Xiao-Jiao Nie, Yonghua Shi, Tingting Cui, Chen Lin
Magnesium (Mg) based biomaterials have gained increased attention in various health care applications, as orthopedic transplants in particular. It is also reported that they also have anti-tumor properties. Mg based alloy materials can actively interfere with the growth of tumor cells, which may be its degradation products, including OH− and H2. During the degradation of Mg, ions and hydrogen (H2) are continuously increasing and pH value and osmotic pressure in the microenvironment of the material surface are increased at the same time. Such near-surface effects can also have a dramatic impact on residual tumor cells, interfere with the cycle of tumor cells as well as reduce the content of reactive oxygen species. Therefore, the intake level of Mg based alloys and Mg content will affect the growth activity of many tumor cells. Keeping these points in view, this article reviews the role of Mg in tumor microenvironment and underlying molecular mechanisms, in particular it’s degradation behavior.
{"title":"Role of Magnesium in Tumor Microenvironment and Underlying Molecular Mechanisms","authors":"Xiao-Jiao Nie, Yonghua Shi, Tingting Cui, Chen Lin","doi":"10.1166/jbt.2023.3247","DOIUrl":"https://doi.org/10.1166/jbt.2023.3247","url":null,"abstract":"Magnesium (Mg) based biomaterials have gained increased attention in various health care applications, as orthopedic transplants in particular. It is also reported that they also have anti-tumor properties. Mg based alloy materials can actively interfere with the growth of tumor cells,\u0000 which may be its degradation products, including OH− and H2. During the degradation of Mg, ions and hydrogen (H2) are continuously increasing and pH value and osmotic pressure in the microenvironment of the material surface are increased at the same time.\u0000 Such near-surface effects can also have a dramatic impact on residual tumor cells, interfere with the cycle of tumor cells as well as reduce the content of reactive oxygen species. Therefore, the intake level of Mg based alloys and Mg content will affect the growth activity of many tumor cells.\u0000 Keeping these points in view, this article reviews the role of Mg in tumor microenvironment and underlying molecular mechanisms, in particular it’s degradation behavior.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46637755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study analyzed the effect of bone marrow mesenchymal stem cells (BMSC) homing with chemotaxis transplantation of SDF-1a on the repair of corneal damage. The SDF-1a with varied concentration was added. They were divided into A group, B group, C group, D group and control group followed by analysis of corneal cell survival by MTT, apoptosis by flow cytometry, and Trkb level by immunohistochemical staining. There was an increasing tendency on the quantity of chemotactic cells (P <0.05) with a highest quantity in C group. The recruitment of BMSC could be prompted by SDF-1a and the chemotactic effect was the best when SDF-1a concentration was 100 ng/ml. The survival rate and Trkb protein level in experimental groups was higher than that in control group with highest survival rate and Trkb level in C group. In conclusion, corneal injury repair is prompted by BMSC homing with chemotaxis transplantation of SDF-1a, indicating that it might be used as a novel approach to promote corneal injury repair.
