MICROPOROUS AND MESOPOROUS MATERIALS
·
2019
·
IF 4.182
Yeqing Wang,Jian Zhang,Xiangju Meng,Shichao Han,Qiuyan Zhu,Na Sheng,Liang Wang,Feng-Shou Xiao
In this work, we show sustainable and efficient synthesis of nanosized EMT zeolite under organotemplate-free and solvent-free conditions, which not only completely avoids the use of organic templates for production of NOx and CO 2 but also effectively reduces the formation of polluted water. In addition, the yield of EMT zeolite is significantly enhanced by this route, compared with conventional hydrothermal synthesis . The nanosized EMT zeolite obtained has good crystallinity, uniform crystal size distribution, and high surface area. Ion-exchange tests show that the nanosized EMT zeolite owes high Ca 2+ and Mg 2+ ion exchange capacity at room temperature, which is potentially important for softening hard water in the industrial processes. Catalytic tests in Knoevenagel condensation show that the nanosized EMT zeolite exhibits higher activity than that of the EMT zeolite synthesized using organic template, indicating the importance of the nanosized EMT zeolite as a base catalyst.
研究领域:
材料科学
·
环境科学
·
催化化学
✓ 已验证
产品关联
DOI
高影响因子
BIOSENSORS & BIOELECTRONICS
·
2021
·
IF 10.618
Yuwei Tian,Limin Zhang,Fangjie Liu,Minxuan Wang,Lingyun Li,Mingmei Guo,Hangyu Xu,Zhiying Yu,Weizhi Wang
Epithelial-mesenchymal transition (EMT) is closely related to tumor metastasis and invasion. Thereinto, mesenchymal tumor mitochondria are the critical target for tumor inhibition. Therefore, real-time in vivo monitoring of EMT as well as inhibiting mesenchymal tumor mitochondria is of great diagnosis and therapy significance. Herein, we construct a multi-stage recognition and morphological transformable self-assembly-peptide nano biosensor N DRP which can response the EMT marker and specifically damage the mesenchymal tumor cell in vivo . This nano-molar-affinity sensor is designed and screened with sensitive peptides containing a molecular switching which could be specifically triggered by the receptor to achieve the vesicle-to-fibril transformation in living system with enhanced fluorescent signal. N DRP nanosensor could target the tumor lesion in circulatory system, recognize mesenchymal tumor marker DDR2 (Discoidin domain receptor 2) in cellular level and specifically achieve mitochondria in subcellular level as well as damaged mitochondria which could be applied as a in vivo theranostic platform.
研究领域:
癌症生物学
·
纳米技术
·
分子生物学
·
诊疗学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MEDICAL SCIENCE MONITOR
·
2020
·
IF 1.918
Shudong Chen,Chenglei Ren,Hui Zheng,Xianchun Sun,Jundi Dai
Background lncRNA HCP5 plays a cancer-promoting role in a variety of cancers. This study was the first to explore the mechanism of HCP5 in gastric carcinoma (GC). Material/Methods The differences in HCP5 between GC patients and healthy people were revealed in the TCGA database. The expression of HCP5 in GC tissues and adjacent tissues was compared by qRT-PCR. At the same time, the clinic pathological features of the patients were counted. Starbase and luciferase assay predicted and verified that miR-27b-3p is a targeted miRNA for HCP5. The expression of HCP5 and miR-27b-3p in various GC cells was detected by qRT-PCR. Cell viability and metastasis in different treatment groups were assessed by use of Cell Couting Kit-8 assay and clone formation assay, wound-healing assay, and transwell assay. Finally, expression of epithelial-mesenchymal transition (EMT)-associated markers was detected by Western blot. Results We found that HCP5 was overexpressed in GC tissues. Patients with higher expression of HCP5 had larger tumors, were more likely to have lymph node metastasis, and had higher TNM stage. HCP5 was overexpressed in GC cells, but this was reversed by miR-27b-3p. Silencing HCP5 inhibited GC cell viability and metastasis by downregulating Vimentin and N-cadherin and up-regulating E-cadherin, but this effect was partially reversed by miR-27b-3p inhibitor. Conclusions The effect of silencing HCP5 on repressing GC cells viability and metastasis by regulating EMT-associated markers can be partially reversed by miR-27b-3p inhibitor.
