Hong Li, Fei Gao, Tian Yang, Sifang Feng, Qian Ning, Ya Liu, Tian-jun Chen
Lung cancer is one of the most common causes of cancer-related deaths for cancer patients, the specific role of cyclic RNA in non-small cell lung cancer still needs further exploration. The effect of Hsa-Circ-0002360 and the relative pathway participated in the development of non-small cell lung cancer cells, lentivirus expression vector shcirc0002360, miRNA-511-5p mimics and recombinant protein SMURF2 were used in this study. The function of cell proliferation, migration and apoptosis were compared by flow cytometry, wound healing, RT-qPCR and western blot. We found circRNA 0002360 knockout significantly inhibited A549 cell functions. After further overexpression of miR-511-5p, the migration function, proliferation function, and cell viability of cells are significantly decreased while apoptosis rate increased, and quite the opposite after adding SMURF2. Smurf2 promotes the development of non-small cell lung cancer cells by regulating tumor cell migration, dissemination, and apoptosis, and this process is also regulated by Hsa-cic-000236 and miR-511-5p.
{"title":"Hsa-Circ-0002360 Promotes the Development of Non-Small Cell Lung Cancer Cells by Regulating Specific E3 Ubiquitin Protein Ligase 2 Pathway Through miRNA-511-5p","authors":"Hong Li, Fei Gao, Tian Yang, Sifang Feng, Qian Ning, Ya Liu, Tian-jun Chen","doi":"10.1166/jbn.2023.3700","DOIUrl":"https://doi.org/10.1166/jbn.2023.3700","url":null,"abstract":"Lung cancer is one of the most common causes of cancer-related deaths for cancer patients, the specific role of cyclic RNA in non-small cell lung cancer still needs further exploration. The effect of Hsa-Circ-0002360 and the relative pathway participated in the development of non-small cell lung cancer cells, lentivirus expression vector shcirc0002360, miRNA-511-5p mimics and recombinant protein SMURF2 were used in this study. The function of cell proliferation, migration and apoptosis were compared by flow cytometry, wound healing, RT-qPCR and western blot. We found circRNA 0002360 knockout significantly inhibited A549 cell functions. After further overexpression of miR-511-5p, the migration function, proliferation function, and cell viability of cells are significantly decreased while apoptosis rate increased, and quite the opposite after adding SMURF2. Smurf2 promotes the development of non-small cell lung cancer cells by regulating tumor cell migration, dissemination, and apoptosis, and this process is also regulated by Hsa-cic-000236 and miR-511-5p.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"264 1 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139291174","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}
Colon cancer is a severe digestive system malignant tumor. It is particularly urgent to make a thorough inquiry into colon cancer. The role of lncRNA SBF2 Antisense RNA 1 (SBF2-AS1) in the progression of this disease was explored. RT-PCR was undertaken to detect lncRNA SBF2-AS1 expression, miR-506-3p, and ZEB1 in normal HIEC, HCT116, LoVo, SW480, and SW620 cells. Sh-SBF2-AS1, miR-506-3p mimic, ZEB1 inhibitor, and controls were transfected. Proliferation was verified by CCK-8 assay. Invasion and migration ability were monitored via wound healing and Transwell assay. The colon cancer model was established to research the role of lncRNA SBF2-AS1 in vivo. LncRNA SBF2-AS1 was with high level in colon cancer samples, and the survival rate was positively related to SBF2-AS1 level of patients. Down-expressed SBF2-AS1 decreased the development of colon cells. Furthermore, we predicted SBF2-AS1 targeted binding to miR-506-3p and proved that the downstream gene was ZEB1 by the bioinformatic and experimental means. In addition, we observed that the tumor-accelerate effects of SBF2-AS1 in colon cancer were mediated by PI3K/Akt/mTOR pathway. Finally, we referred that sh-SBF2-AS1 effectively inhibits the development of colon cancer in vivo. LncRNA SBF2-AS1 has involved the PI3K/Akt/mTOR signaling pathway of colon cancer via regulating the miR-506-3p/ZEB1 axis.
