Background: LncRNA PINK1-AS is an identified key modifier in cancers, but its biological function in bladder cancer (BC) remains unclear. The current work tried to explore the function and mechanism of PINK1-AS in BC. Methods: Fifty-five pairs of BC tissue and matched para-cancer normal tissue were excised to analyze PINK1-AS, miR-98-5p, and IGF1R expression. Based on T24 cells, the proliferative, apoptotic, invasive, and migratory activities were evaluated by CCK-8, flow cytometry, and Transwell assay correspondingly. RIP and dual luciferase reporter assays verified binding relationships between genes. Results: PINK1-AS expression was abnormally high in BC tissues, and was associated with TNM staging and lymph node metastasis in BC patients. PINK1-AS knockdown delayed the malignant progression in BC. Overexpressing PINK1-AS had the opposite effect. The impacts of silencing or promoting PINK1-AS on BC were mitigated by overexpression of IGF1R and miR-98-5p, respectively. PINK1-AS was competitively bound to miR-98-5p to mediate IGF1R expression. Conclusion: Targeting the abnormally overexpressed lncRNA, PINK1-AS, can release the inhibition of IGF1R by miR-98-5p, thereby promoting BC malignancy. PINK1-AS/miR-98-5p/IGF1R axis can be used as a potential therapeutic target for BC.
{"title":"LncRNA Phosphatase and Tensin Homolog Induced Kinase 1-AS Promotes Insulin Like Growth Factor 1 Receptor Expression Through Sponge miR-98-5p and Contributes to Bladder Cancer Progression","authors":"Shunping Wang, DanPing Cheng, Bin Zheng","doi":"10.1166/jbt.2023.3259","DOIUrl":"https://doi.org/10.1166/jbt.2023.3259","url":null,"abstract":"Background: LncRNA PINK1-AS is an identified key modifier in cancers, but its biological function in bladder cancer (BC) remains unclear. The current work tried to explore the function and mechanism of PINK1-AS in BC. Methods: Fifty-five pairs of BC tissue and matched\u0000 para-cancer normal tissue were excised to analyze PINK1-AS, miR-98-5p, and IGF1R expression. Based on T24 cells, the proliferative, apoptotic, invasive, and migratory activities were evaluated by CCK-8, flow cytometry, and Transwell assay correspondingly. RIP and dual luciferase reporter assays\u0000 verified binding relationships between genes. Results: PINK1-AS expression was abnormally high in BC tissues, and was associated with TNM staging and lymph node metastasis in BC patients. PINK1-AS knockdown delayed the malignant progression in BC. Overexpressing PINK1-AS had the opposite\u0000 effect. The impacts of silencing or promoting PINK1-AS on BC were mitigated by overexpression of IGF1R and miR-98-5p, respectively. PINK1-AS was competitively bound to miR-98-5p to mediate IGF1R expression. Conclusion: Targeting the abnormally overexpressed lncRNA, PINK1-AS, can release\u0000 the inhibition of IGF1R by miR-98-5p, thereby promoting BC malignancy. PINK1-AS/miR-98-5p/IGF1R axis can be used as a potential therapeutic target for BC.","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":"42092653","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 probe the role and specific mechanism of Bushen Huoxue Recipe in inhibiting renal fibrosis (RF), 150 healthy adult male Sprague-Dawley rats were randomized to sham operated group (SO group), model group (UUO group), conventional treatment group (UUO+EPL group), high-dose Bushen Huoxuefang group (UUO+H group), and low-dose Bushen Huoxue Recipe group (UUO+L group), with 30 mice in each group. The UUO, UUO+EPL, UUO+H, and UUO+L groups showed decreased pathological damage scores in rat renal tissue and increased blood urea nitrogen (BUN), serum creatinine (Cr), interleukin-1β (IL-1β), IL-18, high-sensitivity C-reactive protein (hs-CRP), and caspase-1 levels compared with the SO group. The expression of NLRP3, type III collagen (Col-III), matrix fibronectin (FN), and α-smooth actin (α-SMA) increased (P <0.05). Inflammatory cells aggregated in rat kidney tissue, and some renal tubular cells atrophied, fell off, vacuolized, underwent pyknosis, and the shape of tubules was incomplete. The lumen was enlarged, and the DNA damage was greater. The UUO+EPL, UUO+H and UUO+L groups showed increased pathological damage score of rat renal tissue and decreased expression levels of Cr, BUN, hs-CRP, IL-1β, IL-18, caspase-1, NLRP3, FN, Col-III, and α-SMA than UUO group. After a longer period, the UUO+EPL and UUO+H groups decreased more significantly than the UUO+L group. We conclude that Bushen Huoxue Recipe inhibits RF by regulating reactive oxygen species (ROS)/NLRP3-induced pyroptosis pathway.
