The role of peroxiredoxin V in (-)-epigallocatechin 3-gallate-induced multiple myeloma cell death.

Ren, Lina,Yang, Hee-Young,Choi, Hoon-In,Chung, Kyoung-Jin,Yang, Ung,Lee, Il-Kwon,Kim, Hyeoung-Joon,Lee, Dong-Seok,Park, Byung-Ju,Lee, Tae-Hoon Pergamon Press 2011 Oncology Research Vol.19 No.8

<P>(-)-Epigallocatechin 3-gallate (EGCG) is a potent antioxidant polyphenol in green tea that acts as an anticancer agent via both direct and indirect pathways. Although the relationship between EGCG's anticancer effects and its antioxidant activity is not fully understood, it is known that EGCG stimulates production of reactive oxygen species (ROS), which induce oxidative stress leading to cell death. In IM9 multiple myeloma cells, EGCG acted in a dose- and time-dependent manner to induce apoptotic cell death. Among the antioxidant enzymes expressed in IM9 cells, levels of peroxiredoxin V (PrdxV) were selectively and significantly reduced by EGCG. Moreover, the ROS scavenger NAC completely inhibited EGCG-induced apoptosis and PrdxV reduction, while overexpression of PrdxV, but not a Prdx(VC48S) mutant, protected IM9 cells from EGCG-induced apoptosis. EGCG-induced reductions in cell viability and PrdxV levels were also observed in primary CD138+ multiple myeloma cells from patients. These results suggest that PrdxV is a key target via which EGCG mediates its anticancer effects.</P>

Chemical Investigation of Volatiles Emitted from Flowers of Three Varieties of Damask Rose Cultivated in Beijing

Lina Yang,Jianwu Ren,Yan Wang 한국원예학회 2014 Horticulture, Environment, and Biotechnology Vol.55 No.6

Three varieties of Damask rose named ‘Four Seasons’, ‘Celsiana’ and ‘Rose de Rescht’, were studied inBeijing in dry and frozen climate. The volatiles emitted from flowers were collected by dynamic headspace collectionmethod and were detected and identified via thermal-desorption cold trap/gas chromatography/mass spectrometer technique(TCT-GC/MS). The results revealed that 63, 68 and 55 species of individual compounds were found from ‘FourSeasons’, ‘Celsiana’ and ‘Rose de Rescht’, respectively. The results demonstrated that ‘Celsiana’ possessed most diversevolatile components; the relative abundance of terpenes was as much as 49%, whereas it was 20 and 40% for ‘FourSeasons’ and ‘Rose de Rescht’, respectively. It meant that the rose oil from flowers of ‘Celsiana’ might be of highquality. Therefore, industrial plantation of ‘Celsiana’ is probably reasonable in Beijing area.

Role of Estrogen Receptor-α in the Regulation of Claudin-6 Expression in Breast Cancer Cells

Liu Yafang,Wu Qiong,Ren Yue,Xu Xiaoming,Yu Lina,Zhang Mingzi,Zhang Ting,Li Yulin,Quan Chengshi 한국유방암학회 2011 Journal of breast cancer Vol.14 No.1

Purpose: In our previous studies we showed that upregulating claudin-6 (CLDN6) expression may contribute to preventing breast cancer, and that 17β-estradiol induces a concentration- and time-related effect on CLDN6 mRNA and protein expression in MCF-7 cells. However, the mechanisms of 17β-estradiol regulation of CLDN6 are still unclear. We determined the role of estrogen receptors in the regulation of CLDN6 expression in human breast cancer tissues and a cell line. Methods: CLDN6, estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) expression in breast cancer tissues were examined using immunohistochemistry. The human breast cancer cell line, MCF-7, which expresses ERα but not ERβ was used. CLDN6 and ERα expression were measured by reverse transcriptase-PCR, Western blotting and immunofluorescent staining. Treatments with propyl pyrazole triol (PPT) and ICI 182, 780 (ICI) were performed. Results: The results revealed that CLDN6 expression was related to ERα in breast cancer tissues (p=0.033). PPT, an ERα-selective ligand, upregulated CLDN6 expression at 10^(-5) mol/L after 24 hours. The effect of PPT on regulating CLDN6 expression in MCF-7 cells was blocked by ICI. Conclusion: These findings suggest that Erα reulates CLDN6 expression in breast cancer tissues and that 17β- estradiol induces CLDN6 expression through an ERα pathway in MCF-7 cells.