{"title":"LncRNA SBF2 Antisense RNA 1 Accelerates the Progression of Colon Cancer via PI3K/Akt/mTOR Signaling Pathway by Targeting miR-506-3p/ZEB1 Axis","authors":"Fei Yang, Min Tao","doi":"10.1166/jbn.2023.3692","DOIUrl":"https://doi.org/10.1166/jbn.2023.3692","url":null,"abstract":"Colon cancer is a severe digestive system malignant tumor. It is particularly urgent to make a thorough inquiry into colon cancer. The role of lncRNA SBF2 Antisense RNA 1 (SBF2-AS1) in the progression of this disease was explored. RT-PCR was undertaken to detect lncRNA SBF2-AS1 expression, miR-506-3p, and ZEB1 in normal HIEC, HCT116, LoVo, SW480, and SW620 cells. Sh-SBF2-AS1, miR-506-3p mimic, ZEB1 inhibitor, and controls were transfected. Proliferation was verified by CCK-8 assay. Invasion and migration ability were monitored via wound healing and Transwell assay. The colon cancer model was established to research the role of lncRNA SBF2-AS1 in vivo. LncRNA SBF2-AS1 was with high level in colon cancer samples, and the survival rate was positively related to SBF2-AS1 level of patients. Down-expressed SBF2-AS1 decreased the development of colon cells. Furthermore, we predicted SBF2-AS1 targeted binding to miR-506-3p and proved that the downstream gene was ZEB1 by the bioinformatic and experimental means. In addition, we observed that the tumor-accelerate effects of SBF2-AS1 in colon cancer were mediated by PI3K/Akt/mTOR pathway. Finally, we referred that sh-SBF2-AS1 effectively inhibits the development of colon cancer in vivo. LncRNA SBF2-AS1 has involved the PI3K/Akt/mTOR signaling pathway of colon cancer via regulating the miR-506-3p/ZEB1 axis.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"263 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139298415","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}
Previous studies have identified that ring finger protein 38 (RNF38) induces proliferative potential in many types of tumors. However, its functions in colorectal cancer (CRC) are unclear. This study aims to elucidate the regulatory effects of RNF38 on CRC proliferation in vitro and in vivo. Expression pattern and prognostic potential of RNF38 in clinically collected CRC cases were analyzed. After intervening RNF38 levels in SW480 and HT29 cells, viability, cell cycle progression and apoptosis were examined. Subsequently, we generated RNF38 overexpressed transgenic mice and xenograft model in nude mice. in vivo regulation of RNF38 on CRC proliferation was assessed. RNF38 was upregulated in CRC tissues. Overexpression of RNF38 stimulated proliferative ability and inhibited apoptosis in CRC cells. In addition, in vivo overexpression of RNF38 triggered tumor growth of CRC in nude mice. Silence of RNF38 markedly suppressed in vivo proliferation of CRC and induced apoptosis by activating the PI3K/AKT signaling.
