scholarly journals Circular RNA ciRs-126 promotes hypoxia/reoxygenation cardiac injury possibly through miR-21

2022 ◽  
Vol 20 (1) ◽  
Author(s):  
Changming Tan ◽  
Jianming Li ◽  
Zhaoshun Yuan ◽  
Yongxin Mu
Keyword(s):  
Cell Apoptosis ◽  
Cardiac Injury ◽  
Circular Rna ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Inhibitory Effects ◽  
Apoptosis Assay ◽  
Induced Apoptosis ◽  
Hypoxia Reoxygenation

Abstract Background This study aimed to analyze the role of circular RNA ciRs-126 in hypoxia/reoxygenation cardiac injury (H/R). Methods Expression of ciRs-126 and miR-21 in plasma samples from patients with H/R and healthy controls was determined by RT-qPCR. Correlations were analyzed by linear regression. Overexpression of ciRs-126 and miR-21 was achieved in cardiomyocytes to explore their crosstalk. The roles of ciRs-126 and miR-21 in H/R-induced apoptosis of cardiomyocytes were analyzed using cell apoptosis assay. Results CiRs-126 was upregulated and miR-21 was downregulated in H/R patients. They were inversely correlated across plasma samples from H/R patients. In H/R cardiomyocytes, ciRs-126 was upregulated and miR-21 was downregulated. In cardiomyocytes, ciRs-126 overexpression decreased miR-21 level and reduced the inhibitory effects of miR-21 overexpression on H/R-induced cell apoptosis. Conclusions Circular RNA ciRs-126 may suppress miR-21 expression to promote H/R cardiac injury.

scholarly journals Circular RNA circFADS2 is overexpressed in sepsis and suppresses LPS-induced lung cell apoptosis by inhibiting the maturation of miR-15a-5p

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xiaoyang Hong ◽  
Shuanglei Li ◽  
Jie Wang ◽  
Zhe Zhao ◽  
Zhichun Feng
Keyword(s):  
Cell Apoptosis ◽  
Expression Vector ◽  
Circular Rna ◽  
Lung Cells ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Apoptosis Assay ◽  
Induced Apoptosis ◽  
Lps Treatment

Abstract Background Circular RNA circFADS2 plays protective roles in LPS-induced inflammation, which promotes sepsis, suggesting its involvement in sepsis. Methods Expression of circFADS2, mature miR-15a-5p, and miR-15a-5p precursor in plasma samples from sepsis patients and healthy controls was determined by RT-qPCR. The circFADS2 expression vector was transfected in lung cells, followed by the measurement of the expression levels of mature miR-15a-5p and miR-15a-5p precursor to study the role of circFADS2 in miR-15a-5p maturation. Cell apoptosis was analyzed by cell apoptosis assay. Results CircFADS2 was upregulated in sepsis and inversely correlated with mature miR-15a-5p, but not miR-15a-5p precursor. In lung cells, circFADS2 overexpression decreased the level of mature miR-15a-5p, but not miR-15a-5p precursor. LPS treatment decreased miR-15a-5p expression and increased circFADS2 level. Cell apoptosis analysis showed that circFADS2 overexpression reduced miR-15a-5p overexpression-induced apoptosis of LPS-treated lung cells. Conclusions CircFADS2 is upregulated in sepsis to suppress LPS-induced lung cell apoptosis by inhibiting miR-15a-5p maturation.

Circular RNA circZNF652 is overexpressed in osteoarthritis and positively regulates LPS-induced apoptosis of chondrocytes by upregulating PTEN

2020 ◽  
Author(s):  
Xuefeng Yuan ◽  
Yingchi Zhang ◽  
Cong Cai ◽  
Chaoxu Liu ◽  
Jie Xie ◽  
...  
Keyword(s):  
Synovial Fluid ◽  
Cell Apoptosis ◽  
Circular Rna ◽  
Healthy Controls ◽  
Inhibitory Effects ◽  
Pten Mrna ◽  
Apoptosis Assay ◽  
Sirna Silencing ◽  
Induced Apoptosis

