20(S)- Protopanaxadiol suppresses hepatic stellate cell activation via WIF1 demethylation-mediated inactivation of the Wnt/β-catenin pathway

Chunxue Li,Yating Zhan,Rongrong Zhang,Qiqi Tao,Zhichao Lang,Jianjian Zheng 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.4

Ginsenoside Rg1 Epigenetically Modulates Smad7 Expression in Liver Fibrosis via MicroRNA-152

Rongrong Zhang,Xinmiao Li,Yuxiang Gao,Qiqi Tao,Zhichao Lang,Yating Zhan,Chunxue Li,Jianjian Zheng 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.4

MiR-144-3p and Its Target Gene β-Amyloid Precursor Protein Regulate 1-Methyl-4-Phenyl-1,2-3,6-Tetrahydropyridine-Induced Mitochondrial Dysfunction

Li, Kuo,Zhang, Junling,Ji, Chunxue,Wang, Lixuan Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.7

MicroRNAs (miRNAs) have been reported to be involved in many neurodegenerative diseases. The present study focused on the role of hsa-miR-144-3p in one of the neuro-degenerative diseases, Parkinson's disease (PD). Our study showed a remarkable down-regulation of miR-144-3p expression in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-treated SH-SY5Y cells. MiR-144-3p was then overexpressed and silenced in human SH-SY5Y cells by miRNA-mimics and miRNA-inhibitor transfections, respectively. Furthermore, ${\beta}$-amyloid precursor protein (APP) was identified as a target gene of miR-144-3p via a luciferase reporter assay. We found that miR-144-3p overexpression significantly inhibited the protein expression of APP. Since mitochondrial dysfunction has been shown to be one of the major pathological events in PD, we also focused on the role of miR-144-3p and APP in regulating mitochondrial functions. Our study demonstrated that up-regulation of miR-144-3p increased expression of the key genes involved in maintaining mitochondrial function, including peroxisome proliferator-activated receptor ${\gamma}$ coactivator-$1{\alpha}$(PGC-$1{\alpha}$), nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM). Moreover, there was also a significant increase in cellular ATP, cell viability and the relative copy number of mtDNA in the presence of miR-144-3p overexpression. In contrast, miR-144-3p silencing showed opposite effects. We also found that APP overexpression significantly decreased ATP level, cell viability, the relative copy number of mtDNA and the expression of these three genes, which reversed the effects of miR-144-3p overexpression. Taken together, these results show that miR-144-3p plays an important role in maintaining mitochondrial function, and its target gene APP is also involved in this process.

PRR11 and SKA2 gene pair is overexpressed and regulated by p53 in breast cancer

Wang, Yitao,Zhang, Chunxue,Mai, Li,Niu, Yulong,Wang, Yingxiong,Bu, Youquan Korean Society for Biochemistry and Molecular Biol 2019 BMB Reports Vol.52 No.2

Our previous study found that two novel cancer-related genes, PRR11 and SKA2, constituted a classic gene pair that was regulated by p53 and NF-Y in lung cancer. However, their role and regulatory mechanism in breast cancer remain elusive. In this study, we found that the expression levels of PRR11 and SKA2 were upregulated and have a negative prognotic value in breast cancer. Loss-of-function experiments showed that RNAi-mediated knockdown of PRR11 and/or SKA2 inhibited proliferation, migration, and invasion of breast cancer cells. Mechanistic experiments revealed that knockdown of PRR11 and/or SKA2 caused dysregulation of several downstream genes, including CDK6, TPM3, and USP12, etc. Luciferase reporter assays demonstrated that wild type p53 significantly repressed the PRR11-SKA2 bidirectional promoter activity, but not NF-Y. Interestingly, NF-Y was only essential for and correlated with the expression of PRR11, but not SKA2. Consistently, adriamycin-induced (ADR) activation of endogenous p53 also caused significant repression of the PRR11 and SKA2 gene pair expression. Notably, breast cancer patients with lower expression levels of either PRR11 or SKA2, along with wild type p53, exhibited better disease-free survival compared to others with p53 mutations and/or higher expression levels of either PRR11 or SKA2. Collectively, our study indicates that the PRR11 and SKA2 transcription unit might be an oncogenic contributor and might serve as a novel diagnostic and therapeutic target in breast cancer.