{"title":"Ring Finger Protein 38 Induces Colorectal Cancer Proliferation by Activating the Phosphatidyl- Inositol 3-Kinase/Serine-Threonine Kinase Signaling","authors":"Junde Zhou, Meng Qiao, Haiyan Zhao, Nannan Lu, Xinxin Lv, Xin Wang, Jing Li, Lixia Ke","doi":"10.1166/jbn.2023.3698","DOIUrl":"https://doi.org/10.1166/jbn.2023.3698","url":null,"abstract":"Previous studies have identified that ring finger protein 38 (RNF38) induces proliferative potential in many types of tumors. However, its functions in colorectal cancer (CRC) are unclear. This study aims to elucidate the regulatory effects of RNF38 on CRC proliferation in vitro and in vivo. Expression pattern and prognostic potential of RNF38 in clinically collected CRC cases were analyzed. After intervening RNF38 levels in SW480 and HT29 cells, viability, cell cycle progression and apoptosis were examined. Subsequently, we generated RNF38 overexpressed transgenic mice and xenograft model in nude mice. in vivo regulation of RNF38 on CRC proliferation was assessed. RNF38 was upregulated in CRC tissues. Overexpression of RNF38 stimulated proliferative ability and inhibited apoptosis in CRC cells. In addition, in vivo overexpression of RNF38 triggered tumor growth of CRC in nude mice. Silence of RNF38 markedly suppressed in vivo proliferation of CRC and induced apoptosis by activating the PI3K/AKT signaling.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"237 1 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139302082","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 assesses the role of a scaffold constructed by co-cultivating autologous oxygen-releasing nano-bionic materials and bone marrow stromal cells (BMSCs) in joint repairing. A scaffold constructed of autologous oxygen-releasing nano-bionic materials and BMSCs was transplanted into SD rats. The immunofluorescence detected the expression of nuclear antigen (PCNA) and analyzed the proliferation of BMSCs. Reverse transcription polymerase chain reaction (RT-PCR) examined the expression of osteogenic markers and TUNEL staining analyzed BMSCs apoptosis. There was a significant difference in the apoptosis and proliferation cell number of BMSCs in ankle joint between solely autologous oxygen-releasing nano-bionic material scaffold group and composite BMSCs nano-bionic scaffold (P <0.05). There was a statistical difference in PCNA and TUNEL expression between two groups at 4 weeks and 8 weeks (P <0.05). The expression of osteogenesis markers in ankle joint at 1 week, 4 weeks, and 8 weeks were continuously reduced, and the composite of autologous oxygen-releasing nanomaterials and BMSCs increased the expression of osteogenic markers (P <0.05). The composite scaffold constructed by autologous oxygen-releasing nano-bionic materials and BMSCs has a good two-way immune regulation function and is able to carry lipids, proteins, nutritional factors, and growth factors, which can effectively promote tissue engineering repairing and delay the scaffold degradation. Combined with the nano-release system to repair bone tissue, composite material can effectively promote the proliferation of joint osteoblasts and osteogenic differentiation, thus help repairing the ankle joint.
{"title":"The Construction of Foot and Ankle Joint by Autologous Oxygen-Releasing Nano-Bionic Scaffold Combined with Bone Marrow Mesenchymal Stem Cells","authors":"Zhi Zhao, Mengkun Liu, Rifei Zha, Tingbao Zhang, Lijia Pei, Yang Liu, Xinshe Zhou","doi":"10.1166/jbn.2023.3707","DOIUrl":"https://doi.org/10.1166/jbn.2023.3707","url":null,"abstract":"This study assesses the role of a scaffold constructed by co-cultivating autologous oxygen-releasing nano-bionic materials and bone marrow stromal cells (BMSCs) in joint repairing. A scaffold constructed of autologous oxygen-releasing nano-bionic materials and BMSCs was transplanted into SD rats. The immunofluorescence detected the expression of nuclear antigen (PCNA) and analyzed the proliferation of BMSCs. Reverse transcription polymerase chain reaction (RT-PCR) examined the expression of osteogenic markers and TUNEL staining analyzed BMSCs apoptosis. There was a significant difference in the apoptosis and proliferation cell number of BMSCs in ankle joint between solely autologous oxygen-releasing nano-bionic material scaffold group and composite BMSCs nano-bionic scaffold (P <0.05). There was a statistical difference in PCNA and TUNEL expression between two groups at 4 weeks and 8 weeks (P <0.05). The expression of osteogenesis markers