{"title":"Bone Marrow Mesenchymal Stem Cells (BMSC) Homing with Chemotaxis Transplantation of Stromal Cell-Derived Factor 1a Promotes the Corneal Damage Repair","authors":"Xia Zhang, Jing Dai, Ying Q Lin, H. Su, Xi Luo","doi":"10.1166/jbt.2023.3215","DOIUrl":"https://doi.org/10.1166/jbt.2023.3215","url":null,"abstract":"This study analyzed the effect of bone marrow mesenchymal stem cells (BMSC) homing with chemotaxis transplantation of SDF-1a on the repair of corneal damage. The SDF-1a with varied concentration was added. They were divided into A group, B group, C group, D group and control group followed\u0000 by analysis of corneal cell survival by MTT, apoptosis by flow cytometry, and Trkb level by immunohistochemical staining. There was an increasing tendency on the quantity of chemotactic cells (P <0.05) with a highest quantity in C group. The recruitment of BMSC could be prompted\u0000 by SDF-1a and the chemotactic effect was the best when SDF-1a concentration was 100 ng/ml. The survival rate and Trkb protein level in experimental groups was higher than that in control group with highest survival rate and Trkb level in C group. In conclusion, corneal injury repair is prompted\u0000 by BMSC homing with chemotaxis transplantation of SDF-1a, indicating that it might be used as a novel approach to promote corneal injury repair.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47774528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wei Su, Yinshan Wu, Huijun Zheng, Xiuliu Guo, Binbin Feng, F. Guo
The therapeutic effects of bone marrow mesenchymal stem cells (BMSCs) on severe acute pancreatitis (SAP) and miRNAs are currently the research hotspots. This study intends to explore the potential impact of miR-141-modified BMSCs on SAP. After establishment of rat model of SAP, the animals were grouped into control group, model group, BMSCs group, miR-141 group, positive control group, and PI3K/mTOR signaling agonist group (agonist group) followed by analysis of miR-141 expression by RT-qPCR and the expression of serum amylase, IL-6, TNF-α, TAP, PI3K, mTOR, and LC3-II by Western blot and ELISA. miR-141 was significantly up-regulated in the miR-141-modified BMSCs group (p > 0.05). The contents of serum amylase, IL-6, TNF-α, and TAP was increased in SAP rats and decreased after BMSC treatment (p > 0.05). The increased autophagy flux in the rats with SAT was reduced upon treatment with BMSCs and autophagy flux was decreased in miR-141 group but increased in positive control group. The model and positive control group presented highest expression of LC3-II, p-PI3K and p-mTOR, followed by BMSCs group and miR-141 group (p < 0.05). In conclusion, miR-141-modified BMSCs decrease the phosphorylation of PI3K and mTOR to inhibit PI3K/mTOR signaling activity and downregulate LC3-II protein to inhibit autophagy, thereby ameliorating the development of SAP, indicating that miR-141 might be a therapeutic target for SAP.
{"title":"miR-141-Modified Bone Marrow Mesenchymal Stem Cells (BMSCs) Inhibits the Progression of Severe Acute Pancreatitis","authors":"Wei Su, Yinshan Wu, Huijun Zheng, Xiuliu Guo, Binbin Feng, F. Guo","doi":"10.1166/jbt.2023.3190","DOIUrl":"https://doi.org/10.1166/jbt.2023.3190","url":null,"abstract":"The therapeutic effects of bone marrow mesenchymal stem cells (BMSCs) on severe acute pancreatitis (SAP) and miRNAs are currently the research hotspots. This study intends to explore the potential impact of miR-141-modified BMSCs on SAP. After establishment of rat model of SAP, the\u0000 animals were grouped into control group, model group, BMSCs group, miR-141 group, positive control group, and PI3K/mTOR signaling agonist group (agonist group) followed by analysis of miR-141 expression by RT-qPCR and the expression of serum amylase, IL-6, TNF-α, TAP, PI3K, mTOR,\u0000 and LC3-II by Western blot and ELISA. miR-141 was significantly up-regulated in the miR-141-modified BMSCs group (p > 0.05). The contents of serum amylase, IL-6, TNF-α, and TAP was increased in SAP rats and decreased after BMSC treatment (p > 0.05). The increased\u0000 autophagy flux in the rats with SAT was reduced upon treatment with BMSCs and autophagy flux was decreased in miR-141 group but increased in positive control group. The model and positive control group presented highest expression of LC3-II, p-PI3K and p-mTOR, followed by BMSCs group and miR-141\u0000 group (p < 0.05). In conclusion, miR-141-modified BMSCs decrease the phosphorylation of PI3K and mTOR to inhibit PI3K/mTOR signaling activity and downregulate LC3-II protein to inhibit autophagy, thereby ameliorating the development of SAP, indicating that miR-141 might be a therapeutic\u0000 target for SAP.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42349800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaobo Wang, Yili Hu, Diandian Chen, Le Cheng, Lili Yu, Quanjun Yang