研究领域:
肿瘤学
·
分子生物学
·
癌症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
International Journal of Biological Sciences
·
2021
·
IF 6.582
Deng-Pan Wu,Yan Zhou,Li-Xiang Hou,Xiao-Xiao Zhu,Wen Yi,Si-Man Yang,Tian-Yu Lin,Jin-Lan Huang,Bei Zhang,Xiao-Xing Yin
Tamoxifen (TAM) resistance has indicated a significant challenge during endocrine therapy for hormone-sensitive breast cancer. Thus, it is significant to elucidate the molecular events endowing TAM resistance to endocrine therapy. In this study, we found that epithelial-mesenchymal transition (EMT) was an important event to confer TAM resistance, and attenuating EMT by elevating connexin (Cx) 43 expression could reverse TAM resistance. Specifically, Cx43 overexpression improved TAM sensitivity, while Cx43 depletion facilitated TAM insensitivity by modulating EMT in T47D TAM-resistant and -sensitive cells, and transplanted xenografts. Importantly, we found a novel reciprocal regulation between Cx43 and c-Src/PI3K/Akt pathway contributing to EMT and TAM resistance in breast cancer. Moreover, we identified that Cx43 deficiency was significantly correlated with poor relapse-free survival in patients undergoing TAM treatment. Therefore, Cx43 represents a prognostic marker and an attractive target for breast cancer treatments. Therapeutic strategies designed to increase or maintain Cx43 function may be beneficial to overcome TAM resistance.
研究领域:
肿瘤学
·
分子生物学
·
癌症治疗
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Biomaterials Science
·
2022
·Vol. 11
·期 1
·235-247
·
IF 7.59
Xiaomeng Wang,Xiaoduo Tang,Nuo Li,Yihan Sun,Ruotong Yu,Junhu Zhang,Daowei Li,Bai Yang,Hongchen Sun
The ultimate goal of cutaneous wound healing is to reform a stratified epithelium to restore the normal epidermal barrier, which involves the epithelial-to-mesenchymal transition (EMT) process. However, healing strategies based on EMT induction are immature and ambiguous to date. Excessive induction of EMT may cause fibrosis, hypertrophic scarring, and increased risk of malignancy. Here, we present a new EMT-inducing strategy for eliciting partial EMT to facilitate proper epithelial cell migration. The new EMT-inducing system integrates black phosphorus nanosheets (BPNSs), catechol-modified chitosan (CA-CS), and oxidized dextran (Odex) to engineer an adhesive hydrogel patch (C&BP-Patch) with remarkable efficacy on infectious burn wound healing. The C&BP-Patch can orchestrate key early skin wound healing processes including hemostasis, inflammation, and proliferation, which enable fast partial EMT induction to restore an intact epithelial barrier. The C&BP-Patch acts initially as a high-performance bio-sealant to create a moist and stable microenvironment for EMT. Moreover, the photothermal effects of the C&BP-Patch can eliminate bacteria, accelerate microcirculation and reduce inflammation to maintain a proper EMT. Most importantly, the BPNSs can intrinsically induce partial EMT of epithelial cells via a Snail1-mediated signaling pathway. Therefore, our study proposes a new strategy for effective infectious burn wound healing based on inducing partial EMT.
