The increasing incidence of lung cancer seriously threatens the safety of human life and property. At present, it is difficult for relevant drugs in clinical treatment to accurately identify and act on cancer cells. Therefore, liposome nanoparticles are used to carry related drugs and genes for targeted therapy, which is of great significance. Hippo/YAP signaling is related to the proliferation and apoptosis of cancer cells. Therefore, in this study, the mechanism of lung cancer cells inhibition was further analyzed by constructing miR-429 liposome nanoparticles. miR-429 liposome nanoparticles were prepared and characterized and then injected into experimental group mice after successful modeling and divided into model group, miR-429 lipid nanoparticle group, Hippo/YAP inhibitor (TDI-011536) group, and Hippo/YAP activator (XMU-MP-1) group. Lung cancer cells were taken to construct miR-429 gene silencing and miR-429 gene overexpression groups, followed by analysis of cell proliferation and levels of miR-429, Hippo and YAP. The miR-429 liposome nanoparticles promote the occurrence and development of lung cancer. The miR-429 has a certain inhibitory effect on Hippo/YAP signaling, where it reduces Hippo/YAP signaling activity and inhibits the growth of lung cancer cells. The miR-429 liposome nanoparticles can inhibit Hippo/YAP signaling, reduce their expression, thereby inhibiting lung cancer cell growth and inducing apoptosis, so miR-429 liposome nanoparticles might be used in treating lung cancer.
{"title":"miR-429 Liposome Nanoparticles Inhibit Lung Cancer via Targeting of Hippo/YAP in Lung Cancer Mice","authors":"Hui Jing, Xubo Cao, Jinghao Zhang, Xin Yao, Yanmin Wu","doi":"10.1166/jbn.2023.3686","DOIUrl":"https://doi.org/10.1166/jbn.2023.3686","url":null,"abstract":"The increasing incidence of lung cancer seriously threatens the safety of human life and property. At present, it is difficult for relevant drugs in clinical treatment to accurately identify and act on cancer cells. Therefore, liposome nanoparticles are used to carry related drugs and\u0000 genes for targeted therapy, which is of great significance. Hippo/YAP signaling is related to the proliferation and apoptosis of cancer cells. Therefore, in this study, the mechanism of lung cancer cells inhibition was further analyzed by constructing miR-429 liposome nanoparticles. miR-429\u0000 liposome nanoparticles were prepared and characterized and then injected into experimental group mice after successful modeling and divided into model group, miR-429 lipid nanoparticle group, Hippo/YAP inhibitor (TDI-011536) group, and Hippo/YAP activator (XMU-MP-1) group. Lung cancer cells\u0000 were taken to construct miR-429 gene silencing and miR-429 gene overexpression groups, followed by analysis of cell proliferation and levels of miR-429, Hippo and YAP. The miR-429 liposome nanoparticles promote the occurrence and development of lung cancer. The miR-429 has a certain inhibitory\u0000 effect on Hippo/YAP signaling, where it reduces Hippo/YAP signaling activity and inhibits the growth of lung cancer cells. The miR-429 liposome nanoparticles can inhibit Hippo/YAP signaling, reduce their expression, thereby inhibiting lung cancer cell growth and inducing apoptosis, so miR-429\u0000 liposome nanoparticles might be used in treating lung cancer.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 72","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138619984","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}
In this research, the potential healing function of regular exercise on spinal cord injury healing response was investigated in a rat model. The animals were treated with curcumin-loaded chitosan nanoparticles dispersed in a calcium alginate hydrogel containing endometrial stem cells. Study showed the animals that received both regular exercise and hydrogel showed significantly better histopathological signs and functional recovery than the other groups. Histopathological studies showed that edema, vacuolation, and fibrosis were significantly lower in this group. Gene expression studies showed that the hybrid treatment upregulated the expression levels of VEGF, b-FGF, and TGF-β genes.