Maternal nutrition altered embryonic MYOD1, MYF5, and MYF6 gene expression in genetically fat and lean lines of chickens

Li Feng,Yang Chunxu,Xie Yingjie,Gao Xiang,Zhang Yuanyuan,Ning Hangyi,Liu Guangtao,Chen Zhihui,Shan Anshan 아세아·태평양축산학회 2022 Animal Bioscience Vol.35 No.8

Objective: The objectives of this study were to evaluate the effects of daily feed intake during the laying period on embryonic myogenic differentiation 1 (MYOD1), myogenic factor 5 (MYF5), and myogenic factor 6 (MYF6) gene expression in genetically fat and lean lines of chickens. Methods: An experiment in a 2×2 factorial design was conducted with two dietary intake levels (100% and 75% of nutrition recommendation) and two broiler chicken lines (fat and lean). Two lines of hens (n = 384 for each line) at 23th week of age were randomly divided into 4 treatments with 12 replicates of 16 birds. The experiment started at 27th week of age (5% egg rate) and ended at 54th week of age. Hatched eggs from the medium laying period were collected. Real time polymerase chain reaction analysis was used to analyse the MYOD1, MYF5, and MYF6 mRNA levels of E7, E9, E11, E13, and E15 body tissues and E17, E19, and E21 chest and thigh muscle samples. Results: The results indicated that there were significant effects of line, dietary intake, and interactions between them on MYOD1, MYF5, and MYF6 gene mRNA expression levels in embryonic tissues. Low daily feed intake did not change the expression trend of MYOD1 mRNA in either line, but changed the peak values, especially in lean line. Low daily feed intake altered the trend in MYF5 mRNA expression level in both lines and apparently delayed its onset. There was no apparent effect of low daily feed intake on the trends of MYF6 mRNA expression levels in either line, but it significantly changed the values on many embryonic days. Conclusion: Maternal nutrient restriction affects myogenesis and is manifested in the expression of embryonic MYOD1, MYF5, and MYF6 genes. Long term selection for fat deposition in broiler chickens changes the pattern and intensity of myogenesis. Objective: The objectives of this study were to evaluate the effects of daily feed intake during the laying period on embryonic myogenic differentiation 1 (<i>MYOD1</i>), myogenic factor 5 (<i>MYF5</i>), and myogenic factor 6 (<i>MYF6</i>) gene expression in genetically fat and lean lines of chickens.Methods: An experiment in a 2×2 factorial design was conducted with two dietary intake levels (100% and 75% of nutrition recommendation) and two broiler chicken lines (fat and lean). Two lines of hens (n = 384 for each line) at 23th week of age were randomly divided into 4 treatments with 12 replicates of 16 birds. The experiment started at 27th week of age (5% egg rate) and ended at 54th week of age. Hatched eggs from the medium laying period were collected. Real time polymerase chain reaction analysis was used to analyse the <i>MYOD1</i>, <i>MYF5</i>, and <i>MYF6</i> mRNA levels of E7, E9, E11, E13, and E15 body tissues and E17, E19, and E21 chest and thigh muscle samples.Results: The results indicated that there were significant effects of line, dietary intake, and interactions between them on <i>MYOD1</i>, <i>MYF5</i>, and <i>MYF6</i> gene mRNA expression levels in embryonic tissues. Low daily feed intake did not change the expression trend of <i>MYOD1</i> mRNA in either line, but changed the peak values, especially in lean line. Low daily feed intake altered the trend in <i>MYF5</i> mRNA expression level in both lines and apparently delayed its onset. There was no apparent effect of low daily feed intake on the trends of <i>MYF6</i> mRNA expression levels in either line, but it significantly changed the values on many embryonic days.Conclusion: Maternal nutrient restriction affects myogenesis and is manifested in the expression of embryonic <i>MYOD1</i>, <i>MYF5</i>, and <i>MYF6</i> genes. Long term selection for fat deposition in broiler chickens changes the pattern and intensity of myogenesis.

