Artificial Cells, Nanomedicine, and Biotechnology

Journal Information
ISSN / EISSN : 21691401 / 2169141X
Current Publisher: Informa UK Limited (10.1080)
Former Publisher: Informa UK Limited (10.3109)
Total articles ≅ 1,740
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Latest articles in this journal

Wencui Wan, Weiwei Wan, Yang Long, Qiuming Li, Xuemin Jin, Guangming Wan, Fengyan Zhang, Yong Lv
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 463-472; doi:10.1080/21691401.2019.1709861

Jianhua Gong, Feihu Guo, Weihua Cheng, Hongqiang Fan, Qingfang Miao, Jigang Yang
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 408-414; doi:10.1080/21691401.2019.1709857

Abstract:Overexpression of CD30 has been reported on the surface of some T-cell lymphomas, especially on Hodgkin’s lymphoma (HL) and anaplastic large cell lymphoma (ALCL). CD30 targeted immunotherapy has good clinical therapy response. We have produced a novel antibody drug conjugates (ADCs)-anti-CD30-LDM, which shows attractive tumour-targeting capability and extremely potent antitumor efficacy. To further investigate biological characteristics and promote clinical translation of anti-CD30-LDM, we constructed a radiolabeled 123I-anti-CD30-LDM to evaluate the biodistribution characteristics. The anti-CD30-LDM was radioiodinated by the Iodogen method. The radiochemical purity of 123I-anti-CD30-LDM was more over 98%, and the specific activity of 240.5 MBq/mg. The stability and the specificity of 123I-anti-CD30-LDM were evaluated in vitro. Cellular binding assays were used to evaluate the binding capabilities in CD30-positive Karpas299 cells and CD30-negative Raji cells. B-NDG mice bearing Karpas 299 and Raji xenografts were used for in vivo biodistribution studies. Our results demonstrated that anti-CD30-LDM as an ideal ADC targeted to CD30, which was labelled easily with 123I and obtained the sufficient yields. The 123I-anti-CD30-LDM preserved specific binding to CD30 in vitro and uptake in tumour xenografts in B-NDG mice. These results are encouraging for anti-CD30-LDM as a promising clinical translational candidate for various CD30 positive lymphomas and other diseases.
Gang Su, Guangli Sun, Hai Liu, Liliang Shu, Weiwei Zhang, Zhenxing Liang
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 345-352; doi:10.1080/21691401.2019.1709850

Abstract:Prokineticin 2 (PK2) was reported to be decreased in the hearts of end-state heart failure patients. Our study aimed to explore the effects of PK2 on hypoxia/reoxygenation (H/R) injury and the underlying mechanism. H9c2 cardiomyocytes were treated with 5 nM PK2 in the presence or absence of 5 mM dual phosphatidylinositol 3-kinase (PI3K)/the mammalian target of rapamycin (mTOR) inhibitor (BEZ235) for 24 h and then subjected to H/R treatment. Cell viability and lactate dehydrogenase (LDH) release were evaluated by CCK-8 and LDH release assays, respectively. Apoptosis was determined by flow cytometry analysis. Oxidative stress was assessed by measuring superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) content. Results showed that H/R treatment decreased PK2 expression and inactivated the Akt/mTOR pathway in H9c2 cardiomyocytes. PK2 treatment activated the Akt/mTOR pathway in H/R-exposed H9c2 cardiomyocytes. H/R stimulation suppressed cell viability, increased LDH release, induced apoptosis and oxidative stress in H9c2 cardiomyocytes, while these effects were neutralised by treatment with PK2. However, the inhibitory effects of PK2 on H/R-induced injury in H9c2 cardiomyocytes were abolished by the addition of BEZ235. In conclusion, PK2 relieved H/R-induced injury in H9c2 cardiomyocytes by activation of the Akt/mTOR pathway.
Xin-Chun Qi, Bo Li, Wen-Liang Wu, Hai-Chun Liu, Yun-Peng Jiang
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 377-383; doi:10.1080/21691401.2019.1709851

Abstract:Oxidative stress can induce apoptosis and decrease activities of osteoblasts. Hyperoside (HYP) is a potent antioxidant derived from Chinese herb. This study aims to evaluate the protective effects provided by HYP to osteoblastic MC3T3-E1 cells. MC3T3-E1 cells were pre-treated with HYP for 24 h before being treated with 0.3 mM hydrogen peroxide (H2O2) for 24 h. Cell viability, flow cytometric analysis and mRNA expression of alkaline phosphatase (ALP), collagen I (COL-I) and osteocalcin (OCN) in MC3T3-E1 cells were examined. We next examined apoptosis-related and mitogen-activated protein kinase (MAPK) related proteins in HYP and H2O2 groups. HYP over the dose of 40 μmol/L could obviously increase the MC3T3-E1 cell viability at 24 h and 48 h (p < .05). HYP significantly (p < .05) increased mRNA expression of ALP, COL-I and OCN than H2O2 group. Moreover, HYP decreased the apoptosis rate and apoptosis-related proteins that induced by H2O2. In addition, HYP decreased the production of phosphorylated Jun N-terminal kinase (JNK) and p38 levels of osteoblastic MC3T3-E1 cells induced by H2O2. These results demonstrated that the protective effect provided by HYP to osteoblastic MC3T3-E1 cells was mediated, at least in part, via inhibition of MAPK signalling pathway and oxidative damage of the cells.
Rongli Ge, Guanglei Gao
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 384-392; doi:10.1080/21691401.2019.1709863