研究领域:
材料科学
·
生物医学工程
·
伤口愈合
·
纳米技术
·
组织工程
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF HAZARDOUS MATERIALS
·
2024
·
IF 12.2
Zhe Du,Qingping Liu,Mengruo Wang,Yifu Gao,Qi Li,Yizhe Yang,Tianyu Lu,Lei Bao,Yaxian Pang,Haijun Wang,Yujie Niu,Rong Zhang
Accumulating evidence indicates that maternal exposure to carbon black nanoparticles (CBNPs) during gestation can induce multiple system abnormalities in offspring, whereas its potential mechanism in respiratory disease is still largely unknown. In order to explore the effect of maternal exposure to CBNPs on offspring’s lung and latent pathogenesis, we respectively established in vivo model of pregnant rats exposed to CBNPs and ex vivo model of lung epithelial cells treated with pups’ serum of pregnant rats exposed to CBNPs. After maternal exposure to CBNPs, epithelial-mesenchymal transition (EMT) and fibrosis levels increased as a result of DDRGK1-mediated reticulophagy upregulated in offspring’s lung. DDRGK1 as FAM134B’s cargo bound with FAM134B to mediate reticulophagy. Transcription factor “SP1” positively regulated DDRGK1 gene expression by binding to its promoter. Furthermore, the upregulation of NSUN2 elevated m 5 C methylation of SP1 mRNA and the protein level of SP1 subsequently increased through Ybx1 recognizing and stabilizing m 5 C-methylated SP1 mRNA, followed by the increased levels of reticulophagy and fibrosis in lung epithelial cells treated with offspring’s serum of matrix exposed to CBNPs during gestation. In conclusion, NSUN2/Ybx1/m 5 C-SP1 axis promoted DDRGK1-mediated reticulophagy, which played an important role in EMT-induced fibrosis in offspring’s lung tissue after maternal exposure to CBNPs during gestation.
研究领域:
呼吸系统疾病
·
纳米毒理学
·
分子生物学
·
表观遗传学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PLACENTA
·
2024
·
IF 3
Gaoying Wang,Ruirui Dong,Haijian Zhao,Ningzhen Ye,Jing Wang,Jing Cheng,Xinrui Shi,Liang Luo,Ting Zhang
Background Abnormal bile acid metabolism leading to changes in placental function during pregnancy. To determine whether endoplasmic reticulum protein 29 (ERp29) can mediate the pregnancy effects of cholestasis by altering the level of trophoblast cell apoptosis. Methods ERp29 in serum of 66 intrahepatic cholestasis of pregnancy (ICP) pregnant women and 74 healthy were detected by ELISA. Subcutaneous injection of ethinyl estradiol (E2) was used to induce ICP in pregnant rats. Taurocholic acid (TCA) was used to simulate the ICP environment, and TGF-β1 was added to induce the epithelial mesenchymal transformation (EMT) process. The scratch, migration, and invasion test were used to detect the EMT process. ERp29 overexpression/knockdown vector were constructed and transfected to verify the role of ERp29 in the EMT process. Downstream gene was obtained through RNA-seq. Results Compared with the healthy pregnant women, the expression levels of ERp29 in serum of ICP pregnancy women were significantly increased (P < 0.001). ERp29 in the placenta tissue of the ICP pregnant rats increased significantly, and the level of apoptosis increased. The placental tissues of the ICP had high expression of E-cadherin and low expression of N-cadherin, snail1, vimentin. After HTR-8/SVneo cells were induced by TCA, EMT was inhibited, while the ERp29 increased. Cell and animal experiments showed that, knockdown of ERp29 reduced the inhibition of EMT, the ICP progress was alleviated. Overexpression of FOS salvaged the inhibitory effects of ERp29 on cell EMT. Discussion The high level of ERp29 in placental trophoblast cells reduced FOS mRNA levels, inhibited the EMT process and aggravated the occurrence and development of ICP.