{"title":"Bushen Huoxue Recipe Inhibits Renal Fibrosis by Regulating the Reactive Oxygen Species/Nucleotide-Binding Oligomerization Domain-Like Receptor Family Pyrin Domain-Containing 3-Induced Pyroptosis Pathway","authors":"Xian Chen, Jianrao Lu","doi":"10.1166/jbt.2023.3249","DOIUrl":"https://doi.org/10.1166/jbt.2023.3249","url":null,"abstract":"To probe the role and specific mechanism of Bushen Huoxue Recipe in inhibiting renal fibrosis (RF), 150 healthy adult male Sprague-Dawley rats were randomized to sham operated group (SO group), model group (UUO group), conventional treatment group (UUO+EPL group), high-dose Bushen Huoxuefang\u0000 group (UUO+H group), and low-dose Bushen Huoxue Recipe group (UUO+L group), with 30 mice in each group. The UUO, UUO+EPL, UUO+H, and UUO+L groups showed decreased pathological damage scores in rat renal tissue and increased blood urea nitrogen (BUN), serum creatinine (Cr), interleukin-1β\u0000 (IL-1β), IL-18, high-sensitivity C-reactive protein (hs-CRP), and caspase-1 levels compared with the SO group. The expression of NLRP3, type III collagen (Col-III), matrix fibronectin (FN), and α-smooth actin (α-SMA) increased (P <0.05). Inflammatory\u0000 cells aggregated in rat kidney tissue, and some renal tubular cells atrophied, fell off, vacuolized, underwent pyknosis, and the shape of tubules was incomplete. The lumen was enlarged, and the DNA damage was greater. The UUO+EPL, UUO+H and UUO+L groups showed increased pathological damage\u0000 score of rat renal tissue and decreased expression levels of Cr, BUN, hs-CRP, IL-1β, IL-18, caspase-1, NLRP3, FN, Col-III, and α-SMA than UUO group. After a longer period, the UUO+EPL and UUO+H groups decreased more significantly than the UUO+L group. We conclude that\u0000 Bushen Huoxue Recipe inhibits RF by regulating reactive oxygen species (ROS)/NLRP3-induced pyroptosis pathway.","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":"43651634","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 assessed the mechanism of BMSC combined with bone transport in improving bone defect. Fifty rats were divided into five sets randomly including NC set, DEX set, BMSC set and BT set. There were ten rats in each set. The BMSC was isolated using whole bone marrow adherent method and then cultivated. The general condition of rats in each set was observed and morphological parameter, pathological change in bone defect tissue was detected along with analysis of the expression of MCP-1, p53, TNF-α and STAT1 in bone tissue. The primary BMSC was cultivated for seven days and the fusiform BMSC was enlarged and the quantity of binucleate or multinucleate cells was increased after passage. The bone defect model was prepared successfully when the degree of fusion reached 100%. The mental condition was good. DEX set showed significantly reduced TBV and increased TRS compared with NC set. However, TBV was increased and TRS was reduced in BMSC set, BT set and BMSC+BT set significantly compared with DEX set. MCP-1 mRNA level in DEX set was lower and increased in the treatment group. In addition, p53, TNF-α and STAT1 was increased in DEX set but reduced in BMSC set, BT set and BMSC+BT set. In conclusion, MCP-1 in rats’ bone defect tissue is upregulated and the p53/TNF-α/STAT1 signal activity is restrained by BMSC combined with bone transport so as to treat the bone defect.