Oxymatrine has been applied to anti-cancer therapies for various cancers. The present study aimed to investigate the potential impact of miR-188 on breast cancer (BC) cell progression and underlying mechanism. After establishment of a rat model of BC, rats were administered with oxymatrine (4 mg/kg, 8 mg/kg), Xihuang pill (XH) (positive control), and miR-188 mimic (1 mg/kg) followed by analysis of tumor growth, the expression of miR-188, MMP-9, MMP-2, and PTEN, and BC cell behaviors. Oxymatrine significantly decreased tumor incidence and reduced tumor mass (p<0.05) with 8 mg/kg intervention group and positive control group exhibiting higher tumor inhibition rate (p<0.05). In addition, oxymatrine or XH effectively reduced cell proliferation, invasion and migration rate. Of note, compared to 4 mg/kg oxymatrine, 8 mg/kg oxymatrine and XH showed more significantly inhibitory effects on BC cells. Moreover, oxymatrine or XH significantly downregulated miR-188, MMP-9, and MMP-2 and upregulated PTEN. Mechanically, PTEN was indicated as the target of miR-188 with specific binding between them. In conclusion, Oxymatrine inhibits BC cell behaviors through down-regulation of miR-188 to increase PTEN expression. This study might provide a new basis for the management of BC.
{"title":"Oxymatrine Inhibits Malignant Behaviors of Breast Cancer Cells by Inhibiting miR-188 Expression to Up-Regulate Phosphatase and Tensin Homolog (PTEN)","authors":"Xiaobo Wang, Yili Hu, Diandian Chen, Le Cheng, Lili Yu, Quanjun Yang","doi":"10.1166/jbt.2023.3220","DOIUrl":"https://doi.org/10.1166/jbt.2023.3220","url":null,"abstract":"Oxymatrine has been applied to anti-cancer therapies for various cancers. The present study aimed to investigate the potential impact of miR-188 on breast cancer (BC) cell progression and underlying mechanism. After establishment of a rat model of BC, rats were administered with oxymatrine\u0000 (4 mg/kg, 8 mg/kg), Xihuang pill (XH) (positive control), and miR-188 mimic (1 mg/kg) followed by analysis of tumor growth, the expression of miR-188, MMP-9, MMP-2, and PTEN, and BC cell behaviors. Oxymatrine significantly decreased tumor incidence and reduced tumor mass (p<0.05)\u0000 with 8 mg/kg intervention group and positive control group exhibiting higher tumor inhibition rate (p<0.05). In addition, oxymatrine or XH effectively reduced cell proliferation, invasion and migration rate. Of note, compared to 4 mg/kg oxymatrine, 8 mg/kg oxymatrine and XH showed\u0000 more significantly inhibitory effects on BC cells. Moreover, oxymatrine or XH significantly downregulated miR-188, MMP-9, and MMP-2 and upregulated PTEN. Mechanically, PTEN was indicated as the target of miR-188 with specific binding between them. In conclusion, Oxymatrine inhibits BC cell\u0000 behaviors through down-regulation of miR-188 to increase PTEN expression. This study might provide a new basis for the management of BC.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42618377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
W. Su, Pan Liu, Yang Zhang, Zhongcheng Gong, Hua-rong Zhao
Background: The paper aimed to investigate the role of Glut1 in the inhibition of the invasion and migration capabilities of tongue squamous carcinoma cell by Catechin. Materials and Methods: Transwell assay and scratch test were applied to measure the effect of Catechin on the invasion and migration of the cells, and WB to detect the expression of each protein. Overexpressed lentivirus was used to up-regulate Glut1 in tongue squamous carcinoma cells, detecting whether the process can be reversed. After silencing RAP1GDS1 in tongue squamous carcinoma cells by RNAi technology, the effect of Catechin on Glut1 expression was measured. Results: The results of Transwell assay and scratch test verified that Catechin can inhibit the invasion and migration. Subsequent WB experiments confirmed that Catechin can inhibit the expression of Glut1, N-cadherin and Vimentin, while promote the expression of E-cadherin. The up-regulation of Glut1 can significantly reverse the inhibitory effect of Catechin. Silencing of RAP1GDS1 can inhibit the expression of Glut1. However, the up-regulation of Glut1 expression can significantly reverse this process. WB result verified the inhibitive effect of Catechin on RAP1GDS1 in tongue squamous carcinoma cells. Conclusion: Catechin affects glycolytic activity by down-regulating Glut1 and induces EMT process inhibition. It is speculated that, through regulating Glut1 by silencing RAP1GDS1.