in ankle joint at 1 week, 4 weeks, and 8 weeks were continuously reduced, and the composite of autologous oxygen-releasing nanomaterials and BMSCs increased the expression of osteogenic markers (P <0.05). The composite scaffold constructed by autologous oxygen-releasing nano-bionic materials and BMSCs has a good two-way immune regulation function and is able to carry lipids, proteins, nutritional factors, and growth factors, which can effectively promote tissue engineering repairing and delay the scaffold degradation. Combined with the nano-release system to repair bone tissue, composite material can effectively promote the proliferation of joint osteoblasts and osteogenic differentiation, thus help repairing the ankle joint.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"29 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139305860","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}
miR-29c is related to renal fibrosis. Lipid nanoparticles can inhibit cell growth. This study mainly explores whether miR-29c carried by lipid nanoparticles may regulate the expression of TGF-β signaling and then involves in renal fibrosis. Kidney fibrosis cells HK-2 were intervened with 20 μmol/L miR-29c carried by lipid nanoparticles followed by analysis of the proliferation number and cell cycle changes of HK-2 cells, expression of TGF-β pathway protein, and relationship between TGF-β and miR-29c. Mice were infused with Ang II (1000 ng/kg/min) for 4 weeks to establish a mouse model of renal fibrosis. After treatment with miR-29c carried by lipid nanoparticles and PBS, the changes of renal fibrosis and the expression of TGF-β were measured. The higher the concentration of miR-29c carried by lipid nanoparticles, the more significant the decrease in cell proliferation, and cells in S phase began to decline significantly (P <0.05). Cell number in lipid nanoparticle+PBS group was the lowest and cells in PBS group and lipid nanoparticle+TGF-β inhibitor group were higher. TGF-β is a target gene of miR-29c. When the concentration of miR-29c in lipid nanoemulsion was 20 μmol/L, the expression of TGF-β protein decreased. miR-29c-carried lipid nanoparticles significantly attenuated Ang II-induced kidney injury. TGF-β was highly expressed in renal fibrosis compared with control mice and the expression of TGF-β was decreased after lipid nanoparticle treatment. miR-29c carried by lipid nanoparticles can inhibit the proliferation of renal fibrosis cells, regulate the TGF-β pathway, and ultimately control abnormal cell proliferation.
{"title":"miR-29c Carried by Lipid Nanoparticles Mediates TGF-β Signaling Pathway in Renal Fibrosis","authors":"Yuting Gong, Yumei Liang, Yinyin Chen, Ying Chen, Qinghua Zeng, Shuyi Qian","doi":"10.1166/jbn.2023.3711","DOIUrl":"https://doi.org/10.1166/jbn.2023.3711","url":null,"abstract":"miR-29c is related to renal fibrosis. Lipid nanoparticles can inhibit cell growth. This study mainly explores whether miR-29c carried by lipid nanoparticles may regulate the expression of TGF-β signaling and then involves in renal fibrosis. Kidney fibrosis cells HK-2 were intervened with 20 μmol/L miR-29c carried by lipid nanoparticles followed by analysis of the proliferation number and cell cycle changes of HK-2 cells, expression of TGF-β pathway protein, and relationship between TGF-β and miR-29c. Mice were infused with Ang II (1000 ng/kg/min) for 4 weeks to establish a mouse model of renal fibrosis. After treatment with miR-29c carried by lipid nanoparticles and PBS, the changes of renal fibrosis and the expression of TGF-β were measured. The higher the concentration of miR-29c carried by lipid nanoparticles, the more significant the decrease in cell proliferation, and cells in S phase began to decline significantly (P <0.05). Cell number in lipid nanoparticle+PBS group was the lowest and cells in PBS group and lipid nanoparticle+TGF-β inhibitor group were higher. TGF-β is a target gene of miR-29c. When the concentration of miR-29c in lipid nanoemulsion was 20 μmol/L, the expression of TGF-β protein decreased. miR-29c-carried lipid nanoparticles significantly attenuated Ang II-induced kidney injury. TGF-β was highly expressed in renal fibrosis compared with control mice and the expression of TGF-β was decreased after lipid nanoparticle treatment. miR-29c carried by lipid nanoparticles can inhibit the proliferation of renal fibrosis cells, regulate the TGF-β pathway, and ultimately control abnormal cell proliferation.