{"title":"Bone Marrow Mesenchymal Stem Cells Combined with Bone Transport Improves Bone Defect in Rats","authors":"Ting Qiu, Chenhuan Wu, Ying Cai","doi":"10.1166/jbt.2023.3242","DOIUrl":"https://doi.org/10.1166/jbt.2023.3242","url":null,"abstract":"This study assessed the mechanism of BMSC combined with bone transport in improving bone defect. Fifty rats were divided into five sets randomly including NC set, DEX set, BMSC set and BT set. There were ten rats in each set. The BMSC was isolated using whole bone marrow adherent method\u0000 and then cultivated. The general condition of rats in each set was observed and morphological parameter, pathological change in bone defect tissue was detected along with analysis of the expression of MCP-1, p53, TNF-α and STAT1 in bone tissue. The primary BMSC was cultivated\u0000 for seven days and the fusiform BMSC was enlarged and the quantity of binucleate or multinucleate cells was increased after passage. The bone defect model was prepared successfully when the degree of fusion reached 100%. The mental condition was good. DEX set showed significantly reduced TBV\u0000 and increased TRS compared with NC set. However, TBV was increased and TRS was reduced in BMSC set, BT set and BMSC+BT set significantly compared with DEX set. MCP-1 mRNA level in DEX set was lower and increased in the treatment group. In addition, p53, TNF-α and STAT1 was increased\u0000 in DEX set but reduced in BMSC set, BT set and BMSC+BT set. In conclusion, MCP-1 in rats’ bone defect tissue is upregulated and the p53/TNF-α/STAT1 signal activity is restrained by BMSC combined with bone transport so as to treat the bone defect.","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":"42961595","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 mechanism of BMSC modified with ADAMTS-1 inhibitor in regulating the myocardial fibrosis in myocarditis through TGFβ1/MMP9/TIMP1 pathway and collagen metabolism. Model of viral myocarditis (VMC) rats was established and then assigned into control set, carrier set, inhibitor set and carrier and inhibitor set randomly followed by analysis of CVF% in atrial tissue, ADAMTS-1 level by RT-PCR and TGFβ1, MMP9 and TIMP1 level by IHC. ADAMTS-1 mRNA level in control set was highest and lowest in inhibitor set. There was fibrosis in every set inordinately. The degree of myocardial fibrosis was reduced in inhibitor set and carrier and inhibitor set. The quantity of inflammatory cells was also reduced significantly. There was no or sporadic mall focal necrosis. The level of TGFβ1, MMP9 and TIMP1 in the treated three sets was significant decreased compared with control set with more significant changes in the inhibitor set and carrier and inhibitor set. Collagen metabolism in VMC rats was restrained by BMSC modified with ADAMTS-1 inhibitor and therefore the myocardial fibrosis was ameliorated with the possible mechanism being through regulation of the TGFβ1/MMP9/TIMP1 signaling pathway.
{"title":"Bone Marrow Mesenchymal Stem Cell Modified with A Disintegrin and Metalloproteinase with Thrombospondin Motifs 1 Inhibitor Regulates Myocardial Fibrosis in Myocarditis","authors":"Kexin Yuan, Peng Qi, Xiao Hao, Qingqing Hao, Pei Zhao","doi":"10.1166/jbt.2023.3244","DOIUrl":"https://doi.org/10.1166/jbt.2023.3244","url":null,"abstract":"This study assesses the mechanism of BMSC modified with ADAMTS-1 inhibitor in regulating the myocardial fibrosis in myocarditis through TGFβ1/MMP9/TIMP1 pathway and collagen metabolism. Model of viral myocarditis (VMC) rats was established and then assigned into control\u0000 set, carrier set, inhibitor set and carrier and inhibitor set randomly followed by analysis of CVF% in atrial tissue, ADAMTS-1 level by RT-PCR and TGFβ1, MMP9 and TIMP1 level by IHC. ADAMTS-1 mRNA level in control set was highest and lowest in inhibitor set. There was fibrosis\u0000 in every set inordinately. The degree of myocardial fibrosis was reduced in inhibitor set and carrier and inhibitor set. The quantity of inflammatory cells was also reduced significantly. There was no or sporadic mall focal necrosis. The level of TGFβ1, MMP9 and TIMP1 in the treated\u0000 three sets was significant decreased compared with control set with more significant changes in the inhibitor set and carrier and inhibitor set. Collagen metabolism in VMC rats was restrained by BMSC modified with ADAMTS-1 inhibitor and therefore the myocardial fibrosis was ameliorated with\u0000 the possible mechanism being through regulation of the TGFβ1/MMP9/TIMP1 signaling pathway.","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":"42883833","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}
Irisin is a cytokine mainly secreted by skeletal muscles, widely distributed in the body with functions of anti-oxidation, anti-inflammation, prevention of reperfusion injury, immune stimulation, and reduction of cerebral infarction. In this study, rats with subarachnoid hemorrhage (SAH) were used as experimental subjects, and irisin was injected intraperitoneally to investigate irisin’s effect on cerebral vasospasm and early brain injury (EBI). After establishment of the animal model of SAH, animals were administered with irisin through intraperitoneal injection. The animal tissues were taken out to assess the morphological changes, and neurons apoptosis by TUNEL staining and Nissl staining. Brain edema score was used to assess the severity of brain injury, and the relationship between related signal pathways was detected by Western blot. Administration of irisin significantly reduced cerebral vasospasm and decreased neuronal apoptosis induced by SAH. Irisin inhibited the apoptosis of prefrontal cortex mitochondrial neurons, and decreased Bax/Bcl-2 and cytochrome C in the cytoplasm. The expressions of PSD-95 and GAP-43 and BDNF in brain tissues were decreased upon SAH, but their expressions were partially restored after treatment with irisin. Irisin decreases neuronal apoptosis and mitochondrial function with up-regulation of synapse proteins, thereby exerting a protective effect on EBI and SAH.