Effect of kaolin pretreatment on the structure and properties of metakaolin phosphate-based geopolymers

Xin Yu,Chengxin Ren,Wenlong Xu,Lina Xu,Qingbo Tian 한양대학교 청정에너지연구소 2024 Journal of Ceramic Processing Research Vol.25 No.1

This study focused on the preparation of metakaolin-based phosphate-activated geopolymers (MKPGs) using kaolin pretreatedat 950 °C for varying times as a precursor. It was found that kaolinite quickly transformed into amorphous metakaolin (MK)and then transitioned from a disordered phase to an ordered phase, resulting in precipitation of kyanite and mullite withincreasing calcination time. The formation of the kyanite phase had an adverse effect on geopolymerization, which causeda decrease in the strength of the MKPGs. The precipitation of the mullite phase hindered the geopolymerization reactionbetween phosphoric acid and MK, and the geopolymer failed to solidify. As the calcination time increased from 10 min to 60min, the compressive strength of the geopolymers increased and then decreased. The maximum strength of the geopolymerscreated from MK calcined for 30 min was 132.1 MPa.

Punicalagin Reversed the Hepatic Injury of Tetrachloromethane by Antioxidation and Enhancement of Autophagy

Jingfang Luo,Yi Long,Guofeng Ren,Yahui Zhang,Jihua Chen,Ruixue Huang,Lina Yang 한국식품영양과학회 2019 Journal of medicinal food Vol.22 No.12

Hepatic injury is significant in the pathogenesis and development of many types of liver diseases. Punicalagin (PU) is a bioactive antioxidant polyphenol found in pomegranates. To explore its protective effect against carbon tetrachloride (CCl4)-induced liver injury and the mechanism, Institute of Cancer Research (ICR) mice and L02 cells were used to observe the changes of serum biochemical indicators, histopathological liver structure, cell viability, antioxidative indices, and autophagy-related proteins were assessed. In ICR mice, PU ameliorated the CCl4-induced increase of the serum aspartate aminotransferase, alanine aminotransferase, the activity of liver lactate dehydrogenase, and the damage of histopathological structure, and exhibited a hepatoprotective effect against CCl4. PU attenuated oxidative stress by decreasing the liver malondialdehyde level and increasing the activities of liver superoxide dismutase, glutathione peroxidase, and the expression of the liver nuclear factor E2-related factor (Nrf2) protein. Furthermore, according to the vivo and vitro experiments, PU might activate autophagy through the mediation of the Akt/FOXO3a and P62/Nrf2 signaling pathway. Taken together, these results suggest that PU may protect against CCl4-induced liver injury through the upregulation of antioxidative activities and autophagy.

Peroxiredoxin V selectively regulates IL-6 production by modulating the Jak2–Stat5 pathway

Choi, Hoon-In,Chung, Kyoung-Jin,Yang, Hee-Young,Ren, Lina,Sohn, Sungoh,Kim, Poo-Reun,Kook, Min-Suk,Choy, Hyon E.,Lee, Tae-Hoon Elsevier 2013 FREE RADICAL BIOLOGY AND MEDICINE Vol.65 No.-