{"title":"Sport Medicine Principles Augment Healing Response in Spinal Cord Injury in a Rat Model Treated with a Curcumin-Loaded Nanocomposite Hydrogel","authors":"Bo Zhao, Hao Huang","doi":"10.1166/jbn.2023.3564","DOIUrl":"https://doi.org/10.1166/jbn.2023.3564","url":null,"abstract":"In this research, the potential healing function of regular exercise on spinal cord injury healing response was investigated in a rat model. The animals were treated with curcumin-loaded chitosan nanoparticles dispersed in a calcium alginate hydrogel containing endometrial stem cells.\u0000 Study showed the animals that received both regular exercise and hydrogel showed significantly better histopathological signs and functional recovery than the other groups. Histopathological studies showed that edema, vacuolation, and fibrosis were significantly lower in this group. Gene expression\u0000 studies showed that the hybrid treatment upregulated the expression levels of VEGF, b-FGF, and TGF-β genes.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138611326","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 Wang, Jia-Hong Jian, Nai-Kei Wong, Jie Li, Long Jin, Yi Zhang, Bai-Ou Guan
Hydrogels are an important category of polymeric materials with physicochemical features such as moisturizability and biocompatibility that are ideal for developing dressings for diabetic wounds. However, conventional non-ionic hydrogel materials generally exhibit poor mechanical properties and poor adhesion, which compromise their ability to self-sustain in mechanically dynamic wound microenvironments. In this research, we developed a hybrid hydrogel as a highly biocompatible adhesive wound dressing that met the mechanical requirements of the skin to promote chronic wound healing in diabetic mouse models. A 7.5% (w/v) hydrogel corresponded to a Young’s modulus of 6.3 kPa. In vitro cell-based and subcutaneous implantation experiments in mice demonstrated the excellent biocompatibility and optimal biodegradability of hydrogel dressings. In a diabetic mouse splint wound model for evaluating wound healing in vivo, the hydrogel dressing showed robust adhesion to the wound and efficiently accommodated mechanical deformations around the wound, resulting in significantly improved healing rates of chronic diabetic wounds. Thus, our work illustrates a newly alternative strategy for the simple and efficacious treatment of chronic wounds in the context of diabetes care.
{"title":"A Facilely Prepared Adhesive Dressing Derived from Non-Ionic Hydrogel for Accelerated Diabetic Wound Healing","authors":"Wei Wang, Jia-Hong Jian, Nai-Kei Wong, Jie Li, Long Jin, Yi Zhang, Bai-Ou Guan","doi":"10.1166/jbn.2023.3654","DOIUrl":"https://doi.org/10.1166/jbn.2023.3654","url":null,"abstract":"Hydrogels are an important category of polymeric materials with physicochemical features such as moisturizability and biocompatibility that are ideal for developing dressings for diabetic wounds. However, conventional non-ionic hydrogel materials generally exhibit poor mechanical properties\u0000 and poor adhesion, which compromise their ability to self-sustain in mechanically dynamic wound microenvironments. In this research, we developed a hybrid hydrogel as a highly biocompatible adhesive wound dressing that met the mechanical requirements of the skin to promote chronic wound healing\u0000 in diabetic mouse models. A 7.5% (w/v) hydrogel corresponded to a Young’s modulus of 6.3 kPa. In vitro cell-based and subcutaneous implantation experiments in mice demonstrated the excellent biocompatibility and optimal biodegradability of hydrogel dressings. In a diabetic mouse\u0000 splint wound model for evaluating wound healing in vivo, the hydrogel dressing showed robust adhesion to the wound and efficiently accommodated mechanical deformations around the wound, resulting in significantly improved healing rates of chronic diabetic wounds. Thus, our work illustrates\u0000 a newly alternative strategy for the simple and efficacious treatment of chronic wounds in the context of diabetes care.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 16","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138613033","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}
To explore the expression of circ_0000615 in HTFs and its effect on cell proliferation and migration. With in vitro culture of HTFs, qRT-PCR was performed to detect the expression of circ_0000615 in HTFs. Cells in logarithmic phase were taken for subsequent experiments, and the following groups were constructed, including HTF blank control group (C group); HTFs+10 ng/mL TGF-β1 group (TGF-β1 group); HTFs+si-NC group (si-NC group); and HTFs+si-circ_0000615 group (si-circ_0000615 group). CCK-8 assay was performed to detect cell proliferation, Cell Monoclonal Assay was used to detect Cell Monoclonal Formationand, Transwell assay was conducted simultaneously to detect cell migration. According to the results of qRT-PCR, compared with C group, after induction of HTFs with TGF-β1 for 24 h and 48 h, TGF-β1 group showed significantly increased expressions of circ_0000615, with statistically significant differences (P < 0.05). After induction of HTFs with TGF-β1, compared with C group, TGF-β1 group had enhanced cell proliferation, monoclonal formation and migration, showing statistically significant differences (P < 0.05). Furthermore, after cell transfections for HTFs, compared with si-NC group, si-circ_0000615 group showed obviously downregulated expression of circ_0000615 in HTFs, accompanied by evidently weakened cell proliferation, monoclonal formation and migration, statistically significant differences (P < 0.05). Circ_0000615 is highly expressed in HTFs. A silenced expression of circ_0000615 may inhibit the proliferation and migration of HTFs.