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"252 3 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139296201","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 inflammatory-immune response secondary to nerve injury is an important mechanism for craniocerebral injury. Procyanidins from lotus seedpods (LSPCs) are one of the main active ingredients isolated from the mature receptacles of the Nymphaeaceae family lotus plant. LSPCs exhibit strong free radical scavenging and antioxidant activities. The objective of this study was to determine the effects of LSPC nanoliposomes on traumatic brain injury (TBI). In a TBI rat model, LSPC nanoliposomes were injected intraperitoneally. Inflammatory factors and oxidative stress molecules were detected with ELISAs and RT-PCR. The TLR4/NF- κ B signaling pathway was explored using Western blotting. The modified neurological severity scores (mNSS) increased in the TBI group compared with the scores in the Sham group. The water maze test indicated latency in finding the platform was prolonged and staying time in the platform quadrant and the number of times crossing the platform were reduced in the TBI group. Treatment with LSPCs significantly reduced the mNSS scores in rats with TBI and significantly reduced the time to find the platform, increased the residence time in the platform quadrant, and increased the frequency of crossing the platform during the water maze test. In addition, brain edema was reduced in rats with TBI after intraperitoneal injection of LSPCs. Iba-1, IL-1 β , IL-6, and TNF- α levels were reduced after intraperitoneal injection of LSPCs. MDA levels were also reduced, while GSH-Px and SOD levels increased. After intraperitoneal injection of LSPCs, TLR4, MyD88, and pNF- κ B p65 were significantly attenuated. Activation of TLR4 prevented the protective effects of LCPCs in rats with TBI. The results of this study demonstrate that LSPCs attenuate activation of the TLR4/NF- κ B pathway in rats with TBI, thereby reducing microglia activation, inflammation, and oxidative stress.
{"title":"Lotus Seedpod Oligomeric Procyanidin Nanoliposomes Targeting TLR4/NF-<i>κ</i>B Reduce Inflammation and Oxidative Stress in Patients with Traumatic Brain Injury","authors":"Wenlong Hao, Sulan Luo, Lamei Hao, Feifei Zhang","doi":"10.1166/jbn.2023.3688","DOIUrl":"https://doi.org/10.1166/jbn.2023.3688","url":null,"abstract":"The inflammatory-immune response secondary to nerve injury is an important mechanism for craniocerebral injury. Procyanidins from lotus seedpods (LSPCs) are one of the main active ingredients isolated from the mature receptacles of the Nymphaeaceae family lotus plant. LSPCs exhibit strong free radical scavenging and antioxidant activities. The objective of this study was to determine the effects of LSPC nanoliposomes on traumatic brain injury (TBI). In a TBI rat model, LSPC nanoliposomes were injected intraperitoneally. Inflammatory factors and oxidative stress molecules were detected with ELISAs and RT-PCR. The TLR4/NF- κ B signaling pathway was explored using Western blotting. The modified neurological severity scores (mNSS) increased in the TBI group compared with the scores in the Sham group. The water maze test indicated latency in finding the platform was prolonged and staying time in the platform quadrant and the number of times crossing the platform were reduced in the TBI group. Treatment with LSPCs significantly reduced the mNSS scores in rats with TBI and significantly reduced the time to find the platform, increased the residence time in the platform quadrant, and increased the frequency of crossing the platform during the water maze test. In addition, brain edema was reduced in rats with TBI after intraperitoneal injection of LSPCs. Iba-1, IL-1 β , IL-6, and TNF- α levels were reduced after intraperitoneal injection of LSPCs. MDA levels were also reduced, while GSH-Px and SOD levels increased. After intraperitoneal injection of LSPCs, TLR4, MyD88, and pNF- κ B p65 were significantly attenuated. Activation of TLR4 prevented the protective effects of LCPCs in rats with TBI. The results of this study demonstrate that LSPCs attenuate activation of the TLR4/NF- κ B pathway in rats with TBI, thereby reducing microglia activation, inflammation, and oxidative stress.