<P><B>Abstract</B></P> <P>Mammalian peroxiredoxin V (PrdxV) is a multifunctional protein that protects cells from DNA damage and inhibits stress-induced apoptosis. However, PrdxV is also known to be involved in modulating lipopolysaccharide (LPS)-induced host cell signaling, but its precise role is not fully understood. In this study, we used stably transfected RAW264.7 cells and transiently transfected 293-mTLR4-MD2-CD14 cells expressing wild-type (WT) or mutant (C48S) PrdxV to characterize the function and mechanism of action of PrdxV in LPS-induced immune responses. We found that PrdxV selectively reduces production of interleukin 6 (IL-6) by inhibiting activation of signal transducer and activator of transcription 5 (Stat5) through interaction with Jak2. Notably, this activity of PrdxV was dependent on its catalytic Cys48 residue, but not its peroxidase activity. The binding of to Jak2 effectively inhibited Jak2 phosphorylation, but PrdxV did not act as efficiently as SOCS1 (suppressor of cytokine signaling 1). Our results suggest that PrdxV is a key mediator contributing to the regulation of LPS/TLR4-induced immune responses.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Cytosolic PrdxV is up-regulated in LPS-stimulated macrophages. </LI> <LI> PrdxV regulates IL-6 production in a catalytic Cys48-dependent manner. </LI> <LI> PrdxV modulates the activation of the Jak2–Stat5 signal cascades. </LI> <LI> PrdxV interacts with Jak2 via catalytic Cys48. </LI> </UL> </P>

Peroxiredoxin V Regulates Aco2, Acadm, and Acox1 Activity in Hypoxic Kidney

Tae‐Hoon Lee,Hee‐Young Yang,Joseph Kwon,Hoon‐In Choi,Lina Ren,Ung Yang,Byung‐Ju Park,Zae Young Ryoo 한국동물생명공학회(구 한국동물번식학회) 2011 발생공학 국제심포지엄 및 학술대회 Vol.2011 No.1

Peroxiredoxin V, an atypical thioredoxin peroxidase, is widely expressed in mammalian tissues. In addition, Prdx V is localized in mitochondria, peroxisome, cytosol, and nucleus. Prdx V has been reported to protect a wide range of cellular environments as antioxidant enzyme, and its dysfunctions may be implicated in several diseases, such as cancer, inflammation, and neurodegenerative disease. Identification and relative quantification of proteins affected by Prdx V may help identify novel signaling mechanisms that are important for oxidative stress response. However, the role of Prdx V in the modulation of hypoxia‐related cellular response is not studied yet. In order to examine the function of endogenous Prdx V in hypoxic condition in vivo, we generated a transgenic mouse model with Prdx V siRNA expression controlled by U6 promoter. Of many tissues, the knockdown of Prdx V expression was displayed in kidney, lung, and liver, but not spleen and skin. We conducted on the basis of nano‐UPLC‐MSE proteomic study to identify the Prdx V‐affected protein networks in hypoxic kidneys. In this study, we identified protein networks associated with oxidative stress, fatty acid metabolism, and mitochondrial dysfunction. Our results indicated that Prdx V affected to regulation of kidney homeostasis under hypoxia stress.

Targeting Multiple Myeloma Cell Death with Polyphenol EGCG

Tae‐Hoon Lee,Hee‐Young Yang,Hoon‐In Choi,Ung Yang,Kyoung‐Jin Chung,Lina Ren 한국동물생명공학회(구 한국동물번식학회) 2011 발생공학 국제심포지엄 및 학술대회 Vol.2011 No.1

(‐)‐Epigallocatechin 3‐gallate (EGCG) is a potent antioxidant polyphenol in green tea that acts as an anticancer agent via both direct and indirect pathways. Although the relationship between EGCG’s anticancer effects and its antioxidant activity is not fully understood, it is known that EGCG stimulates production of reactive oxygen species (ROS), which induce oxidative stress leading to cell death. In IM9 multiple myeloma cells, EGCG acted in a dose‐ and time‐dependent manner to induce apoptotic cell death. Among the antioxidant enzymes expressed in IM9 cells, levels of peroxiredoxin (Prdx) V were selectively and significantly reduced by EGCG. Moreover, the ROS scavenger NAC completely inhibited EGCG‐induced apoptosis and PrdxV reduction, while overexpression of PrdxV, but not a PrdxVC48S mutant, protected IM9 cells from EGCG‐induced apoptosis. EGCG‐induced reductions in cell viability and PrdxV levels were also observed in primary CD138+ multiple myeloma cells from patients. These results suggest that PrdxV is a key target via which EGCG mediates its anticancer effects.