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Hypoxanthine induces cholesterol accumulation and incites atherosclerosis in apolipoprotein E ‐deficient mice and cells
In this study, we investigated the role of hypoxanthine on cholesterol synthesis and atherosclerosis development, particularly in apolipoprotein E (APOE)‐deficient mice. The effect of hypoxanthine on the regulation of cholesterol synthesis and atherosclerosis were evaluated in Apoe knockout (KO) mice and cultured HepG2 cells. Hypoxanthine markedly increased serum cholesterol levels and the atherosclerotic plaque area in Apoe KO mice. In HepG2 cells, hypoxanthine increased intracellular ROS production. Hypoxanthine increased cholesterol accumulation and decreased APOE and ATP‐binding cassette transporter A1 (ABCA1) mRNA...
Source: Journal of Cellular and Molecular Medicine - July 10, 2016 Category: Molecular Biology Authors: Hye ‐Myung Ryu, You‐Jin Kim, Eun‐Joo Oh, Se‐Hyun Oh, Ji‐Young Choi, Jang‐Hee Cho, Chan‐Duck Kim, Sun‐Hee Park, Yong‐Lim Kim Tags: Original Article Source Type: research

Suppressive effect of epigallocatechin ‐3‐O‐gallate on endoglin molecular regulation in myocardial fibrosis in vitro and in vivo
In conclusion, epigallocatechin‐3‐O‐gallate (EGCG) attenuated the endoglin expression and myocardial fibrosis by anti‐inflammatory effect in vitro and in vivo, the novel suppressive effect was mediated through JNK/AP‐1 pathway.
Source: Journal of Cellular and Molecular Medicine - June 15, 2016 Category: Molecular Biology Authors: Chiu ‐Mei Lin, Hang Chang, Bao‐Wei Wang, Kou‐Gi Shyu Tags: Original Article Source Type: research

Suppressive effect of epigallocatechin‐3‐O‐gallate on endoglin molecular regulation in myocardial fibrosis in vitro and in vivo
In conclusion, epigallocatechin‐3‐O‐gallate (EGCG) attenuated the endoglin expression and myocardial fibrosis by anti‐inflammatory effect in vitro and in vivo, the novel suppressive effect was mediated through JNK/AP‐1 pathway.
Source: Journal of Cellular and Molecular Medicine - June 15, 2016 Category: Molecular Biology Authors: Chiu‐Mei Lin, Hang Chang, Bao‐Wei Wang, Kou‐Gi Shyu Tags: Original Article Source Type: research

Mitofusin ‐2 knockdown increases ER–mitochondria contact and decreases amyloid β‐peptide production
Abstract Mitochondria are physically and biochemically in contact with other organelles including the endoplasmic reticulum (ER). Such contacts are formed between mitochondria‐associated ER membranes (MAM), specialized subregions of ER, and the outer mitochondrial membrane (OMM). We have previously shown increased expression of MAM‐associated proteins and enhanced ER to mitochondria Ca2+ transfer from ER to mitochondria in Alzheimer's disease (AD) and amyloid β‐peptide (Aβ)‐related neuronal models. Here, we report that siRNA knockdown of mitofusin‐2 (Mfn2), a protein that is involved in the tethering of ER and ...
Source: Journal of Cellular and Molecular Medicine - May 19, 2016 Category: Molecular Biology Authors: Nuno Santos Leal, Bernadette Schreiner, Catarina Moreira Pinho, Riccardo Filadi, Birgitta Wiehager, Helena Karlstr öm, Paola Pizzo, Maria Ankarcrona Tags: Original Article Source Type: research

Mitofusin‐2 knockdown increases ER–mitochondria contact and decreases amyloid β‐peptide production
Abstract Mitochondria are physically and biochemically in contact with other organelles including the endoplasmic reticulum (ER). Such contacts are formed between mitochondria‐associated ER membranes (MAM), specialized subregions of ER, and the outer mitochondrial membrane (OMM). We have previously shown increased expression of MAM‐associated proteins and enhanced ER to mitochondria Ca2+ transfer from ER to mitochondria in Alzheimer's disease (AD) and amyloid β‐peptide (Aβ)‐related neuronal models. Here, we report that siRNA knockdown of mitofusin‐2 (Mfn2), a protein that is involved in the tethering of ER and ...
Source: Journal of Cellular and Molecular Medicine - April 30, 2016 Category: Molecular Biology Authors: Nuno Santos Leal, Bernadette Schreiner, Catarina Moreira Pinho, Riccardo Filadi, Birgitta Wiehager, Helena Karlström, Paola Pizzo, Maria Ankarcrona Tags: Original Article Source Type: research