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"24 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135708171","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 role of KLF5 (Kruppel-like factor 5) in the abnormal dedifferentiation of chondrocytes (CHs) observed in osteoarthritis (OA) and monolayer culture conditions. Human primary CHs were cultured in a monolayer for 14 days, and various analyses were conducted. The area and aspect ratio of the cells were measured, and protein expression levels of KLF5, acetylated KLF5 (Ac-KLF5), and Runx2 were assessed using western blotting. Additionally, mRNA levels of chondrogenic genes (type II collagen, Col-II), hypertrophic genes (type X collagen, Col-X), and MMP-13 were determined through RT-PCR. The effects of TGF- β and Am80 supplementation on KLF5 acetylation and Runx2 expression were examined, and siRNA was used to silence Runx2 gene expression. Results showed that CHs exhibited dedifferentiation after 7 days of culture, characterized by increased cell size, larger aspect ratio, elevated Ac-KLF5 levels, decreased Col-II expression, and increased Col-X and MMP-13 expression. TGF- β treatment enhanced Ac-KLF5 and Runx2 expression, thereby accelerating dedifferentiation within 3 days. In contrast, Am80 suppressed Ac-KLF5 and Runx2 expression, leading to delayed dedifferentiation over 14 days. Silencing Runx2 mitigated KLF5 acetylation-induced CH dedifferentiation without affecting Ac-KLF5 levels. In conclusion, KLF5 acetylation promotes Runx2 expression and subsequently contributes to CH dedifferentiation during monolayer culture.
{"title":"Kruppel-Like Factor 5 Acetylation Upregulates Runx2 Expression and Accelerates the Dedifferentiation Process of Chondrocyte in Monolayer Culture","authors":"Peng Hu, Hongliang Du, Lizhen Duan, Xiaomei Lu","doi":"10.1166/jbn.2023.3679","DOIUrl":"https://doi.org/10.1166/jbn.2023.3679","url":null,"abstract":"This study aimed to investigate the role of KLF5 (Kruppel-like factor 5) in the abnormal dedifferentiation of chondrocytes (CHs) observed in osteoarthritis (OA) and monolayer culture conditions. Human primary CHs were cultured in a monolayer for 14 days, and various analyses were conducted. The area and aspect ratio of the cells were measured, and protein expression levels of KLF5, acetylated KLF5 (Ac-KLF5), and Runx2 were assessed using western blotting. Additionally, mRNA levels of chondrogenic genes (type II collagen, Col-II), hypertrophic genes (type X collagen, Col-X), and MMP-13 were determined through RT-PCR. The effects of TGF- β and Am80 supplementation on KLF5 acetylation and Runx2 expression were examined, and siRNA was used to silence Runx2 gene expression. Results showed that CHs exhibited dedifferentiation after 7 days of culture, characterized by increased cell size, larger aspect ratio, elevated Ac-KLF5 levels, decreased Col-II expression, and increased Col-X and MMP-13 expression. TGF- β treatment enhanced Ac-KLF5 and Runx2 expression, thereby accelerating dedifferentiation within 3 days. In contrast, Am80 suppressed Ac-KLF5 and Runx2 expression, leading to delayed dedifferentiation over 14 days. Silencing Runx2 mitigated KLF5 acetylation-induced CH dedifferentiation without affecting Ac-KLF5 levels. In conclusion, KLF5 acetylation promotes Runx2 expression and subsequently contributes to CH dedifferentiation during monolayer culture.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"54 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135708233","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 underlying mechanism through which moxibustion intervention therapy improves platelet activation in rats with atherosclerosis using Next Generation Sequencing (NGS). Atherosclerosis models were established in 15 Apolipoprotein E knockout mice (ApoE-/- mice) aged 8 weeks, while non-transgenic mice (C57BL/6) were used as the control group. The mice were divided into four groups: moxibustion group, clopidogrel group, model group, and blank control group. Following 12 weeks of intervention, platelet-rich plasma was prepared from venous blood collected from the mice’s eyeballs. RNA extraction and analysis were performed to assess gene expression patterns. In the moxibustion group, the expression of PPBP was downregulated, while PTPN7 expression was upregulated, indicating involvement in the MAPK classical pathway. The moxibustion group exhibited significantly higher PTPN7 mRNA expression compared to both the clopidogrel and model groups, while Robo4 mRNA expression was significantly reduced in both the moxibustion and clopidogrel groups. The PTPN7 gene locus, acting through the MAPK pathway, may serve as a potential target for enhancing atherosclerosis management by modulating platelet activation.