研究领域:
妇产科学
·
分子生物学
·
细胞生物学
·
病理学
✓ 已验证
DOI
PubMed
高影响因子
Journal of Materials Chemistry C
·
2023
·Vol. 11
·期 48
·17080-17086
·
IF 6.4
Jinping Yuan,Qianrui Li,Chunmei Yue,Na Wang,Peng Li,Huanrong Li
Zeolite confined silver clusters (AgCLs) are favored by scientific researchers due to their unique luminescent properties. However, it remains a challenge to optimize luminescent silver-loaded zeolites through simple and effective methods. In this work, the effect of surface modification on the dynamic luminescence abilities of silver clusters in zeolites was discussed for the first time. A series of luminescent silver nanoclusters (from yellow-green emission to blue emission) were fabricated by introducing Ag+ ions into EMT zeolites and PEG400-modified EMT zeolites, respectively. It is also noteworthy that modification of the EMT zeolite surface with PEG400 significantly improves the luminescence intensity and photoluminescence quantum yields, which may be ascribed to the increase of hydroxyl (–OH) functional groups in the surface of PEG400-modified EMT zeolites, thereby promoting the reduction of Ag+ and accelerating the nucleation rate of luminescent silver nanoclusters. Moreover, even at increasing thermal temperature, the sample modified by PEG400 still maintains intense blue light and only presents a slight thermal quenching effect, showing superior stability. Therefore, in terms of optical properties and stability, such a sample synthesized by us possessing a high PLQY of 53% and good thermal stability can be considered as a suitable candidate to replace the traditional commercial blue-emitting phosphor (BaMgAl10O17:Eu2+) for full spectrum white lighting. Furthermore, a white LED lamp was obtained by combining the composites and commercial phosphors on a 365 nm NUV-LED. This work contributes to a valuable reference for the rational design of luminescent silver-loaded zeolites with promising new functionalities and stimulates the great potential of luminescent silver nanocluster zeolite composites in developing promising phosphors for high-quality lighting.
✓ 已验证
产品关联
DOI
高影响因子
Journal of Advanced Research
·
2025
·
IF 13
Shize Zhang,Yuang Chen,Nan Aa,Chen Xu,Tao Xie,Yi Wang,Tian Cheng,Mengqin Wang,Hong Yu,Xinqiang Ji,Song Zhao,Yaohui Wang,Jun Xiao,Yuan Xie,Guangji Wang,Jiye Aa
Introduction The repair of structural damage of the intestinal barrier is critical to rescue ulcerative colitis (UC), but there lacks effective targets currently. Objectives This study aims to explore mechanisms and identify potential targets for repairing the damaged intestinal barrier involved in UC. Methods Nontargeted metabolomic and transcriptomic analyses were utilized to characterize the metabolic features of DSS-induced colitis and identify potential therapeutic targets. Pantothenate kinase 3 (PANK3) was pharmacologically and genetically modulated to elucidate its mechanistic role. Chromatin immunoprecipitation and dual-luciferase reporter assays were employed to identify upstream regulators of PANK3, and PANK3 agonists were screened by high-throughput docking and further confirmed by in vitro and in vivo experiments. Results Metabolomic data indicated that perturbed metabolism involves pantothenate kinase. Clinical database, qPCR, WB, and immunohistochemical staining revealed a significant decrease of PANK3 in both patients and murine models of colitis. Pharmacological activation or overexpression of PANK3 restored the integrity of the intestinal barrier in UC mice, whereas PANK3 knockdown or inhibition exacerbated barrier dysfunction. PANK3 is negatively regulated by upstream c-Myc, and affects downstream, epithelial‒mesenchymal transition (EMT). In general, elevated c-Myc suppressed PANK3 transcription, promoted the EMT process and induced barrier disruption. The natural vitamin folic acid was identified as an agonist of PANK3, which could markedly improve the intestinal barrier in DSS-induced colitis. Conclusion The c-Myc-PANK3-EMT axis plays a critical role in preserving the structure and function of intestinal barrier. PANK3 is a potential target and folic acid is a candidate agonist of PANK3 to repair intestinal barrier in UC.