{"title":"Irisin Ameliorates Cerebral Vasospasm and Early Brain Injury in Rats with Experimental Subarachnoid Hemorrhage","authors":"Zhumin Liu, D. Lei","doi":"10.1166/jbt.2023.3257","DOIUrl":"https://doi.org/10.1166/jbt.2023.3257","url":null,"abstract":"Irisin is a cytokine mainly secreted by skeletal muscles, widely distributed in the body with functions of anti-oxidation, anti-inflammation, prevention of reperfusion injury, immune stimulation, and reduction of cerebral infarction. In this study, rats with subarachnoid hemorrhage\u0000 (SAH) were used as experimental subjects, and irisin was injected intraperitoneally to investigate irisin’s effect on cerebral vasospasm and early brain injury (EBI). After establishment of the animal model of SAH, animals were administered with irisin through intraperitoneal injection.\u0000 The animal tissues were taken out to assess the morphological changes, and neurons apoptosis by TUNEL staining and Nissl staining. Brain edema score was used to assess the severity of brain injury, and the relationship between related signal pathways was detected by Western blot. Administration\u0000 of irisin significantly reduced cerebral vasospasm and decreased neuronal apoptosis induced by SAH. Irisin inhibited the apoptosis of prefrontal cortex mitochondrial neurons, and decreased Bax/Bcl-2 and cytochrome C in the cytoplasm. The expressions of PSD-95 and GAP-43 and BDNF in brain tissues\u0000 were decreased upon SAH, but their expressions were partially restored after treatment with irisin. Irisin decreases neuronal apoptosis and mitochondrial function with up-regulation of synapse proteins, thereby exerting a protective effect on EBI and SAH.","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":"49653793","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 miR-663 in the oxidative damage in myocardial cells through regulating BMSC from exosome. BMSC from rats was cultivated and transfected with miR-663 mimics to measure miR-663 level, BMSC proliferation and apoptosis and cTnT level. Exosome in supernatant was collected. The myocardial cells were assigned into control set, damage set and exo-miR-663-BMSC set followed by analysis of cell proliferative and apoptotic activity, miR-663 level, ROS, MDA, SOD and GSH-Px content as well as the expression of Nrf2, keap1 and HO-1. BMSC proliferation was prompted and apoptosis was restrained by miR-663 mimics and BMSC was prompted to be differentiated into myocardial cells. The target gene of miR-663 was keap1. Exo-miR-663-BMSC set showed increased myocardial cell proliferation and decreased apoptosis, reduced ROS and MDA as well as increased SOD and GSH-Px level along with downregulation of keap1 and upregulated of Nrf2 and HO-1. In addition, the recovery of heart injury caused by IRI was significantly prompted by exo-miR-663-BMSC. In conclusion, exo-miR-663 BMSC is capable to ameliorate heart injury induced by IRI.