{"title":"Research on the Mechanism of Moxibustion Intervention in Atherosclerosis Based on Next Generation Sequencing","authors":"Jia Yang, Hanxi Dai, Shiwan Hu, Kun Cai","doi":"10.1166/jbn.2023.3673","DOIUrl":"https://doi.org/10.1166/jbn.2023.3673","url":null,"abstract":"This study aimed to investigate the underlying mechanism through which moxibustion intervention therapy improves platelet activation in rats with atherosclerosis using Next Generation Sequencing (NGS). Atherosclerosis models were established in 15 Apolipoprotein E knockout mice (ApoE-/- mice) aged 8 weeks, while non-transgenic mice (C57BL/6) were used as the control group. The mice were divided into four groups: moxibustion group, clopidogrel group, model group, and blank control group. Following 12 weeks of intervention, platelet-rich plasma was prepared from venous blood collected from the mice’s eyeballs. RNA extraction and analysis were performed to assess gene expression patterns. In the moxibustion group, the expression of PPBP was downregulated, while PTPN7 expression was upregulated, indicating involvement in the MAPK classical pathway. The moxibustion group exhibited significantly higher PTPN7 mRNA expression compared to both the clopidogrel and model groups, while Robo4 mRNA expression was significantly reduced in both the moxibustion and clopidogrel groups. The PTPN7 gene locus, acting through the MAPK pathway, may serve as a potential target for enhancing atherosclerosis management by modulating platelet activation.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"31 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135708236","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 significance of miR-141 expression, tumor-associated macrophages (TAMs), and CD147 expression in bladder cancer (BCa) cells, and their relationship with tumor grade. A total of 80 BCa patients were selected, and they were categorized into two groups: Group G1 (56 cases) with poorly differentiated tumors, and Group G2 (24 cases) with moderately to well-differentiated tumors according to the WHO classification criteria for urothelial carcinoma. We analyzed the differences in miR-141, TAMs, and CD147 expression levels among different tumor grades. The miR-141 level in BCa tissues of patients in Group G2 showed a significant decrease (1.88±0.4) compared to Group G1 ( P <0.05). As the tumor grade increased, TAMs levels in tumor tissues also increased ( P <0.05). Notably, 66.7% of CD147-positive patients in Group G2 exhibited a clear increase compared to Group G1 ( P <0.05). Importantly, significant correlations were observed between miR-141, TAMs, CD147 levels, and tumor grade ( P <0.05). These findings suggest that as BCa grades increase, miR-141 levels decrease while TAMs and CD147 levels increase. The levels of miR-141, TAMs, and CD147 in BCa tissue cells can serve as indicators for evaluating the prognosis of BCa patients.