研究领域:
胃肠病学
·
分子生物学
·
免疫学
·
代谢组学
·
转化医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
XiaoMing Zhou,ChenXi Zhang,Wen Shen,RuiFei Zhuang,ShenLin Liu,JinDi Liu
Background Curzerene, a bioactive compound from Curcuma zedoaria, exhibits anticancer effects, but its role in gastric precancerous lesions remains poorly understood. This study investigates the potential of Curzerene in inhibiting gastric precancerous lesions progression by regulating the long non-coding RNA (LncRNA) AFAP1-AS1 and the Hippo/YAP signaling pathway. Methods In vitro, a gastric precancerous cell model (MC cells) was established by treating GES-1 cells with MNNG. The effects of Curzerene on cell proliferation, migration, and EMT were assessed using CCK-8, scratch assays, RT-PCR, and Western blot. In vivo, a gastric precancerous mouse model was induced by MNU, and the therapeutic effects of Curzerene (14 mg/kg and 28 mg/kg) were evaluated through histological and molecular analysis. Results Curzerene treatment significantly inhibited MC cell proliferation, migration, and EMT, downregulating LncRNA AFAP1-AS1 and YAP while upregulating E-cadherin and downregulating N-cadherin. In vivo, Curzerene alleviated gastric mucosal damage, reduced cancer markers (P53 and CD133), and improved histopathology. Transcriptomic analysis identified the Hippo/YAP pathway as a key mediator of Curzerene’s effects. YAP activation reversed Curzerene’s inhibitory effects on EMT, confirming the involvement of this pathway. Conclusion Curzerene effectively inhibits gastric precancerous lesion progression by targeting the YAP signaling and the following LncRNA AFAP1-AS1 to suppress EMT. These findings suggest Curzerene’s novel potential as a promising therapeutic agent for early intervention and prevention of gastric cancer.
研究领域:
肿瘤学
·
分子生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHINESE JOURNAL OF CHEMICAL ENGINEERING
·
2026
·
IF 3.5
Yuze Zhang,Xiaoqing Wang,Yuan Li,Yating Wang,Yang Zhou,Feifei Zhang,Jinping Li,Jiangfeng Yang
Adsorptive CH 4 /N 2 separation holds great promise, yet remains a challenging effort owing to the limited availability of effective adsorbents. In this study, a series of tetramethylammonium (TMA)-modified EMT zeolites (EMT-TMA) were developed via ion exchange for CH 4 /N 2 adsorption separation. The suitable pore and incorporated functional groups of EMT-TMA contribute to a pronounced increase in CH 4 adsorption capacity, accompanied by a significant decrease in N 2 adsorption, resulting in a substantial enhancement of CH 4 /N 2 selectivity. In particular, EMT-TMA-34% exhibits a selectivity of CH 4 /N 2 up to 5.4 at 298 K and 100 kPa, far surpassing that of the pristine EMT (1.8). Grand canonical Monte Carlo (GCMC) calculations indicate that introducing TMA markedly increases the difference for CH 4 and N 2 affinity on the adsorbent. Breakthrough experiments and pressure swing adsorption (PSA) simulation further confirm its outstanding CH 4 /N 2 separation performances. This study converts previously ineffective materials in this area into highly efficient CH 4 adsorbents, with significant potential for industrial coalbed methane (CBM) upgrading. Download: Download high-res image (245KB) Download: Download full-size image
✓ 已验证
产品关联
DOI
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2019
·
IF 3.585
Guangxu Cao,Shuang Li,Hezhan Shi,Peidi Yin,Jialing Chen,Huifeng Li,Ying Zhong,Li-Ting Diao,Bin Du
Tubulointerstitial fibrosis (TIF) is the main pathologic feature of end-stage renal disease. Epithelial-mesenchymal transition (EMT) of proximal tubular cells (PTCs) is one of the most significant features of TIF. MicroRNAs play critical roles during EMT in TIF. However, whether miRNAs can be used as therapeutic targets in TIF therapy remains undetermined. We found that miR-30e, a member of the miR-30 family, is deregulated in TGF-β1-induced PTCs, TIF mice and human fibrotic kidney tissues. Moreover, transcription factors that induce EMT, such as snail, slug, and Zeb2, were direct targets of miR-30e. Using a cell-based miR-30e promoter luciferase reporter system, Schisandrin B (Sch B) was selected for the enhancement of miR-30e transcriptional activity. Our results indicate that Sch B can decrease the expression of snail, slug, and Zeb2, thereby attenuating the EMT of PTCs during TIF by upregulating miR-30e, both in vivo and in vitro. This study shows that miR-30e can serve as a therapeutic target in the treatment of patients with TIF and that Sch B may potentially be used in therapy against renal fibrosis
研究领域:
肾病学
·
分子生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）