Abstract Background Circular RNA circZNF652 promotes LPS-induced inflammation, which contributes to the development of osteoarthritis (OA), indicating the potential involvement of CRNDE in OA. This study was carried to explore the involvement of circZNF652 in OA. Methods RT-qPCR was performed to analyze the expression of circZNF652 and PTEN mRNA in synovial fluid samples from 60 OA patients and 60 healthy controls. Correlations between circZNF652 and PTEN mRNA were analyzed by Pearson’s correlation coefficient. Overexpression and siRNA silencing of circZNF652 were achieved in chondrocytes, followed by performing RT-qPCR and Western blot to analyze the expression of PTEN. The role of circZNF652 and PTEN in regulating the apoptosis of chondrocytes induced by LPS was analyzed by cell apoptosis assay. Results We found that circZNF652 was overexpressed in OA and positively correlated with PTEN mRNA. In chondrocytes, circZNF652 overexpression increased the expression of PTEN, and circZNF652 siRNA silencing decreased the expression of PTEN. Moreover, circZNF652 and PTEN positively regulated the apoptosis of chondrocytes induced by LPS. PTEN overexpression reversed the inhibitory effects of circZNF652 siRNA silencing on cell apoptosis. Conclusion CircZNF652E is overexpressed in OA and positively regulates LPS-induced apoptosis of chondrocytes by upregulating PTEN.

Overexpression of lncRNA MCM3AP-AS1 in Sepsis Suppresses the Maturation of miR-223 to Promote LPS-induced Lung Cells

2020 ◽  
Author(s):  
Chunzhi Gong ◽  
Jianying Wang ◽  
Shupeng Liu ◽  
Zunfeng Li ◽  
Zhaoguo Liu ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Lung Cells ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Inhibitory Effects ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Apoptosis Assay ◽  
Induced Apoptosis ◽  
Lps Treatment

Abstract Background: Previous studies have showed that lncRNA MCM3AP-AS1 and miR-223 play opposite roles in LPS-induced inflammation, which contributes to the progression of sepsis. This study was therefore carried out to analyze the interactions between MCM3AP-AS1 and miR-223 in sepsis. Methods: Plasma samples were obtained from 62 sepsis patients and 62 healthy controls. Expression of MCM3AP-AS1, miR-223 precursor and mature miR-223 in plasma samples was determined by RT-qPCR. In human bronchial epithelial cells (HBEpCs), the interaction between MCM3AP-AS1 and miR-223 was analyzed by overexpression experiments. Cell apoptosis assay was analyzed by cell apoptosis assay.Results: We found that MCM3AP-AS1 was upregulated in sepsis, while miR-223 was downregulated in sepsis. MCM3AP-AS1 and mature miR-223 were inversely correlated, while MCM3AP-AS1 and miR-223 precursor were not. In HBEpCs, LPS treatment resulted in the upregulation of MCM3AP-AS1 and downregulation of miR-223. In HBEpCs, MCM3AP-AS1 overexpression downregulated mature miR-223 but failed to affect miR-223 precursor. In addition, MCM3AP-AS1 overexpression reduced the inhibitory effects of miR-223 on LPS-induced apoptosis of HBEpCs.Conclusions: LncRNA MCM3AP-AS1 is upregulated in sepsis and may suppress the maturation of miR-223 to promote LPS-induced lung cells.

scholarly journals CircRNA circFADS2 is Downregulated in Osteoporosis and Suppresses LPS-induced Apoptosis of Osteoblast by Downregulating miR-16-5p

2020 ◽  
Author(s):  
Hailong Zhou ◽  
Jianmin Jiang ◽  
Xiaohua Chen ◽  
Zhiwei Zhang
Keyword(s):  
Correlation Coefficient ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Apoptosis Assay ◽  
Primary Osteoblasts ◽  
Induced Apoptosis ◽  
Lps Treatment

Abstract Background: CircRNA circFADS2 plays protective roles in LPS-induced cell injury, which promotes osteoporosis (OS), suggesting the involvement of circFADS2 in OS. This study aimed to explore the role of circFADS2 in OS.Methods: RT-qPCRs were performed to analyze the expression of circFADS2 and miR-16-5p in plasma samples from OS patients (n=64) and healthy controls (n=64). Correlations between circFADS2 and miR-16-5p were explored by Pearson’s correlation coefficient. In primary osteoblasts, circFADS2 and miR-16-5p were overexpressed to study the interactions between them. Cell apoptosis assay was performed to study the functions of circFADS2 and miR-16-5p in the apoptosis of osteoblasts induced by LPS.Results: CircFADS2 was downregulated in OA and inversely correlated with miR-16-5p. After treatment, circFADS2 was upregulated and miR-16-5p was downregulated. In osteoblasts, LPS treatment decreased the expression of circFADS2 but increased the expression of miR-16-5p. Overexpression of circFADS2 decreased the expression of miR-16-5p. Cell apoptosis analysis showed that circFADS2 overexpression reduced the apoptosis of osteoblasts under LPS-treatment, while miR-16-5p overexpression increased cell apoptosis. Moreover, overexpression of miR-16-5p reduced the effects of circFADS2 overexpression on the apoptosis of osteoblasts. Conclusion: Therefore, CircFADS2 is downregulated in OS and promotes LPS-induced apoptosis of osteoblast by downregulating miR-16-5p.

