CTGF (结缔组织生长因子)和TGF-β1 (转化生长因子-β1)是两种具有广泛生物学活性的细胞信号分子,参与细胞增殖、迁移、分化及细胞外基质的合成与沉积,尤其在纤维化过程中起重要作用。TGF-β1是CTGF表达的最强诱导剂之一,两者在多种病...CTGF (结缔组织生长因子)和TGF-β1 (转化生长因子-β1)是两种具有广泛生物学活性的细胞信号分子,参与细胞增殖、迁移、分化及细胞外基质的合成与沉积,尤其在纤维化过程中起重要作用。TGF-β1是CTGF表达的最强诱导剂之一,两者在多种病理过程中表现出协同作用。目前,已有大量研究表明两者在心肌纤维化中起到关键作用。同时多项研究表明,血清CTGF和TGF-β1水平与冠状动脉粥样硬化的发展进程存在密切关系,可为临床提供更敏感的疾病评估指标。其与冠状动脉病变复杂及严重程度的相关性,一直作为近年来学者的研究热点。非ST段抬高急性冠状动脉(冠脉)综合征(non-ST segment elevation acute coronary syndrome, NSTE-ACS)的核心病理机制为冠状动脉粥样病变基础上继发血栓形成和/或痉挛。临床上NSTE-ACS患者在冠状动脉狭窄基础上,往往同时伴有弥漫性多支血管病变。本文旨在分析NSTE-ACS患者中CTGF和TGF-β1水平与SYNTAX评分之间的相关性并进行比较。CTGF (connective tissue growth factor) and TGF-β1 (transforming growth factor-β1) are two cell signaling molecules with extensive biological activities, participating in cell proliferation, migration, differentiation, and the synthesis and deposition of extracellular matrix, especially playing a significant role in the process of fibrosis. TGF-β1 is one of the strongest inducers of CTGF expression, and the two exhibit a synergistic effect in various pathological processes. Currently, numerous studies have demonstrated that they play a crucial role in myocardial fibrosis. Meanwhile, multiple studies have shown that the levels of serum CTGF and TGF-β1 are closely related to the development process of coronary atherosclerosis, providing more sensitive disease assessment indicators for clinical practice. The correlation between them and the complexity and severity of coronary artery lesions has been a research hotspot in recent years. The core pathological mechanism of non-ST segment elevation acute coronary syndrome (NSTE-ACS) lies in the secondary thrombosis and/or spasm on the basis of coronary atherosclerotic lesions. Clinically, patients with NSTE-ACS often have diffuse multi-vessel lesions in addition to coronary artery stenosis. This article aims to analyze and compare the correlation between the levels of CTGF and TGF-β1 and the SYNTAX score in patients with NSTE-ACS.展开更多
Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whe...Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.展开更多
文摘CTGF (结缔组织生长因子)和TGF-β1 (转化生长因子-β1)是两种具有广泛生物学活性的细胞信号分子,参与细胞增殖、迁移、分化及细胞外基质的合成与沉积,尤其在纤维化过程中起重要作用。TGF-β1是CTGF表达的最强诱导剂之一,两者在多种病理过程中表现出协同作用。目前,已有大量研究表明两者在心肌纤维化中起到关键作用。同时多项研究表明,血清CTGF和TGF-β1水平与冠状动脉粥样硬化的发展进程存在密切关系,可为临床提供更敏感的疾病评估指标。其与冠状动脉病变复杂及严重程度的相关性,一直作为近年来学者的研究热点。非ST段抬高急性冠状动脉(冠脉)综合征(non-ST segment elevation acute coronary syndrome, NSTE-ACS)的核心病理机制为冠状动脉粥样病变基础上继发血栓形成和/或痉挛。临床上NSTE-ACS患者在冠状动脉狭窄基础上,往往同时伴有弥漫性多支血管病变。本文旨在分析NSTE-ACS患者中CTGF和TGF-β1水平与SYNTAX评分之间的相关性并进行比较。CTGF (connective tissue growth factor) and TGF-β1 (transforming growth factor-β1) are two cell signaling molecules with extensive biological activities, participating in cell proliferation, migration, differentiation, and the synthesis and deposition of extracellular matrix, especially playing a significant role in the process of fibrosis. TGF-β1 is one of the strongest inducers of CTGF expression, and the two exhibit a synergistic effect in various pathological processes. Currently, numerous studies have demonstrated that they play a crucial role in myocardial fibrosis. Meanwhile, multiple studies have shown that the levels of serum CTGF and TGF-β1 are closely related to the development process of coronary atherosclerosis, providing more sensitive disease assessment indicators for clinical practice. The correlation between them and the complexity and severity of coronary artery lesions has been a research hotspot in recent years. The core pathological mechanism of non-ST segment elevation acute coronary syndrome (NSTE-ACS) lies in the secondary thrombosis and/or spasm on the basis of coronary atherosclerotic lesions. Clinically, patients with NSTE-ACS often have diffuse multi-vessel lesions in addition to coronary artery stenosis. This article aims to analyze and compare the correlation between the levels of CTGF and TGF-β1 and the SYNTAX score in patients with NSTE-ACS.
基金This work was supported by the Hunan Provincial Education Department General Project Research Fund(No.20C1412)the Hunan Graduate Scientific Research Innovation Project(No.CX2018B474)the National Famous Elderly Chinese Medicine Experts Xinyu Chen Inheritance Workshop Construction Project(No.[2022]75).
文摘Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.