{"title":"miR-663-Containing Exosomes Secreted by Bone Marrow Mesenchymal Stem Cells Ameliorate Cardiomyocyte Oxidative Damage","authors":"X. Xia, Baoan Xu","doi":"10.1166/jbt.2023.3246","DOIUrl":"https://doi.org/10.1166/jbt.2023.3246","url":null,"abstract":"This study assesses the role of miR-663 in the oxidative damage in myocardial cells through regulating BMSC from exosome. BMSC from rats was cultivated and transfected with miR-663 mimics to measure miR-663 level, BMSC proliferation and apoptosis and cTnT level. Exosome in supernatant\u0000 was collected. The myocardial cells were assigned into control set, damage set and exo-miR-663-BMSC set followed by analysis of cell proliferative and apoptotic activity, miR-663 level, ROS, MDA, SOD and GSH-Px content as well as the expression of Nrf2, keap1 and HO-1. BMSC proliferation was\u0000 prompted and apoptosis was restrained by miR-663 mimics and BMSC was prompted to be differentiated into myocardial cells. The target gene of miR-663 was keap1. Exo-miR-663-BMSC set showed increased myocardial cell proliferation and decreased apoptosis, reduced ROS and MDA as well as increased\u0000 SOD and GSH-Px level along with downregulation of keap1 and upregulated of Nrf2 and HO-1. In addition, the recovery of heart injury caused by IRI was significantly prompted by exo-miR-663-BMSC. In conclusion, exo-miR-663 BMSC is capable to ameliorate heart injury induced by IRI.","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":"49388722","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}
Glioblastoma (GBM) is the most frequently identified malignancy of the brain. Due to the special tumor location, it is extremely urgent to explore key genes involved in the pathogenesis of GBM. In this study, we tried to identify vital genes that participate in the GBM progression by analyzing TCGA-sourced transcriptome data and identified 3183 differentially expressed genes (DEGs). Meanwhile, we also observed that CRYGN, MICAL2, BICDL1, PLK2, MTHFD2, OSMR, COL22A1, MSTN, and G0S2 expressions were significantly associated with patients’ survival. Immune infiltration analysis indicated that eight genes enhanced the immune infiltration in GBM, while BICDL1 had no significant effect. In conclusion, our study demonstrates that the eight genes are potential key genes involved in GBM and significantly connected to patients’ prognosis.
{"title":"Identification of Key Genes Involved in Glioblastoma by Integrated Bioinformatics Analysis","authors":"Dongke Yan, Yanchao Gong, Yongling Wang, Longmei Li, Wenhui Tong, Jingjie Pang","doi":"10.1166/jbt.2023.3251","DOIUrl":"https://doi.org/10.1166/jbt.2023.3251","url":null,"abstract":"Glioblastoma (GBM) is the most frequently identified malignancy of the brain. Due to the special tumor location, it is extremely urgent to explore key genes involved in the pathogenesis of GBM. In this study, we tried to identify vital genes that participate in the GBM progression by\u0000 analyzing TCGA-sourced transcriptome data and identified 3183 differentially expressed genes (DEGs). Meanwhile, we also observed that CRYGN, MICAL2, BICDL1, PLK2, MTHFD2, OSMR, COL22A1, MSTN, and G0S2 expressions were significantly associated with patients’ survival. Immune infiltration\u0000 analysis indicated that eight genes enhanced the immune infiltration in GBM, while BICDL1 had no significant effect. In conclusion, our study demonstrates that the eight genes are potential key genes involved in GBM and significantly connected to patients’ prognosis.","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":"48535947","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 intends to assess whether BMSCs inhibits inflammation and promotes chondrocyte activity in knee arthritis. 36 SD rats were randomly assigned into group H, group K, group M and group B. The rat models of knee arthritis were established in Group K, group M and group B. After modeling, BMSCs were infused into rats in group B and methotrexate to rats in group M for 6 weeks followed by analysis of TNF-α, IL-6 and IL-1 levels, morphology of knee cartilage, chondrocyte activity and the expression of NO, ERα and cGMP protein. H&E staining found that the surface of knee cartilage in group H was smooth and the morphology of chondrocytes was normal. In group K, bone fissure was formed on articular cartilage surface, and the hyperplasia of deep cells was disorder. The surface of articular cartilage in group B and M gradually became smooth. Compared to group H, TNF-α, IL-6 and IL-1 levels in group K were increased (P < 0.05); their levels in group M and group B were decreased relative to K group (P < 0.05). Compared to group K, chondrocytes activity in groups H, M and B was increased (P < 0.05). NO, ERα and cGMP levels were decreased in knee cartilage of group K relative to H group (P < 0.05) and increased in group M and group B (P < 0.05). In conclusion, BMSCs can down-regulate IL-6, IL-1 and TNF-α, enhance chondrocytes activity, and up-regulate the levels of NO, ERα and cGMP, thus providing a new idea for treating knee arthritis.