Abstract:Background: CircZNF609 (cZNF609) is previously revealed as an essential mediator in oxidative stress. This paper determined the role of cZNF609 in skin oxidative damage to evaluate its importance in pressure ulcer. Methods: HaCaT cells treated by H2O2 were considered as a cell model of pressure ulcer. The role of cZNF609 in the model was checked by conducting CCK-8 assay, FITC-PI double-staining, ROS detection and Western blot. The downstream gene and signalling of cZNF609 were studied by utilizing qRT-PCR and Western blot. Results: HaCaT cells were remarkably damaged by H2O2, as evidenced by the viability loss, apoptosis and ROS generation. It was coupled with the elevated expression of p53, p16, Bax and the activated forms of caspase-3 and PARP. Meanwhile, cZNF609 was high-expressed in response to H2O2. The oxidative stress driven by H2O2 was alleviated by transfection with cZNF609 specific siRNA. Further, the anti-antioxidant impacts of cZNF609 silence were impeded by miR-145 silence. The inhibition of JNK and p38MAPK pathways induced by cZNF609 silence was impeded by miR-145 silence. Conclusion: The protective function of cZNF609 silence in H2O2-injured HaCaT cells was revealed in vitro. Silence of cZNF609 exhibited its impact possibly through regulating miR-145, and JNK and p38MAPK pathways.
Yingrui Fan, Weiwei Sheng, Yi Meng, Yundi Cao, Rong Li
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 393-407; doi:10.1080/21691401.2019.1709852

Abstract:LncRNA PTENP1 is a competitive endogenous RNA (ceRNA) involved in decoying miR-106b in multiple diseases. This study investigates the interaction of PTENP1 and miR-106b in cell proliferation, apoptosis and epithelial–mesenchymal transition (EMT) in cervical cancer. The expressions of PTENP1, miR-106b and PTEN were determined in cervical cancer tissues, adjacent normal tissues, cervical cancer cells (HeLa, SiHa, C33A and CasKi) and normal cervical epithelial H8 cells. Up-regulation of PTENP1 and down-regulation of miR-106b were conducted in HeLa and CasKi cells by transfecting cells with corresponding miRNA mimics and inhibitors. Bioinformatics analysis, luciferase reporter assay and RNA-pull down assay were performed to verify the association of miR-106b, PTEN, and PTENP1. Cell growth and cell apoptosis were determined by CCK-8 and flow cytometry analysis. It was found that the expressions of PTENP1 and PTEN were up-regulated and that of miR-106b were down-regulated in cervical cancer tissues and cells. PTENP1 localized in cytoplasm and competitively bound to miR-106b. Up-regulation of PTENP1 and down-regulation of miR-106b contributed to increased expressions of PTEN and E-cadherin. Decreased expression of miR-106b, ZEB1, Snail and Vimentin, resulted in inhibiting cell proliferation and promoting cell apoptosis. Over-expression of PTENP1 and miR-106b accelerated cell proliferation and slowed down cell apoptosis. miR-106b inhibited the expression of PTEN. Our results suggest that LncRNA PTENP1 inhibits cervical cancer progression by competitively binding to miR-106b, leading to promote PTEN expression, inhibit cell proliferation and EMT and induce cell apoptosis in cervical cancer cells
Kexiang Zhu, Zhengcong Zhang, Hui Zhang, Zhengfeng Wang, Fanghong Wang
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 415-424; doi:10.1080/21691401.2019.1652629

Abstract:Objective: To investigate the effects of microRNA-142-3p (miR-142-3p) on the biological characteristics of pancreatic cancer cells and its mechanism. Methods: The expression of miR-142-3p and nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) in pancreatic tissues and four cancer cell lines (Panc-1, BxPC-3, AsPC-1, MIA-PaCa2) were detected by Quantitative PCR (qPCR) or Western blot. The cell viability of pancreatic cancer cells was examined by MTT assay. The apoptosis of pancreatic cancer cells was measured by flow cytometry. Transwell assay was utilized to test the migration and invasion of pancreatic cancer cells. Bioinformatics analysis for miR-142-3p was conducted and the dual luciferase reporter gene assay was utilized to further validate the predicted target relationship. The protein levels of PI3K, p-AKT and T-AKT were analyzed by Western blot. Results: The expression of miR-142-3p was down-regulated, while the expression of NUCKS1 was significantly up-regulated in pancreatic tissues and four cancer cell lines. The expression of miR-142-3p in pancreatic tissues was inversely correlated with NUCKS1 expression. Overexpression of miR-142-3p inhibited the cell viability, cell migration, and invasion, while promoted cell apoptosis of AsPC-1 and MIA-PaCa2 cells. MiR-142-3p targeted NUCKS1 and negatively regulated NUCKS1. Overexpression of miR-142-3p decreased PI3K and p-AKT expression. Up-regulation of NUCKS1 partially reversed the effects of the overexpression of miR-142-3p on the cell viability, cell apoptosis, migration and invasion, as well as PI3K and p-AKT expression in AsPC-1 and MIA-PaCa2 cells. Conclusion: MiR-142-3p regulated the biological characteristics of pancreatic cancer cells by directly targeting NUCKS1.
Zhi-Hai Deng, Gan-Shen Yu, Bin Pan, Zhen-Hua Feng, Qiang Huang, Jian-Zhong Deng, Bo Chen, Shi-Kun Yang
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 435-442; doi:10.1080/21691401.2019.1709859