{"title":"The Expression of Circ_0000615 in Tenon’s Capsule Fibroblasts and Its Effect on Cell Proliferation and Migration","authors":"Yanxi Wang, Xing Chen, Zhenhua Yang, Xuelin Yu, Manhua Xu, Gangjing Kang","doi":"10.1166/jbn.2023.3716","DOIUrl":"https://doi.org/10.1166/jbn.2023.3716","url":null,"abstract":"To explore the expression of circ_0000615 in HTFs and its effect on cell proliferation and migration. With in vitro culture of HTFs, qRT-PCR was performed to detect the expression of circ_0000615 in HTFs. Cells in logarithmic phase were taken for subsequent experiments, and the\u0000 following groups were constructed, including HTF blank control group (C group); HTFs+10 ng/mL TGF-β1 group (TGF-β1 group); HTFs+si-NC group (si-NC group); and HTFs+si-circ_0000615 group (si-circ_0000615 group). CCK-8 assay was performed to detect cell proliferation,\u0000 Cell Monoclonal Assay was used to detect Cell Monoclonal Formationand, Transwell assay was conducted simultaneously to detect cell migration. According to the results of qRT-PCR, compared with C group, after induction of HTFs with TGF-β1 for 24 h and 48 h, TGF-β1 group\u0000 showed significantly increased expressions of circ_0000615, with statistically significant differences (P < 0.05). After induction of HTFs with TGF-β1, compared with C group, TGF-β1 group had enhanced cell proliferation, monoclonal formation and migration,\u0000 showing statistically significant differences (P < 0.05). Furthermore, after cell transfections for HTFs, compared with si-NC group, si-circ_0000615 group showed obviously downregulated expression of circ_0000615 in HTFs, accompanied by evidently weakened cell proliferation, monoclonal\u0000 formation and migration, statistically significant differences (P < 0.05). Circ_0000615 is highly expressed in HTFs. A silenced expression of circ_0000615 may inhibit the proliferation and migration of HTFs.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"22 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138624129","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}
To elucidate the biological function of Rab11-FIP4 in the development of preeclampsia, as well as its clinical significance and underlying mechanism. Relative levels of Rab11-FIP4, IL-6 and TNF-α in placental tissues of PE pregnant women and healthy pregnant women were detected by qRT-PCR. The correlation between Rab11-FIP4 and IL-6 or TNF-α was assessed by Pearson correlation test. After constructing overexpression lentivirus targeting Rab11-FIP4, its influences on biological characteristics of HTR-8/SVneo cells and expression levels of inflammatory cytokines were examined. Rab11-FIP4 was highly expressed in placental tissues of PE pregnant women. Overexpression of Rab11-FIP4 enhanced migratory and invasive capacities of trophoblasts, and upregulated inflammatory proteins. Rab11-FIP4 aggravates the development of PE by upregulating inflammatory proteins, and stimulating migratory and invasive capacities of trophoblasts.