Circular RNA circFADS2 is Overexpressed in Sepsis and Suppresses LPS-Induced Lung Cell Apoptosis by Inhibiting the Maturation of miR-15a-5p

2020 ◽  
Author(s):  
Xiaoyang Hong ◽  
Shuanglei Li ◽  
Jie Wang ◽  
Zhe Zhao ◽  
Zhichun Feng
Keyword(s):  
Cell Apoptosis ◽  
Expression Vector ◽  
Circular Rna ◽  
Lung Cells ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Expression Levels ◽  
Time Points ◽  
Lps Treatment

Abstract Circular RNA circFADS2 plays protective roles in LPS-induced inflammation, which promotes sepsis, suggesting its involvement of circFADS2 in sepsis. We then analysis the involvement of circFADS2 in LOS Expression of circFADS2, mature miR-15a-5p and miR-15a-5p precursor in plasma samples (collected at two time points) from sepsis patients (n=60) and healthy controls (n=60) was determined by RT-qPCR. The expression vector of circFADS2 was transfected in lung cells, followed by the measurement of the expression levels of mature miR-15a-5p and miR-15a-5p precursor to study the role of circFADS2 in the maturation of miR-15a-5p. Cell apoptosis was analyzed by cell apoptosis assay.CircFADS2 was upregulated in sepsis and inversely correlated with mature miR-15a-5p, but not miR-15a-5p precursor. In lung cells, overexpression of circFADS2` decreased the levels of mature miR-15a-5p expression, but not miR-15a-5p precursor. LPS treatment decreased the expression levels of miR-15a-5p, and increased the expression levels of circFADS2. Cell apoptosis analysis showed that circFADS2 overexpression reduced the enhancing effects of miR-15a-5p overexpression on the apoptosis of lung cells induced by LPS.Therefore, circFADS2 is upregulated in sepsis and suppresses LPS-induced lung cell apoptosis by inhibiting the maturation of miR‑15a‑5p.

scholarly journals CircRNA MFACR is Upregulated in Myocardial Infarction and Downregulates miR-125b to Promote Cardiomyocyte Apoptosis-induced by Hypoxia

2020 ◽  
Author(s):  
Shujuan Wang ◽  
Long Li ◽  
Weijie Deng ◽  
Minhua Jiang
Keyword(s):  
Myocardial Infarction ◽  
Cell Apoptosis ◽  
Cardiomyocyte Apoptosis ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Methylation Specific Pcr ◽  
Specific Pcr ◽  
Apoptosis Assay ◽  
Hypoxia Treatment

Abstract Background: CircRNA MFACR promotes cardiomyocyte death, which contributes to myocardial infarction (MI). We analyzed the role of MFACR in MI.Methods: RT-qPCR was applied to determine MFACR and miR-125b expression in plasma samples from both MI patients (n=61) and healthy controls (n=61). MFACR and miR-125b were overexpressed in AC16 cells (cardiomyocytes) to study the interactions between them. Methylation of miR-125b gene in cells with MFACR overexpression was analyzed by methylation-specific PCR. Cell apoptosis after transfections was analyzed by cell apoptosis assay.Results: MFACR was overexpressed in MI and inversely correlated with miR-125b. In AC16 cells, hypoxia treatment increased MFACR expression and decreased miR-125b expression. In AC16 cells, MFACR overexpression decreased miR-125b expression and increased the methylation of miR-125b gene. Under hypoxia, MFACR overexpression increased AC16 cell apoptosis, and miR-125b overexpression decreased cell apoptosis. In addition, miR-125b overexpression reversed the effects of MFACR overexpression on cell apoptosis. Conclusion: MFACR may increase the methylation of miR-125b gene to downregulate its expression, thereby promoting the apoptosis of cardiomyocytes in MI.

scholarly journals CircRNA ACAP2 is Overexpressed in Myocardial Infarction and Promotes the Maturation of miR-532 to Induce the Apoptosis of Cardiomyocyte

2020 ◽  
Author(s):  
Jun Zhang ◽  
Yanrong Tang ◽  
Jing Zhang ◽  
Jing Wang ◽  
Jiyun He ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Correlation Coefficient ◽  
Cell Apoptosis ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Pearson’S Correlation Coefficient ◽  
Apoptosis Assay ◽  
Pearson's Correlation ◽  
Hypoxia Treatment