{"title":"The Role of RAP1GDS1 in the Inhibition of Glut1 Expression by Catechins in Tongue Squamous Carcinoma Cells","authors":"W. Su, Pan Liu, Yang Zhang, Zhongcheng Gong, Hua-rong Zhao","doi":"10.1166/jbt.2023.3237","DOIUrl":"https://doi.org/10.1166/jbt.2023.3237","url":null,"abstract":"Background: The paper aimed to investigate the role of Glut1 in the inhibition of the invasion and migration capabilities of tongue squamous carcinoma cell by Catechin. Materials and Methods: Transwell assay and scratch test were applied to measure the effect of Catechin\u0000 on the invasion and migration of the cells, and WB to detect the expression of each protein. Overexpressed lentivirus was used to up-regulate Glut1 in tongue squamous carcinoma cells, detecting whether the process can be reversed. After silencing RAP1GDS1 in tongue squamous carcinoma cells\u0000 by RNAi technology, the effect of Catechin on Glut1 expression was measured. Results: The results of Transwell assay and scratch test verified that Catechin can inhibit the invasion and migration. Subsequent WB experiments confirmed that Catechin can inhibit the expression of Glut1,\u0000 N-cadherin and Vimentin, while promote the expression of E-cadherin. The up-regulation of Glut1 can significantly reverse the inhibitory effect of Catechin. Silencing of RAP1GDS1 can inhibit the expression of Glut1. However, the up-regulation of Glut1 expression can significantly reverse this\u0000 process. WB result verified the inhibitive effect of Catechin on RAP1GDS1 in tongue squamous carcinoma cells. Conclusion: Catechin affects glycolytic activity by down-regulating Glut1 and induces EMT process inhibition. It is speculated that, through regulating Glut1 by silencing RAP1GDS1.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43618329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aim: To observe Dendrobine (Den) on rats with post-myocardial infarction cardiac dysfunction and mechanism. Materials: Dividing 27 rats as Sham, Model and Den groups, rats treated with two weeks of drug had their cardiac function and structure measured by ultrasound; their myocardial pathological changes observed by HE and Masson staining and observe apoptosis cell number by TUNEL staining; their serum activities of LDH and CK-MB detected by ELISA; myocardial autophagy protein expressions detected by WB and immunohistochemistry. Results: Model group displayed decreased cardiac function levels, enlarged area of myocardial fibrosis, more serum activities of LDH and CK-MB, increased myocardial tissue structural damage and apoptosis cell number, downregulated LAMP2 expression, and up-regulated expressions of Beclin1, LC3-II/LC3-I rate, and P62. To rat victims of myocardial infarction, Den improved cardiac function, reduced area of myocardial fibrosis, compromised activities of serum LDH and CK-MB, and relieved damage in myocardial structure, decreased apoptosis cell number in myocardial tissue, up-regulated the expressions of Beclin1, LAMP2 and LC3-II, and down-regulated P62 to promote the autophagy in myocardium damaged by myocardial infarction. Conclusion: Den alleviates post-myocardial infarction cardiac dysfunction through improvement of autophagosomes formation and autophagic flux via Beclin1/LAMP2 pathway.