{"title":"Biological Function of Rab11-Family Interacting Protein 4 in the Development of Preeclampsia and Their Underlying Mechanism","authors":"Shanshan Yang, Guixia Sun, Yanxia Zhang","doi":"10.1166/jbn.2023.3745","DOIUrl":"https://doi.org/10.1166/jbn.2023.3745","url":null,"abstract":"To elucidate the biological function of Rab11-FIP4 in the development of preeclampsia, as well as its clinical significance and underlying mechanism. Relative levels of Rab11-FIP4, IL-6 and TNF-α in placental tissues of PE pregnant women and healthy pregnant women were\u0000 detected by qRT-PCR. The correlation between Rab11-FIP4 and IL-6 or TNF-α was assessed by Pearson correlation test. After constructing overexpression lentivirus targeting Rab11-FIP4, its influences on biological characteristics of HTR-8/SVneo cells and expression levels of inflammatory\u0000 cytokines were examined. Rab11-FIP4 was highly expressed in placental tissues of PE pregnant women. Overexpression of Rab11-FIP4 enhanced migratory and invasive capacities of trophoblasts, and upregulated inflammatory proteins. Rab11-FIP4 aggravates the development of PE by upregulating inflammatory\u0000 proteins, and stimulating migratory and invasive capacities of trophoblasts.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138615576","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}
Xiangfei Guo, Linbang Wang, Honghao Yang, Guanping He
Osteosarcoma (OS) primarily accurs in adolescents, and is more prevalent in males than females. It is characteristics by local invasive growth and early pulmonary metastases. Nanoparticles (NPs) have emerged as a promising alternative to traditional chemotherapeutic drugs due to their high selectivity and effectiveness. Previous studies have demonstrated the potential of zinc oxide nanoparticles (ZnO NPs) as a treatment for various tumors except OS. In this study, we use RNA-seq analysis to investigate the underlying biological mechanism involved in the process of ZnO NPs-treated different types of OS cell lines. We identified 928 differentially expressed genes (DEGs) in both 143B and MG-63 cells, and we validated the expression of the eight most significant DEGs using RT-qPCR. Gene Ontology (GO) analysis displayed regulation of transcription factor on nucleic acid binding in molecular function term, and extracellular space in cellular components term in both OS cell lines. Additionally, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed the co-enrichment of the MAPK, Toll-like receptor, and NF-κB pathways in both OS cell lines. Protein–protein interaction (PPI) analysis highlighted the involvement of HMOX1, MAFB, CXCL10, and CXCL11 in various biological processes in OS cells treated with ZnO NPs. Furthermore, we confirmed the key protein molecules in the differential signaling pathways of both OS cell lines using Western Blot (WB). Our findings shed light on the potential antitumor mechanisms and exploitable bioeffects of ZnO NPs in the treatment of OS. This study provides more targets and possible mechanisms for the treatment of ZnO NPs, as well as more theoretical basis for the treatment of OS.
骨肉瘤(OS)主要发生在青少年，男性比女性更普遍。它的特点是局部浸润性生长和早期肺转移。纳米粒子(NPs)由于其高选择性和有效性而成为传统化疗药物的一个有希望的替代品。以前的研究已经证明氧化锌纳米颗粒(ZnO NPs)作为除肿瘤外的各种肿瘤的治疗潜力。在这项研究中，我们使用RNA-seq分析来研究ZnO nps处理不同类型OS细胞系过程中涉及的潜在生物学机制。我们在143B和MG-63细胞中鉴定了928个差异表达基因(deg)，并使用RT-qPCR验证了8个最显著的deg的表达。基因本体(Gene Ontology, GO)分析显示，在两种OS细胞系中，转录因子在分子功能方面调控了核酸结合，在细胞组分方面调控了细胞外空间。此外，京都基因和基因组百科全书(KEGG)分析显示，MAPK、toll样受体和NF-κB通路在两种OS细胞系中共同富集。蛋白-蛋白相互作用(PPI)分析强调了HMOX1、MAFB、CXCL10和CXCL11参与氧化锌NPs处理的OS细胞的各种生物过程。此外，我们利用Western Blot (WB)技术确认了两种OS细胞系差异信号通路中的关键蛋白分子。我们的研究结果揭示了ZnO NPs治疗OS的潜在抗肿瘤机制和可开发的生物效应。本研究为ZnO NPs的处理提供了更多的靶点和可能的机制，也为OS的处理提供了更多的理论依据。