MicroRNA‐20a‐5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression
In conclusion, we found novel evidence suggesting that as a member of miR‐17 family, miR‐20a‐5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression.
Source: Journal of Cellular and Molecular Medicine - March 27, 2016 Category: Molecular Biology Authors: Weiwei Fang, Jun Guo, Yuan Cao, Shuyue Wang, Cheng Pang, Meng Li, Lin Dou, Yong Man, Xiuqing Huang, Tao Shen, Jian Li Tags: Original Article Source Type: research

MicroRNA ‐20a‐5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression
In conclusion, we found novel evidence suggesting that as a member of miR‐17 family, miR‐20a‐5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression.
Source: Journal of Cellular and Molecular Medicine - March 27, 2016 Category: Molecular Biology Authors: Weiwei Fang, Jun Guo, Yuan Cao, Shuyue Wang, Cheng Pang, Meng Li, Lin Dou, Yong Man, Xiuqing Huang, Tao Shen, Jian Li Tags: Original Article Source Type: research

Effects of short‐chain acyl‐CoA dehydrogenase on cardiomyocyte apoptosis
In conclusion, for the first time our findings directly demonstrated that SCAD may be as a new target to prevent cardiomyocyte apoptosis through the AMPK/PPARα/SCAD signal pathways.
Source: Journal of Cellular and Molecular Medicine - March 17, 2016 Category: Molecular Biology Authors: Zhenhua Zeng, Qiuju Huang, Zhaohui Shu, Peiqing Liu, Shaorui Chen, Xuediao Pan, Linquan Zang, Sigui Zhou Tags: Original Article Source Type: research

Effects of short ‐chain acyl‐CoA dehydrogenase on cardiomyocyte apoptosis
In conclusion, for the first time our findings directly demonstrated that SCAD may be as a new target to prevent cardiomyocyte apoptosis through the AMPK/PPARα/SCAD signal pathways.
Source: Journal of Cellular and Molecular Medicine - March 16, 2016 Category: Molecular Biology Authors: Zhenhua Zeng, Qiuju Huang, Zhaohui Shu, Peiqing Liu, Shaorui Chen, Xuediao Pan, Linquan Zang, Sigui Zhou Tags: Original Article Source Type: research

Aspirin induces Nrf2‐mediated transcriptional activation of haem oxygenase‐1 in protection of human melanocytes from H2O2‐induced oxidative stress
Abstract The removal of hydrogen peroxide (H2O2) by antioxidants has been proven to be beneficial to patients with vitiligo. Aspirin (acetylsalicylic acid, ASA) has antioxidant activity and has great preventive and therapeutical effect in many oxidative stress‐relevant diseases. Whether ASA can protect human melanocytes against oxidative stress needs to be further studied. Here, we investigated the potential protective effect and mechanisms of ASA against H2O2‐induced oxidative injury in human melanocytes. Human melanocytes were pre‐treated with different concentrations of ASA, followed by exposure to 1.0 mM H2O2. Ce...
Source: Journal of Cellular and Molecular Medicine - March 10, 2016 Category: Molecular Biology Authors: Zhe Jian, Lingzhen Tang, Xiuli Yi, Bangmin Liu, Qian Zhang, Guannan Zhu, Gang Wang, Tianwen Gao, Chunying Li Tags: Original Article Source Type: research

Aspirin induces Nrf2 ‐mediated transcriptional activation of haem oxygenase‐1 in protection of human melanocytes from H2O2‐induced oxidative stress
Abstract The removal of hydrogen peroxide (H2O2) by antioxidants has been proven to be beneficial to patients with vitiligo. Aspirin (acetylsalicylic acid, ASA) has antioxidant activity and has great preventive and therapeutical effect in many oxidative stress‐relevant diseases. Whether ASA can protect human melanocytes against oxidative stress needs to be further studied. Here, we investigated the potential protective effect and mechanisms of ASA against H2O2‐induced oxidative injury in human melanocytes. Human melanocytes were pre‐treated with different concentrations of ASA, followed by exposure to 1.0 mM H2O2. Ce...
Source: Journal of Cellular and Molecular Medicine - March 9, 2016 Category: Molecular Biology Authors: Zhe Jian, Lingzhen Tang, Xiuli Yi, Bangmin Liu, Qian Zhang, Guannan Zhu, Gang Wang, Tianwen Gao, Chunying Li Tags: Original Article Source Type: research