{"title":"Effect of Dendrobine on Cardiac Dysfunction in Rats with Myocardial Infarction by Regulating Autophagy","authors":"Juan Fan, Yi Zhang","doi":"10.1166/jbt.2023.3227","DOIUrl":"https://doi.org/10.1166/jbt.2023.3227","url":null,"abstract":"Aim: To observe Dendrobine (Den) on rats with post-myocardial infarction cardiac dysfunction and mechanism. Materials: Dividing 27 rats as Sham, Model and Den groups, rats treated with two weeks of drug had their cardiac function and structure measured by ultrasound; their myocardial\u0000 pathological changes observed by HE and Masson staining and observe apoptosis cell number by TUNEL staining; their serum activities of LDH and CK-MB detected by ELISA; myocardial autophagy protein expressions detected by WB and immunohistochemistry. Results: Model group displayed decreased\u0000 cardiac function levels, enlarged area of myocardial fibrosis, more serum activities of LDH and CK-MB, increased myocardial tissue structural damage and apoptosis cell number, downregulated LAMP2 expression, and up-regulated expressions of Beclin1, LC3-II/LC3-I rate, and P62. To rat victims\u0000 of myocardial infarction, Den improved cardiac function, reduced area of myocardial fibrosis, compromised activities of serum LDH and CK-MB, and relieved damage in myocardial structure, decreased apoptosis cell number in myocardial tissue, up-regulated the expressions of Beclin1, LAMP2 and\u0000 LC3-II, and down-regulated P62 to promote the autophagy in myocardium damaged by myocardial infarction. Conclusion: Den alleviates post-myocardial infarction cardiac dysfunction through improvement of autophagosomes formation and autophagic flux via Beclin1/LAMP2 pathway.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43339450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Spinal cord injury (SCI) is a spinal cord nerve dysfunction secondary to trauma. Until now, still no appropriate drug with unclear etiology. Therefore, it is to develop effective SCI treatment methods. Herein, we intended to detect the impact of miR-129-5p in SCI After establishment of a mouse SCI model, the animals received intrathecal injection of agomir-miR-129-5p or normal saline. Then, the miR-129-5p’s effect was evaluated by assessing motor function, spinal cord tissue edema, apoptosis and inflammation of mice upon treatments and potential targeted pathways of the miRNA were detected. Overexpressed miR-129-5p facilitated the wound healing with less spare tissue and water content. Additionally, overexpressed miR-129-5p suppressed the in vivo inflammation with decreased apoptotic rate of neurons. As SCI induced increased expression of HMGB1, TLR4, and NF-κB in tissues, but the presence of miR-129-5p reversed the expressions. Collectively, this study elucidate miR-129-5p significantly improves inflammatory response and apoptosis, thereby improving the condition of SCI. These findings might provide a new theory for the disorder, and promote the research progress on the disease.