{"title":"Zinc Oxide Nanoparticles (ZnO NPs) Treated Two Types of Osteosarcoma Cell Lines for Identifying Differentially Expressed Genes","authors":"Xiangfei Guo, Linbang Wang, Honghao Yang, Guanping He","doi":"10.1166/jbn.2023.3722","DOIUrl":"https://doi.org/10.1166/jbn.2023.3722","url":null,"abstract":"Osteosarcoma (OS) primarily accurs in adolescents, and is more prevalent in males than females. It is characteristics by local invasive growth and early pulmonary metastases. Nanoparticles (NPs) have emerged as a promising alternative to traditional chemotherapeutic drugs due to their\u0000 high selectivity and effectiveness. Previous studies have demonstrated the potential of zinc oxide nanoparticles (ZnO NPs) as a treatment for various tumors except OS. In this study, we use RNA-seq analysis to investigate the underlying biological mechanism involved in the process of ZnO NPs-treated\u0000 different types of OS cell lines. We identified 928 differentially expressed genes (DEGs) in both 143B and MG-63 cells, and we validated the expression of the eight most significant DEGs using RT-qPCR. Gene Ontology (GO) analysis displayed regulation of transcription factor on nucleic acid\u0000 binding in molecular function term, and extracellular space in cellular components term in both OS cell lines. Additionally, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed the co-enrichment of the MAPK, Toll-like receptor, and NF-κB pathways in both OS cell lines.\u0000 Protein–protein interaction (PPI) analysis highlighted the involvement of HMOX1, MAFB, CXCL10, and CXCL11 in various biological processes in OS cells treated with ZnO NPs. Furthermore, we confirmed the key protein molecules in the differential signaling pathways of both OS cell lines\u0000 using Western Blot (WB). Our findings shed light on the potential antitumor mechanisms and exploitable bioeffects of ZnO NPs in the treatment of OS. This study provides more targets and possible mechanisms for the treatment of ZnO NPs, as well as more theoretical basis for the treatment of\u0000 OS.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 79","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138620283","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}
As a momentous condition disease, ischemic stroke could lead to physical disability and death. Here, the protective effect of miRNA up-regulated in neural stem cells (NSCs) derived exosomes on ischemic stroke in rats and their molecular mechanisms were investigated to reveal the therapeutic target of exosomes and suggests new approaches to treat ischemic stroke. miRNAs differentially expressed in exosomes derived from NSCs at various differentiation stages were detected by high-throughput sequencing for miRNAs. The impacts of miR-9a-5p upregulation were assessed on the differentiation of NSCs. The effects of exosomes derived from normal NSCs and NSCs with up-regulated miR-9a-5p on cell survival and differentiation and AMPK activation were investigated in vitro and in vivo. The high-throughput sequencing analysis revealed that miR-9a-5p was differentially expressed in NSC-derived exosomes at various stages of differentiation. MiR-9a-5p upregulation in exosomes promoted cell differentiation of NSCs. Furthermore, it can sensitized the AMPK signaling pathway. Following deprivation/reperfusion of oxygen-glucose, the differentiation of NSCs was restored, and exosomes significantly reduced cell apoptosis. MiR-9a-5p exosomes reduced the blood-brain barrier permeability and the infarct volume of rats with ischemic stroke in vivo. Neural cell apoptosis was reduced, thus indicating that miR-9a-5p could inhibit the cell apoptosis in vivo. AMPK activation was induced and increased in the MACO/R rat with miR-9a-5p exosomes. MiR-9a-5p exosomes could promote AMPK phosphorylation, increase NSC survival and enhance cell differentiation; this could inhibit the progression of ischemic stroke by maintaining an adequate number of neural cells and promoting endogenous NSC differentiation.