Abstract:Non-coding RNAs play an important role in the pathogenesis of prostate cancer (PC). This study aims to characterize the role of GAS5 rs145204276 and HOTAIR rs4759314 polymorphisms in the pathogenesis of PC. Both INS allele of GAS5 rs145204276 and A allele of HOTAIR rs4759314 were identified to increase the survival of PC patients. And patients carrying DEL/DEL + AG genotypes tend to present higher levels of HMGB1, GAS5, HOTAIR and lower levels of miR-1284 and miR-22. In addition, the transcription activity of GAS5 promoter was increased by the deletion allele of rs145204276 polymorphism, while the G allele of rs4759314 polymorphism increased the transcription activity of HOTAIR promoter. GAS5 and HOTAIR could bind to miR-1284 and miR-22, respectively, while miR-1284 and miR-22 could bind to the 3′UTR of HMGB1. Compared with the control group, the expressions of miR-1284 or miR-22 were decreased with the presence of GAS5 or HOTAIR, and the expression of HMGB1 was the highest in the GAS5 + HOTAIR group. In summary, the findings of this study demonstrated that both GAS5 rs145204276 and HOTAIR rs4759314 polymorphisms could affect the prognosis of PC by modulating the expression of HMGB1 via modulating the GAS5/miR-1284/HMGB1 and HOTAIR/miR-22/HMGB1 signalling pathways.
Dongchao Yang, Zhicheng Song, Jiali Shen, Heng Song, Jianjun Yang, Peihua Zhang, Yan Gu
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 425-434; doi:10.1080/21691401.2019.1709858

Abstract:Abdominal wall defects are associated with abdominal wall surgery, infection and tumour resection. Polypropylene (PP) mesh, which has excellent mechanical strength, is currently the primary clinical repair material. In repairing the abdominal wall, the mesh can erode the bowel and cause other problems. Constructing a barrier that induces a weak inflammatory response and promotes rapid recovery of the peritoneum is important. We used electrospinning technology to construct a silk fibroin coating on the abdominal surface of a PP patch. A rat model was used to compare the inflammatory responses, regeneration of peritoneal tissue, and antiadhesion effects of electrospun regenerated silk fibroin (RSF) coatings, polycaprolactone (PCL) coatings, and noncoated PP meshes. The inflammatory responses, antiadhesion fractions, and areas of RSF and PCL were better than those of PP at 6 weeks. RSF was associated with complete peritoneal regeneration, in contrast to PCL. At 12 weeks, the structure of the PCL peritoneum was unstable, and the adhesion fraction and area were significantly higher than those of RSF. The intact peritoneum could not be effectively regenerated. The RSF group exhibited lower IL-6 levels than the PCL and PP groups but higher VEGF, IL-10 and TGF-β levels, making RSF more conducive to the regeneration of peritoneal and abdominal wall tissues.
Ying Li, Su Xu, Qingqing Xu, Yijian Chen
Artificial Cells, Nanomedicine, and Biotechnology, Volume 48, pp 452-462; doi:10.1080/21691401.2019.1709856

Abstract:Clostridium difficile (C. difficile) infection results in toxin-induced epithelial injury and marked colonic inflammation. Mitogen-activated protein kinase (MAPK) and NF-κB which regulated by MAP kinase phosphatase (MKP, also known as dual specificity phosphatases, DUSP) are fundamental signalling pathways that mediate multiple cellular processes. However, the regulation of DUSP/MAPKs and NF-κB pathway in C. difficile-induced colonic inflammation remains unclear. Here, we report that TcdB significantly inhibits cell viability and induces production of IL-1β and TNF-α and activation of MAPKs and NF-κB. An E3-ubiquitin ligase, TRIM46, ubiquitinates DUSP1, and its knockdown significantly inhibit TcdB-induced activation of MAPKs and NF-κB and production of IL-1β and TNF-α. Moreover, TRIM46 overexpression induced production of IL-1β and TNF-α also reversed by DUSP1 overexpression. We further found that promoter of TRIM46 also demonstrated binding to NF-κBp65, leading to regulate TRIM46 expression. In addition, the increased colonic inflammation induced by C. difficile administration was inhibited by TRIM46 knockdown in vivo. Taken together, the present study shows that TRIM46, as a new regulator of DUSP1/MAPKs and NF-κB signalling pathway, plays an important role in TcdB-induced colonic inflammation.