul,Moon, Eun-Yi Taylor Francis 2006 Free radical research Vol.40 No.11
<P>Intracellular reactive oxygen species (ROS) were attenuated by the expression of peroxiredoxin II (Prx II). Cellular senescence as judged by senescence-associated (SA)-&bgr;-galactosidase (Gal) positive cell formation was increased in Prx II-deficient mouse embryonic fibroblast (MEF). Ras expression was increased following passages. The level of Ras expression was higher in Prx II<SUP>− / − </SUP> MEF than wild type MEF. ERK activity was also augmented by the deletion of Prx II. SA-&bgr;-Gal-positive cell formation was reduced by PD98059, ERK inhibitor. Activated nuclear transcription factor, nuclear factor-kappaB (NF&kgr;B) by the deletion of Prx II was inhibited by the treatment with PD98059. In contrast, no changes in SA-&bgr;-Gal-positive cell formation were detected by NF&kgr;B inhibitor, <I>N</I>-alpha-tosyl-l-phenylalanyl chloromethyl ketone (TPCK). Collectively, results suggest that Prx II deletion activate Ras–ERK–NF&kgr;B pathways and cellular senescence in Prx II<SUP>− / − </SUP> MEF cells was mediated by ERK activation but not by NF&kgr;B activation.</P>
Han Ying-Hao,Lian Xu-Dong,Lee Seung-Jae,Li Wei-Long,Sun Hu-Nan,Jin Mei-Hua,Kwon Taeho 한국응용생명화학회 2022 Applied Biological Chemistry (Appl Biol Chem) Vol.65 No.5
Patients with triple negative breast cancer (TNBC) lack the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2; thus, conventional hormone and targeted therapies have minimal effect on them. Therefore, clinical treatment of TNBC is still based on chemotherapy and supplemented by other methods. Doxorubicin (DOX), a common drug used in TNBC chemotherapy, has high affinity for cardiolipin, and the nematosomes are rich in cardiolipin; therefore, DOX has high mitochondria-targeting ability. DOX accumulates and plunders the electrons of nicotinamide adenine dinucleotide phosphate (NADPH) and cytochrome C in mitochondria to produce semiquinone DOX. Under the action of oxygen molecules, semiquinone DOX is reduced to DOX and reactive oxygen species (ROS) are generated. The accumulation of ROS can cause mitochondrial dysfunction and lead to mitochondrial dependent apoptosis. Bioinformatic analysis of samples from TNBC patients revealed that peroxiredoxin 1 (PRDX1) was highly expressed in TNBC tissues, and the poor prognosis of patients with high PRDX1 expression was considerably increased. Previous studies determined that DOX can upregulate the expression of the PRDX1 protein in the human TNBC cell line (MDA-MB-231). Thus, we speculate that PRDX1 plays an important role in the process of DOX-induced TNBC cell apoptosis. In this study, we aimed to explore the role of PRDX1 in the process of DOX-induced TNBC cell apoptosis. We found that PRDX1 deletion increased the sensitivity of MDA-MB-231 cells to DOX, which was mainly due to mitochondrial oxidative stress caused by intracellular ROS accumulation, leading to mitochondriadependent apoptosis. Deletion of PRDX1 promotes the PI3K/Akt signaling pathway to mediate the expression of GSK3β. Gsk3β is an upstream signal of mitochondria-dependent apoptosis, and is also an important target of ROS. PRDX1 participates in adriamycin-induced apoptosis of TNBC cells by regulating the expression level of GSK3β. Our findings present new insights to treat breast cancer and TNBC, outlines the clinical use of DOX, and provides a basic theory to develop PRDX1 gene function.
Han Ying-Hao,Mao Ying-Ying,Yu Nan-Nan,Jin Mei-Hua,Jin Ying-Hua,Wang Ai-Guo,Zhang Yong-Qing,Shen Gui-Nan,Cui Yu-Dong,Yu Li-Yun,Lee Dong-Seok,Jo Yu-Jin,Sun Hu-Nan,Kwon Jeongwoo,권태호 한국응용생명화학회 2020 Applied Biological Chemistry (Appl Biol Chem) Vol.63 No.3
In this study, we used RNA sequencing (RNA-seq) to analyze and compare bulk cell samples from wild-type (WT) dermal mesenchymal stem cells (DMSCs) (n = 3) and Prx II knockout DMSCs (n = 3). The purpose of the study was to elucidate the role of Prx II on allogeneic immune rejection of transplanted DMSCs. The results revealed differential expression of 472 genes (176 up-regulated and 296 down-regulated; p ≤ 0.05) between the PrxII+/+ (WT) and PrxII−/− sample groups. When highly regulated genes were categorized according to the Gene Ontology (GO) molecular function classification and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the PrxII−/− samples showed a robust downward trend in allograft rejection. The study identified 43 all immunologically rejected differentially expressed genes, of which 41 showed lower expression in the PrxII−/− vs. PrxII+/+ (WT) samples. These findings suggest that Prx II gene knockout may down-regulate the allograft rejection that occurs during DMSCs transplantation and improve the survival rate of DMSCs in the host. This study provides a new perspective on the clinical treatment of stem cell transplantation.
Han Ying-Hao,Chen Dong-Qin,Jin Mei-Hua,Jin Ying-Hua,Li Jing,Shen Gui-Nan,Li Wei-Long,Gong Yi-Xi,Mao Ying-Ying,Xie Dan-Ping,Lee Dong-Seok,Yu Li-Yun,Kim Sun-Uk,김지수,권태호,Cui Yu-Dong,Sun Hu-Nan 한국응용생명화학회 2020 Applied Biological Chemistry (Appl Biol Chem) Vol.63 No.3
Severe inflammatory reactions caused by macrophage activation can trigger a systemic immune response. In the present study, we observed the anti-inflammatory properties of hispidin on LPS induced RAW264.7 macrophage cells. Our results showed that hispidin treatment significantly reduced the production of cellular NO, IL-6 and reactive oxygen species (ROS) while has not inhibitory effect on TNF-α productions. Excitingly, hispidin treatment retains the phagocytosis ability of macrophages which enabling them to perform the function of removing foreign invaders. Signaling studies showed, hispidin treatment dramatic suppressed the LPS induced mitogen activated protein kinases (MAPK) and JAK/STAT activations. In conclusion, our findings suggest that hispidin may be a new therapeutic target for clinical treatment of macrophages-mediated inflammatory responses.