{"title":"Mechanism of Neural Stem Cell-Derived Exosomal miR-9a-5p Overexpression Improving Survival and Neurogenesis in Ischemic Stroke Rats","authors":"Jiale Liu, Chaoqun Lin, Chenyang Gu, Qiankun Zhang, Tingle Feng, Wenjie Duan, Jiajun Huang, J. Long, Yunhui Qiu, Waqas Ahmed, Ahsan Ali Khan, Hengsen Cai, Yong Hu, Zhihan Zhu, Shiying Huang, Lukui Chen","doi":"10.1166/jbn.2023.3710","DOIUrl":"https://doi.org/10.1166/jbn.2023.3710","url":null,"abstract":"As a momentous condition disease, ischemic stroke could lead to physical disability and death. Here, the protective effect of miRNA up-regulated in neural stem cells (NSCs) derived exosomes on ischemic stroke in rats and their molecular mechanisms were investigated to reveal the therapeutic target of exosomes and suggests new approaches to treat ischemic stroke. miRNAs differentially expressed in exosomes derived from NSCs at various differentiation stages were detected by high-throughput sequencing for miRNAs. The impacts of miR-9a-5p upregulation were assessed on the differentiation of NSCs. The effects of exosomes derived from normal NSCs and NSCs with up-regulated miR-9a-5p on cell survival and differentiation and AMPK activation were investigated in vitro and in vivo. The high-throughput sequencing analysis revealed that miR-9a-5p was differentially expressed in NSC-derived exosomes at various stages of differentiation. MiR-9a-5p upregulation in exosomes promoted cell differentiation of NSCs. Furthermore, it can sensitized the AMPK signaling pathway. Following deprivation/reperfusion of oxygen-glucose, the differentiation of NSCs was restored, and exosomes significantly reduced cell apoptosis. MiR-9a-5p exosomes reduced the blood-brain barrier permeability and the infarct volume of rats with ischemic stroke in vivo. Neural cell apoptosis was reduced, thus indicating that miR-9a-5p could inhibit the cell apoptosis in vivo. AMPK activation was induced and increased in the MACO/R rat with miR-9a-5p exosomes. MiR-9a-5p exosomes could promote AMPK phosphorylation, increase NSC survival and enhance cell differentiation; this could inhibit the progression of ischemic stroke by maintaining an adequate number of neural cells and promoting endogenous NSC differentiation.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"60 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139294713","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}
The skin serves as a natural barrier in the human body, protecting against pathogenic microorganisms and ultraviolet radiation (UV). Skin photoaging is a physiological stress reaction characterized by skin relaxation, dryness, abnormal pigmentation, and increased wrinkles due to prolonged exposure to ultraviolet radiation. The search and development of natural products that can effectively prevent skin photoaging have gained significant attention. We established the photoaging model by subjecting HaCaT cells and ICR mice to UVB+UBA irradiation. We employed CCK8 to assess the impact of Totol Flavonoid of Lichi Seed (TFLS) and Lychee Seed Saponins (LSS) on cell viability. We evaluated the effects of TFLS and LSS on apoptosis using flow cytometry. We utilized SIRT-IN-1 inhibitor to suppress the activity of SIRT1 and examined the mechanism by which TFLS and LSS alleviate UV-induced photoaging damage in cells and mice. We assessed skin inflammation in photoaging ICR mice through HE staining. We evaluated changes in collagen fibers and glia in the skin of photoaging ICR mice using Masson staining. We employed TUNEL staining to evaluate the apoptosis of skin cells in photoaging ICR mice. We extracted nucleic acid using nano-magnetic beads and detected the expression of SIRT1, TGF-β1, and Smad3 in HaCaT cells and mouse skin tissues using qPCR and WB. The study results demonstrate the protective effect of TFLS and LSS against UV-induced photoaging in HaCaT cells and ICR mouse skin, mitigating the damage caused by UV exposure. The mechanism underlying the attenuation of UV-induced photoaging by TFLS and LSS may involve activation of the SIRT1-TGF-β1/Smad3 signaling pathway.