{"title":"Expression of miR-141, TAMs, and CD147 in Bladder Cancer Cells: Implications for Tumor Grade and Prognosis","authors":"Xiaoming You","doi":"10.1166/jbn.2023.3685","DOIUrl":"https://doi.org/10.1166/jbn.2023.3685","url":null,"abstract":"This study aimed to investigate the significance of miR-141 expression, tumor-associated macrophages (TAMs), and CD147 expression in bladder cancer (BCa) cells, and their relationship with tumor grade. A total of 80 BCa patients were selected, and they were categorized into two groups: Group G1 (56 cases) with poorly differentiated tumors, and Group G2 (24 cases) with moderately to well-differentiated tumors according to the WHO classification criteria for urothelial carcinoma. We analyzed the differences in miR-141, TAMs, and CD147 expression levels among different tumor grades. The miR-141 level in BCa tissues of patients in Group G2 showed a significant decrease (1.88±0.4) compared to Group G1 ( P <0.05). As the tumor grade increased, TAMs levels in tumor tissues also increased ( P <0.05). Notably, 66.7% of CD147-positive patients in Group G2 exhibited a clear increase compared to Group G1 ( P <0.05). Importantly, significant correlations were observed between miR-141, TAMs, CD147 levels, and tumor grade ( P <0.05). These findings suggest that as BCa grades increase, miR-141 levels decrease while TAMs and CD147 levels increase. The levels of miR-141, TAMs, and CD147 in BCa tissue cells can serve as indicators for evaluating the prognosis of BCa patients.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"44 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135707287","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 purpose of this study was to prepare liposome-coated poly(lactic-co-glycolic acid) co-loaded with dexamethasone (DXMS, D) and captopril (CAP, C) loading with PLGA nanoparticles (P) and modified polyethylene glycol and integrin α 8 antibody on the surface of nanoparticles to obtain double-drug-loaded core–shell immunoliposome composite nanoparticles (DCPI), and then studied the loading Kidney targeting, anti-inflammatory effects and effects on macrophage differentiation of drug nanoparticles. In vitro cell experiments showed that DCPI could reduce the secretion of M2 macrophage-specific cytokines and the RNA expression levels of markers, and promote M2 macrophages toward unpolarized macrophages differentiation. In vivo experiments showed that DCPI had significant renal targeting, normalized renal index, serum creatinine, and blood urea nitrogen levels in mice with mesangial proliferative glomerulonephritis, and reduced inflammatory cytokines in the kidney’s secretion, and decreased RNA expression of M1 and M2 macrophage markers in kidneys. In conclusion, kidney-targeted DCPI nanoparticles can effectively regulate the polarization of macrophages, play an “anti-inflammatory/anti-fibrotic” therapeutic effect, and be a target for glomerulonephritis. Treatment provides new strategies and evidence.
{"title":"Immuno-Nanoparticles Developed Using Dexamethasone and Captopril Co-Loaded PLGA Improve Glomerulonephritis Through Modulating Macrophage Polarization","authors":"Linping Zhang, Yanting Zhu, Xiaoming Wang, Zhenjiang Li, Qianlan Dong","doi":"10.1166/jbn.2023.3615","DOIUrl":"https://doi.org/10.1166/jbn.2023.3615","url":null,"abstract":"The purpose of this study was to prepare liposome-coated poly(lactic-co-glycolic acid) co-loaded with dexamethasone (DXMS, D) and captopril (CAP, C) loading with PLGA nanoparticles (P) and modified polyethylene glycol and integrin α 8 antibody on the surface of nanoparticles to obtain double-drug-loaded core–shell immunoliposome composite nanoparticles (DCPI), and then studied the loading Kidney targeting, anti-inflammatory effects and effects on macrophage differentiation of drug nanoparticles. In vitro cell experiments showed that DCPI could reduce the secretion of M2 macrophage-specific cytokines and the RNA expression levels of markers, and promote M2 macrophages toward unpolarized macrophages differentiation. In vivo experiments showed that DCPI had significant renal targeting, normalized renal index, serum creatinine, and blood urea nitrogen levels in mice with mesangial proliferative glomerulonephritis, and reduced inflammatory cytokines in the kidney’s secretion, and decreased RNA expression of M1 and M2 macrophage markers in kidneys. In conclusion, kidney-targeted DCPI nanoparticles can effectively regulate the polarization of macrophages, play an “anti-inflammatory/anti-fibrotic” therapeutic effect, and be a target for glomerulonephritis. Treatment provides new strategies and evidence.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"132 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135708223","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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