{"title":"Bone Marrow Mesenchymal Stem Cells Inhibits Inflammation and Promotes Chondrocyte Activity in Knee Arthritis Rats","authors":"Hua Huang, Yang‐xiong Zhu, Sining Li","doi":"10.1166/jbt.2023.3245","DOIUrl":"https://doi.org/10.1166/jbt.2023.3245","url":null,"abstract":"This study intends to assess whether BMSCs inhibits inflammation and promotes chondrocyte activity in knee arthritis. 36 SD rats were randomly assigned into group H, group K, group M and group B. The rat models of knee arthritis were established in Group K, group M and group B. After\u0000 modeling, BMSCs were infused into rats in group B and methotrexate to rats in group M for 6 weeks followed by analysis of TNF-α, IL-6 and IL-1 levels, morphology of knee cartilage, chondrocyte activity and the expression of NO, ERα and cGMP protein. H&E staining\u0000 found that the surface of knee cartilage in group H was smooth and the morphology of chondrocytes was normal. In group K, bone fissure was formed on articular cartilage surface, and the hyperplasia of deep cells was disorder. The surface of articular cartilage in group B and M gradually became\u0000 smooth. Compared to group H, TNF-α, IL-6 and IL-1 levels in group K were increased (P < 0.05); their levels in group M and group B were decreased relative to K group (P < 0.05). Compared to group K, chondrocytes activity in groups H, M and B was increased (P\u0000 < 0.05). NO, ERα and cGMP levels were decreased in knee cartilage of group K relative to H group (P < 0.05) and increased in group M and group B (P < 0.05). In conclusion, BMSCs can down-regulate IL-6, IL-1 and TNF-α, enhance chondrocytes activity,\u0000 and up-regulate the levels of NO, ERα and cGMP, thus providing a new idea for treating knee arthritis.","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":"45003746","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}
Ying Liu, Linyuan Feng, Yang Yang, Zhenhua Lin, Wen-zheng Jiang
Background: To explore expression and immune infiltration of SPARC/osteonectin, cwcv, and maze-like domains proteoglycan 1 (SPOCK1) in Head and Neck squamous cell carcinoma. Methods: A total of 107 HNSC patients’ tissues and 15 adjacent normal tissues were collected in this study. Co-expressed gene and gene set enrichment analysis was detected using STRING and Linked Omics. Immune cell infiltration related to SPOCK1 was analyzed via TIMER. Results: The positive rate of SPOCK1 in HNSC tissues were significantly higher than that in normal tissues by immunohistochemical staining (p< 0.01). The expression of SPOCK1 in HNSC was a positive correlation with the level of immune infiltrating cells. In addition, we discovered that SPOCK1 was major involved in inflammatory response pathways, cancer cell proliferation regulation, cell cycle regulation, apoptosis, adhesion, cell-matrix interaction, etc. Conclusions: SPOCK1 plays a role in promoting cancer in HNSC, which was closely related to the malignant evolution of HNSC, and it was expected to become a prognostic molecular marker for HNSC patients and a potential target for immunotherapy.