{"title":"Effects of Flavonoid and Saponins on Protecting HaCaT Cells and Ameliorating Ultraviolet Radiation B/Ultraviolet Radiation A-Induced Skin Photoaging","authors":"Xiaohuan Hu, Shichen Jiao, Mu Niu, Jie Yang","doi":"10.1166/jbn.2023.3709","DOIUrl":"https://doi.org/10.1166/jbn.2023.3709","url":null,"abstract":"The skin serves as a natural barrier in the human body, protecting against pathogenic microorganisms and ultraviolet radiation (UV). Skin photoaging is a physiological stress reaction characterized by skin relaxation, dryness, abnormal pigmentation, and increased wrinkles due to prolonged exposure to ultraviolet radiation. The search and development of natural products that can effectively prevent skin photoaging have gained significant attention. We established the photoaging model by subjecting HaCaT cells and ICR mice to UVB+UBA irradiation. We employed CCK8 to assess the impact of Totol Flavonoid of Lichi Seed (TFLS) and Lychee Seed Saponins (LSS) on cell viability. We evaluated the effects of TFLS and LSS on apoptosis using flow cytometry. We utilized SIRT-IN-1 inhibitor to suppress the activity of SIRT1 and examined the mechanism by which TFLS and LSS alleviate UV-induced photoaging damage in cells and mice. We assessed skin inflammation in photoaging ICR mice through HE staining. We evaluated changes in collagen fibers and glia in the skin of photoaging ICR mice using Masson staining. We employed TUNEL staining to evaluate the apoptosis of skin cells in photoaging ICR mice. We extracted nucleic acid using nano-magnetic beads and detected the expression of SIRT1, TGF-β1, and Smad3 in HaCaT cells and mouse skin tissues using qPCR and WB. The study results demonstrate the protective effect of TFLS and LSS against UV-induced photoaging in HaCaT cells and ICR mouse skin, mitigating the damage caused by UV exposure. The mechanism underlying the attenuation of UV-induced photoaging by TFLS and LSS may involve activation of the SIRT1-TGF-β1/Smad3 signaling pathway.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"61 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139297085","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}
To detect differential levels of FAM129A and CXCL14 in breast cancer samples, and to explore their influences on breast cancer proliferation. Differential levels of FAM129A and CXCL14 in breast cancer samples were examined by qRT-PCR. The correlation between FAM129A level and clinic pathological factors in breast cancer patients was analyzed. The regulatory effects of FAM129A and CXCL14 on proliferative potential in highly invasive breast cancer cell lines MCF-7 and SKBR-3 were assessed by CCK-8 and EdU assay. The interaction between FAM129A and CXCL14 was explored by bioinformatics analysis and Dual-Luciferase reporter assay. FAM129A was upregulated in breast cancer samples, and it was positively correlated to TNM staging in breast cancer patients. Knockdown of FAM129A markedly attenuated in vitro proliferative ability in breast cancer. CXCL14 was lowly expressed in breast cancer tissues and cell lines, which was able to inhibit breast cancer proliferation. FAM129A could bind CXCL14 and negatively regulate its level in breast cancer samples. Rescue experiments demonstrated that knockdown of CXCL14 could abolish the inhibited proliferative ability in breast cancer cells with FAM129A knockdown. FAM129A is upregulated in breast cancer samples with highly invasive potential, and it is linked to TNM staging. It aggravates the malignant proliferation of breast cancer cells by targeting and downregulating CXCL14.