The mechanisms and significance of up‐regulation of RhoB expression by hypoxia and glucocorticoid in rat lung and A549 cells
In this study, we investigated the effects of hypoxia or/and GC on the expression and activition of RhoB in the lung of rats and human A549 lung carcinoma cells, and further studied its mechanism and significance. We found that hypoxia and dexamethasone (Dex), a synethic GC, not only significantly increased the expression and activation of RhoB independently but also coregulated the expresion of RhoB in vitro and in vivo. Up‐regulation of RhoB by hypoxia was in part through stabilizing the RhoB mRNA and protein. Inhibiting hypoxia‐activated hypoxia‐inducible transcription factor‐1α (HIF‐1α), c‐Jun N‐termina...
Source: Journal of Cellular and Molecular Medicine - February 24, 2016 Category: Molecular Biology Authors: Gao‐Xiang Huang, Xiao‐Yu Pan, Yi‐Duo Jin, Yan Wang, Xiao‐Lian Song, Chang‐Hui Wang, Yi‐Dong Li, Jian Lu Tags: Original Article Source Type: research

The mechanisms and significance of up ‐regulation of RhoB expression by hypoxia and glucocorticoid in rat lung and A549 cells
In this study, we investigated the effects of hypoxia or/and GC on the expression and activition of RhoB in the lung of rats and human A549 lung carcinoma cells, and further studied its mechanism and significance. We found that hypoxia and dexamethasone (Dex), a synethic GC, not only significantly increased the expression and activation of RhoB independently but also coregulated the expresion of RhoB in vitro and in vivo. Up‐regulation of RhoB by hypoxia was in part through stabilizing the RhoB mRNA and protein. Inhibiting hypoxia‐activated hypoxia‐inducible transcription factor‐1α (HIF‐1α), c‐Jun N‐termina...
Source: Journal of Cellular and Molecular Medicine - February 23, 2016 Category: Molecular Biology Authors: Gao ‐Xiang Huang, Xiao‐Yu Pan, Yi‐Duo Jin, Yan Wang, Xiao‐Lian Song, Chang‐Hui Wang, Yi‐Dong Li, Jian Lu Tags: Original Article Source Type: research

HIF‐1α regulates EMT via the Snail and β‐catenin pathways in paraquat poisoning‐induced early pulmonary fibrosis
Abstract Paraquat (PQ) poisoning‐induced pulmonary fibrosis is one of the primary causes of death in patients with PQ poisoning. Hypoxia‐inducible factor‐1α (HIF‐1α) and epithelial‐mesenchymal transition (EMT) are involved in the progression of pulmonary fibrosis. Snail and β‐catenin are two other factors involved in promoting EMT. However, the relationship among HIF‐1α, Snail and β‐catenin in PQ poisoning‐induced pulmonary fibrosis is not clear. Our research aimed to determine whether the regulation of HIF‐1α in EMT occurs via the Snail and β‐catenin pathways in PQ poisoning‐induced pulmonar...
Source: Journal of Cellular and Molecular Medicine - January 19, 2016 Category: Molecular Biology Authors: Yong Zhu, Jiuting Tan, Hui Xie, Jinfeng Wang, Xiaoxiao Meng, Ruilan Wang Tags: Original Article Source Type: research

Epidermal growth factor attenuates blood‐spinal cord barrier disruption via PI3K/Akt/Rac1 pathway after acute spinal cord injury
In this study, we demonstrate that EGF administration inhibits the disruption of BSCB permeability and improves the locomotor activity in SCI model rats. Inhibition of the PI3K/Akt pathways by a specific inhibitor, LY294002, suppresses EGF‐induced Rac1 activation as well as tight junction (TJ) and adherens junction (AJ) expression. Furthermore, the protective effect of EGF on BSCB is related to the activation of Rac1 both in vivo and in vitro. Blockade of Rac1 activation with Rac1 siRNA downregulates EGF‐induced TJ and AJ proteins expression in endothelial cells. Taken together, our results indicate that EGF treatment ...
Source: Journal of Cellular and Molecular Medicine - January 1, 2016 Category: Molecular Biology Authors: Binbin Zheng, Libing Ye, Yulong Zhou, Sipin Zhu, Qingqing Wang, Hongxue Shi, Daqing Chen, Xiaojie Wei, Zhouguang Wang, Xiaokun Li, Jian Xiao, Huazi Xu, Hongyu Zhang Tags: Original Article Source Type: research

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