{"title":"SPOCK1 is a Prognostic-Related Biomarker and Correlated with Immune Infiltrates in Head and Neck Squamous Cell Carcinoma","authors":"Ying Liu, Linyuan Feng, Yang Yang, Zhenhua Lin, Wen-zheng Jiang","doi":"10.1166/jbt.2023.3256","DOIUrl":"https://doi.org/10.1166/jbt.2023.3256","url":null,"abstract":"Background: To explore expression and immune infiltration of SPARC/osteonectin, cwcv, and maze-like domains proteoglycan 1 (SPOCK1) in Head and Neck squamous cell carcinoma. Methods: A total of 107 HNSC patients’ tissues and 15 adjacent normal tissues were collected\u0000 in this study. Co-expressed gene and gene set enrichment analysis was detected using STRING and Linked Omics. Immune cell infiltration related to SPOCK1 was analyzed via TIMER. Results: The positive rate of SPOCK1 in HNSC tissues were significantly higher than that in normal tissues\u0000 by immunohistochemical staining (p< 0.01). The expression of SPOCK1 in HNSC was a positive correlation with the level of immune infiltrating cells. In addition, we discovered that SPOCK1 was major involved in inflammatory response pathways, cancer cell proliferation regulation, cell\u0000 cycle regulation, apoptosis, adhesion, cell-matrix interaction, etc. Conclusions: SPOCK1 plays a role in promoting cancer in HNSC, which was closely related to the malignant evolution of HNSC, and it was expected to become a prognostic molecular marker for HNSC patients and a potential\u0000 target for immunotherapy.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":"1 1","pages":""},"PeriodicalIF":0.1,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64485634","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 role and potential mechanism of TIMP1 in resistance to 5-Fluorouracil (5-Fu) and stem properties in gastric cancer (GC) were investigated. The expressions of HIF-1α and TIMP1, as well as the chemosensitivity of the 5-Fu in GC cell lines (GCCL) (e.g., MGC-803, BGC-823, SGC-7901, HGC-27 and AGS) upon normoxia or hypoxia were analyzed by means of RT-PCR and CCK-8 assay, respectively. Meanwhile, the population of stem cells was determined by using sphere formation assay, while stem cell markers (SCM) (Oct4 and CD44) were detected by western blot to evaluate stem properties. Hypoxia led to upregulated expression of HIF-1α and TIMP1, and enhanced resistance to 5-Fu, sphere formation capability, and expression of SCM in GC cells (GCCs). Indeed, the expressions of TIMP1 and HIF-1α were positively related to each other. The protein levels of both HIF-1α and TIMP1 were increased and decreased by overexpressing and silencing TIMP1, respectively. Under hypoxia conditions, overexpression of TIMP1 conferred 5-Fu-resistance and stem properties to MGC-803 and AGS cells, as revealed by increased IC50 value of 5-Fu, enhanced sphere formation, and up-regulation of Oct4 and CD44; silencing TIMP1 caused the contrary results. TIMP1 is an effective regulator of HIF-1 and plays a critical role in resistance to 5-Fu and stem properties in GCCs upon hypoxia.
{"title":"Tissue Inhibitors of Metalloproteinases 1 Confers 5-Fluorouracil Resistance and Stemness of Gastric Cancer Cells via the Up-Regulation of Hypoxia-Inducible Factor-1α","authors":"Jinxia Jiang, Xiaogu He, Fen Shuang, Xiangming Fang, Feng Zhu","doi":"10.1166/jbt.2023.3240","DOIUrl":"https://doi.org/10.1166/jbt.2023.3240","url":null,"abstract":"The role and potential mechanism of TIMP1 in resistance to 5-Fluorouracil (5-Fu) and stem properties in gastric cancer (GC) were investigated. The expressions of HIF-1α and TIMP1, as well as the chemosensitivity of the 5-Fu in GC cell lines (GCCL) (e.g., MGC-803, BGC-823,\u0000 SGC-7901, HGC-27 and AGS) upon normoxia or hypoxia were analyzed by means of RT-PCR and CCK-8 assay, respectively. Meanwhile, the population of stem cells was determined by using sphere formation assay, while stem cell markers (SCM) (Oct4 and CD44) were detected by western blot to evaluate\u0000 stem properties. Hypoxia led to upregulated expression of HIF-1α and TIMP1, and enhanced resistance to 5-Fu, sphere formation capability, and expression of SCM in GC cells (GCCs). Indeed, the expressions of TIMP1 and HIF-1α were positively related to each other. The\u0000 protein levels of both HIF-1α and TIMP1 were increased and decreased by overexpressing and silencing TIMP1, respectively. Under hypoxia conditions, overexpression of TIMP1 conferred 5-Fu-resistance and stem properties to MGC-803 and AGS cells, as revealed by increased IC50 value\u0000 of 5-Fu, enhanced sphere formation, and up-regulation of Oct4 and CD44; silencing TIMP1 caused the contrary results. TIMP1 is an effective regulator of HIF-1 and plays a critical role in resistance to 5-Fu and stem properties in GCCs upon hypoxia.","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":"43953419","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：