{"title":"miR-129-5p Induces Cell Apoptosis and Inhibits Inflammation by Inflammatory Signaling to Alleviate Spinal Cord Injury (SCI)","authors":"Zhe-Ming Song, Yuwei Gao, Yuhao Zhao, Xiaofei Feng, Zhenjie Zhao, Wenji Wang","doi":"10.1166/jbt.2023.3197","DOIUrl":"https://doi.org/10.1166/jbt.2023.3197","url":null,"abstract":"Spinal cord injury (SCI) is a spinal cord nerve dysfunction secondary to trauma. Until now, still no appropriate drug with unclear etiology. Therefore, it is to develop effective SCI treatment methods. Herein, we intended to detect the impact of miR-129-5p in SCI After establishment\u0000 of a mouse SCI model, the animals received intrathecal injection of agomir-miR-129-5p or normal saline. Then, the miR-129-5p’s effect was evaluated by assessing motor function, spinal cord tissue edema, apoptosis and inflammation of mice upon treatments and potential targeted pathways\u0000 of the miRNA were detected. Overexpressed miR-129-5p facilitated the wound healing with less spare tissue and water content. Additionally, overexpressed miR-129-5p suppressed the in vivo inflammation with decreased apoptotic rate of neurons. As SCI induced increased expression of HMGB1,\u0000 TLR4, and NF-κB in tissues, but the presence of miR-129-5p reversed the expressions. Collectively, this study elucidate miR-129-5p significantly improves inflammatory response and apoptosis, thereby improving the condition of SCI. These findings might provide a new theory for\u0000 the disorder, and promote the research progress on the disease.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":"352 5","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41296453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Acetylcholinesterase degrades the neurotransmitter acetylcholine in nervous system synapses to regulate neurotransmission. It has been demonstrated to be effective as a therapeutic target as well as a target for Alzheimer’s disease drugs. Primary phytoconstituents components of Nigella sativa were identified in this study based on their affinity for an active site binding of Human Acetylcholinesterase. Molecular dynamics and molecular docking methods were used to test the stability of the topmost docking complex. Out of the nine phytochemicals studied in this study, three molecules, Dithymoquinone, Nigellicine, and Nigellidine, were found to have a significant docking score. Based on our findings, Dithymoquinone is the most potent inhibitor of Human Acetylcholinesterase. It is the least energetic protein (10.1 Kcal/mol), resulting in the highest binding affinity. Molecular dynamics studies confirmed the stability of the Dithymoquinone-Human Acetylcholinesterase complex.
{"title":"In silico Identification of Potential Human Acetylcholinesterase Inhibitors from the Nigella sativa Phytochemicals","authors":"Hani S. H. Mohammed Ali","doi":"10.1166/jbt.2023.3221","DOIUrl":"https://doi.org/10.1166/jbt.2023.3221","url":null,"abstract":"Acetylcholinesterase degrades the neurotransmitter acetylcholine in nervous system synapses to regulate neurotransmission. It has been demonstrated to be effective as a therapeutic target as well as a target for Alzheimer’s disease drugs. Primary phytoconstituents components of\u0000 Nigella sativa were identified in this study based on their affinity for an active site binding of Human Acetylcholinesterase. Molecular dynamics and molecular docking methods were used to test the stability of the topmost docking complex. Out of the nine phytochemicals studied in this\u0000 study, three molecules, Dithymoquinone, Nigellicine, and Nigellidine, were found to have a significant docking score. Based on our findings, Dithymoquinone is the most potent inhibitor of Human Acetylcholinesterase. It is the least energetic protein (10.1 Kcal/mol), resulting in the highest\u0000 binding affinity. Molecular dynamics studies confirmed the stability of the Dithymoquinone-Human Acetylcholinesterase complex.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42869379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic sinusitis is an upper respiratory tract disease. miR-134 involves in several diseases. However, its regulatory mechanism in chronic sinusitis has not been assessed. We aim to explore miR-134’s role in chronic sinusitis and the possible mechanism. miR-134 and MMP9 level was measured in chronic sinusitis tissues and normal tissues. The co-expression of miR-134 and MMP9 in PHNECs was detected by immunofluorescence. MMP-9 expression and IκB and α protein phosphorylation was detected by western blot. Immunofluorescence showed positive MMP-9 expression in epithelial cells. miR-134 level was significantly elevated in patients with chronic sinusitis and was co-localized with MMP-9 in the CRSwNP sample of epithelial cells. miR-134 up-regulated MMP-9, which was inhibited after addition of inhibitor BAY 11-7082. In conclusion, miR-134 up-regulates MMP-9 through NF-κB signaling to mediate the occurrence of chronic sinusitis, indicating that miR-134 may participate in the tissue remodeling of chronic sinusitis.