{"title":"FAM129A Aggravates the Malignant Progression of Breast Cancer with the Synergistical Interaction with CXCL14","authors":"Yijie Yuan, Yuxin Zhou, Shuixin Yan, Jiadi Li, Weizhu Wu","doi":"10.1166/jbn.2023.3696","DOIUrl":"https://doi.org/10.1166/jbn.2023.3696","url":null,"abstract":"To detect differential levels of FAM129A and CXCL14 in breast cancer samples, and to explore their influences on breast cancer proliferation. Differential levels of FAM129A and CXCL14 in breast cancer samples were examined by qRT-PCR. The correlation between FAM129A level and clinic pathological factors in breast cancer patients was analyzed. The regulatory effects of FAM129A and CXCL14 on proliferative potential in highly invasive breast cancer cell lines MCF-7 and SKBR-3 were assessed by CCK-8 and EdU assay. The interaction between FAM129A and CXCL14 was explored by bioinformatics analysis and Dual-Luciferase reporter assay. FAM129A was upregulated in breast cancer samples, and it was positively correlated to TNM staging in breast cancer patients. Knockdown of FAM129A markedly attenuated in vitro proliferative ability in breast cancer. CXCL14 was lowly expressed in breast cancer tissues and cell lines, which was able to inhibit breast cancer proliferation. FAM129A could bind CXCL14 and negatively regulate its level in breast cancer samples. Rescue experiments demonstrated that knockdown of CXCL14 could abolish the inhibited proliferative ability in breast cancer cells with FAM129A knockdown. FAM129A is upregulated in breast cancer samples with highly invasive potential, and it is linked to TNM staging. It aggravates the malignant proliferation of breast cancer cells by targeting and downregulating CXCL14.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"55 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139305875","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 aimed to investigate the impact of Homeobox containing1 (HMBOX1) on heart structure and function in Diabetic Cardiomyopathy (DCM) rats. DCM is the leading cause of death in diabetic patients, significantly affecting their quality of life. The DCM rat model was created using a high-fat diet and streptozotocin injection. The success of the model was determined by assessing heart weight, diet, urine output, and cardiac function. HMBOX1 expression in cardiomyocytes of normal and DCM rats was compared. HMBOX1 expression was enhanced in DCM rat cardiomyocytes through jugular vein injection of HMBOX1 lentivirus. The effects of HMBOX1 on myocardial structure, function, collagen levels, inflammatory factors, and the TGF-β/Smad3 signaling pathway in DCM rats were evaluated. DCM rats exhibited increased heart weight, diet, and impaired heart function, confirming successful model creation. HMBOX1 expression was significantly lower in DCM rat cardiomyocytes compared to the control group. Augmenting HMBOX1 expression in DCM rat cardiomyocytes improved cardiac function, myocardial morphology, and reduced collagen I and collagen III expression. HMBOX1 also mitigated inflammation in myocardial tissues. Furthermore, HMBOX1 inhibited the TGF-β/Smad3 signaling pathway in DCM rat cardiomyocytes. Overall, HMBOX1 alleviated DCM by reducing myocardial fibrosis and inflammation via TGF-β/Smad3 signaling pathway inhibition
{"title":"Overexpression of Homeobox Containing1 Relieves Myocardial Fibrosis and Inflammation in Diabetic Cardiomyopathy Rats","authors":"He Huang, Yuan Liu, Qiang Su, Jiayuan Ling","doi":"10.1166/jbn.2023.3697","DOIUrl":"https://doi.org/10.1166/jbn.2023.3697","url":null,"abstract":"This study aimed to investigate the impact of Homeobox containing1 (HMBOX1) on heart structure and function in Diabetic Cardiomyopathy (DCM) rats. DCM is the leading cause of death in diabetic patients, significantly affecting their quality of life. The DCM rat model was created using a high-fat diet and streptozotocin injection. The success of the model was determined by assessing heart weight, diet, urine output, and cardiac function. HMBOX1 expression in cardiomyocytes of normal and DCM rats was compared. HMBOX1 expression was enhanced in DCM rat cardiomyocytes through jugular vein injection of HMBOX1 lentivirus. The effects of HMBOX1 on myocardial structure, function, collagen levels, inflammatory factors, and the TGF-β/Smad3 signaling pathway in DCM rats were evaluated. DCM rats exhibited increased heart weight, diet, and impaired heart function, confirming successful model creation. HMBOX1 expression was significantly lower in DCM rat cardiomyocytes compared to the control group. Augmenting HMBOX1 expression in DCM rat cardiomyocytes improved cardiac function, myocardial morphology, and reduced collagen I and collagen III expression. HMBOX1 also mitigated inflammation in myocardial tissues. Furthermore, HMBOX1 inhibited the TGF-β/Smad3 signaling pathway in DCM rat cardiomyocytes. Overall, HMBOX1 alleviated DCM by reducing myocardial fibrosis and inflammation via TGF-β/Smad3 signaling pathway inhibition","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139297699","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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