Synthesis of Praseodymium-Doped TiO₂ Nanocatalysts by Sol-Microwave and Their Photocatalytic Activity Study

Huang, Fengping,Wang, Shuai,Zhang, Shuang,Fan, Yingge,Li, Chunxue,Wang, Chuang,Liu, Chun Korean Chemical Society 2014 Bulletin of the Korean Chemical Society Vol.35 No.8

The praseodymium-doped $TiO_2$ photocatalyst samples, which could degrade methyl orange under UV irradiation, were prepared by sol-microwave method for improving the photocatalytic activity of $TiO_2$. The resulting materials were analyzed by X-ray diffraction (XRD), scanning electron microscopy (SEM), Transmission electron microscopy (TEM), X-ray photoelectron spectroscopy (XPS), Raman spectra, Fourier transform infrared spectra (FTIR) and Ultraviolet-visible diffuse reflectance spectra (UV-vis DRS). It was found Pr doping retarded the growth of crystalline size and the phase transformation from anatase to rutile, and narrowed the band gap energy. Praseodymium doping brought about remarkable improvement in the photoactivity. The optimal dopant amount of Pr was 2% by molar of cement and the calcination temperature was $500^{\circ}C$ for the best photocatalytic activity. The improvement of photocatalytic activity was ascribed to the occurrence of lattice distortion and the effective containment of the recombination of the electron-hole by $Pr^{3+}$.

MiR-144-3p and Its Target Gene beta-Amyloid Precursor Protein Regulate 1-Methyl-4-Phenyl-1,2-3,6-Tetrahydropyridine-Induced Mitochondrial Dysfunction

Lixuan Wang,Kuo Li,Junling Zhang,Chunxue Ji 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.7

MicroRNAs (miRNAs) have been reported to be involved in many neurodegenerative diseases. The present study focused on the role of hsa-miR-144-3p in one of the neurodegenerative diseases, Parkinson’s disease (PD). Our study showed a remarkable down-regulation of miR-144-3p expression in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-treated SH-SY5Y cells. MiR-144-3p was then overexpressed and silenced in human SH-SY5Y cells by miRNA-mimics and miRNA-inhibitor transfections, respectively. Furthermore, -amyloid precursor protein (APP) was identified as a target gene of miR-144-3p via a luciferase reporter assay. We found that miR-144-3p overexpression significantly inhibited the protein expression of APP. Since mitochondrial dysfunction has been shown to be one of the major pathological events in PD, we also focused on the role of miR-144-3p and APP in regulating mitochondrial functions. Our study demonstrated that up-regulation of miR-144-3p increased expression of the key genes in-volved in maintaining mitochondrial function, including peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1), nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM). Moreover, there was also a significant increase in cellular ATP, cell viability and the relative copy number of mtDNA in the presence of miR-144-3p overexpression. In contrast, miR-144-3p silencing showed opposite effects. We also found that APP overexpression significantly decreased ATP level, cell viability, the relative copy number of mtDNA and the expression of these three genes, which reversed the effects of miR-144-3p overexpression. Taken together, these results show that miR-144-3p plays an important role in maintaining mitochondrial function, and its target gene APP is also involved in this process.

Structure evolution in carbon molecular sieve membranes derived from binaphthol-6FDA polyimide and their gas separation performance

Guoxiong Deng,Yilei Wang,Xueping Zong,Jiangzhou Luo,Xuezhen Wang,Chunxue Zhang,Song Xue 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.94 No.-

Here we reported a causal relationship between the molecular structure of binaphthol-based polyimideprecursor and the pore-size distribution of the derived carbon membrane. The binaphthol-basedpolyamide acid is synthesized from 2,20-diol-1,10-binaphthyl-6,60-diamine and 4,40-(hexafluoroisopro-pylidene)diphthalic anhydride (6FDA). Then, an azeotropic imidiaztion method was used to synthesizethe polyimide with naphthol groups (XS1). When the imidization is carried out by using acetic anhydride,the polyimide with acetyl groups (XS4) is achieved. The CMS membranes prepared by pyrolyzing XS1 andXS4 at 500, 550, and 600 ℃ are named using the temperature as the suffix, such as XS1-500. Their poreevolution has been investigated using TGA, FTIR, XRD, and Raman measurements. The trimodal pore-sizedistribution is in the carbon molecular sieve (CMS) membranes derived from XS4 and the CMS onesderived from XS1 exhibit a bimodal pore structure. Among them, XS4-500 exhibits the highest gaspermeabilities of 3332 barrer for CO2, 773 barrer for O2, and 119 barrer for N2. XS1-500 only affords theCO2, O2, and N2 permeabilities of 1086, 230, and 30.2 barrer. The esterification of naphthol not justdisturbs the hydrogen bonds between polyimide chains but also affects the pore generation of thederived CMS membranes. Our work provides an effective way to enhance the gas permeability of a CMSmembrane derived from the binaphthol-based polyimide.