{"title":"miR-134 Up-Regulates Matrix Metalloproteinase 9 (MMP9) in Chronic Sinusitis","authors":"W. Cao, Yuanzhou Liu, Yandan Chen","doi":"10.1166/jbt.2023.3206","DOIUrl":"https://doi.org/10.1166/jbt.2023.3206","url":null,"abstract":"Chronic sinusitis is an upper respiratory tract disease. miR-134 involves in several diseases. However, its regulatory mechanism in chronic sinusitis has not been assessed. We aim to explore miR-134’s role in chronic sinusitis and the possible mechanism. miR-134 and MMP9 level\u0000 was measured in chronic sinusitis tissues and normal tissues. The co-expression of miR-134 and MMP9 in PHNECs was detected by immunofluorescence. MMP-9 expression and IκB and α protein phosphorylation was detected by western blot. Immunofluorescence showed positive\u0000 MMP-9 expression in epithelial cells. miR-134 level was significantly elevated in patients with chronic sinusitis and was co-localized with MMP-9 in the CRSwNP sample of epithelial cells. miR-134 up-regulated MMP-9, which was inhibited after addition of inhibitor BAY 11-7082. In conclusion,\u0000 miR-134 up-regulates MMP-9 through NF-κB signaling to mediate the occurrence of chronic sinusitis, indicating that miR-134 may participate in the tissue remodeling of chronic sinusitis.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49548769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Non-small cell lung cancer (NSCLC) is a common malignancy worldwide. miR-119-3p is down regulated in many cancers. Nonetheless, the modulatory mechanism of bone marrow mesenchymal stem cells (BMSCs) in NSCLC is unclear. Our research aims to dissect the activity of BMSCs on NSCLC and underlying mechanisms. After isolation and identification, BMSCs were co-cultured with NSCLC cells, which were transfected with miR-119-3p mimics followed by analysis of expression of miR-119-3p and tumor aggressiveness-related proteins, cell invasion/migration and survival. A significantly reduced miR-119-3p level was found in NSCLC cell lines. miR-119-3p mimics inhibited the proliferative, migrating and invasive behaviors of NSCLC cells. Co-culture with BMSCs enhanced miR-119-3p expression in NSCLC cells, thereby suppressing NSCLC cell biological behaviors. Simultaneously, the EMT process was markedly restrained, as indicated by an elevated level of E-cadherin but diminished levels of Vimetnin, N-cadherin and Snail. In conclusion, BMSCs can interfere with the EMT process of NSCLC via up-regulatingmiR-119-3p, thereby retarding the aggressive migration and invasive capability of NSCLC cells.
{"title":"Bone Marrow Mesenchymal Stem Cells (BMSCs) Retard the Aggressive Migrating and Invading Activity of Non-Small Cell Lung Cancer Cells","authors":"Ying Kang, P. Zhang, Kai Xiong, Yuanguo Wang","doi":"10.1166/jbt.2023.3219","DOIUrl":"https://doi.org/10.1166/jbt.2023.3219","url":null,"abstract":"Non-small cell lung cancer (NSCLC) is a common malignancy worldwide. miR-119-3p is down regulated in many cancers. Nonetheless, the modulatory mechanism of bone marrow mesenchymal stem cells (BMSCs) in NSCLC is unclear. Our research aims to dissect the activity of BMSCs on NSCLC and\u0000 underlying mechanisms. After isolation and identification, BMSCs were co-cultured with NSCLC cells, which were transfected with miR-119-3p mimics followed by analysis of expression of miR-119-3p and tumor aggressiveness-related proteins, cell invasion/migration and survival. A significantly\u0000 reduced miR-119-3p level was found in NSCLC cell lines. miR-119-3p mimics inhibited the proliferative, migrating and invasive behaviors of NSCLC cells. Co-culture with BMSCs enhanced miR-119-3p expression in NSCLC cells, thereby suppressing NSCLC cell biological behaviors. Simultaneously,\u0000 the EMT process was markedly restrained, as indicated by an elevated level of E-cadherin but diminished levels of Vimetnin, N-cadherin and Snail. In conclusion, BMSCs can interfere with the EMT process of NSCLC via up-regulatingmiR-119-3p, thereby retarding the aggressive migration and invasive\u0000 capability of NSCLC cells.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45725387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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