Abstract Background: CircRNA ACAP2 and miR-532 both promotes the apoptosis of cardiomyocytes, which contributes to myocardial infarction (MI). Therefore, ACAP2 and miR-532 may interact with each other to participate in MI. Method: Plasma samples from both MI patients (n=65) and healthy controls (n=65) were subjected to RNA extractions and RT-qPCR to analyze the expression of ACAP2, mature miR-532 and premature miR-532. Correlations among them were analyzed by Pearson’s correlation coefficient. Expression of both mature miR-532 and premature miR-532 in cardiomyocytes with ACAP2 overexpression was analyzed by RT-qPCR to study the effects of ACAP2 overexpression on the maturation of miR-532. The role of ACAP2 and miR-532 in regulating the apoptosis of cardiomyocytes induced by hypoxia was analyzed by cell apoptosis assay.Results: In this study we found that ACAP2 and mature miR-532 were both upregulated in plasma from MI patients. ACAP2 and mature miR-532 were inversely correlated, while ACAP2 and premature miR-532 were not closely correlated. In cardiomyocytes, overexpression of ACAP2 decreased the expression of mature miR-532, but not premature miR-532. Cell apoptosis analysis showed that ACAP2 and miR-532 overexpression promoted the apoptosis of cardiomyocytes induced by hypoxia treatment. In addition, miR-532 inhibitor reduced the effects of ACAP2 overexpression. Conclusion: Therefore, ACAP2 is overexpressed in MI and may promote the maturation of miR-532 to induce the apoptosis of cardiomyocyte.

scholarly journals Circular RNA circCTNNA1 is downregulated in osteoarthritis and sponges miR-29a to suppress LPS-induced apoptosis of synoviocytes

2021 ◽  
Author(s):  
Wei Liu ◽  
Haolong Yang ◽  
Xingyu Feng ◽  
Jing Song ◽  
Wei Zhong
Keyword(s):  
Synovial Fluid ◽  
Cell Apoptosis ◽  
Cancer Biology ◽  
Direct Interaction ◽  
Circular Rna ◽  
Human Diseases ◽  
Apoptosis Assay ◽  
Induced Apoptosis

Abstract Introduction: CircRNA circCTNNA1 has been characterized as a critical player in cancer biology, while its role in other human diseases is unknown. This study was carried out to study the role of circCTNNA1 in osteoarthritis (OA). Materials and Methods: OA patients (n = 62) were subjected to extraction of synovial fluid, followed by performing RT-qPCRs to determine the expression of circCTNNA1 and miR-29a. The interaction between circCTNNA1 and miR-29a was predicted by IntaRNA 2.0 and confirmed by RNA pull-down assay. In synoviocytes, overexpression of circCTNNA1 and miR-29a was achieved, followed by performing RT-qPCRs to analyze the crosstalk between them. The role of circCTNNA1 and miR-29a in regulating the apoptosis of synoviocytes was explored by cell apoptosis assay. Results: CircCTNNA1 was downregulated in OA, while miR-29a was overexpressed in OA. CircCTNNA1 and miR-29a were not significantly correlated. RNA pull-down assay illustrated the direct interaction between circCTNNA1 and miR-29a. In synoviocytes, overexpression of circCTNNA1 and miR-29a failed to regulate the expression of each other. CircCTNNA1 overexpression suppressed the enhancing effects of miR-29a overexpression on cell apoptosis induced by LPS. Conclusion: Therefore, circCTNNA1 is downregulates in OA and its overexpression suppresses the apoptosis of synoviocytes by sponging miR-29a.

scholarly journals CircRNA MFACR is Upregulated in Myocardial Infarction and Downregulates miR-125b to Promote Cardiomyocyte Apoptosis-induced by Hypoxia

2020 ◽  
Author(s):  
Shujuan Wang ◽  
Long Li ◽  
Weijie Deng ◽  
Minhua Jiang
Keyword(s):  
Myocardial Infarction ◽  
Cell Apoptosis ◽  
Cardiomyocyte Apoptosis ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Methylation Specific Pcr ◽  
Specific Pcr ◽  
Apoptosis Assay ◽  
Hypoxia Treatment

Abstract Background：CircRNA MFACR promotes cardiomyocyte death, which contributes to myocardial infarction (MI). This study was carried out to explore the involvement of MFACR in MI.RT-qPCRs were performed to analyze the expression of MFACR and miR-125b in plasma samples from both MI patients (n=61) and healthy controls (n=61). MFACR and miR-125b were overexpressed in AC16 cells (cardiomyocytes) to study the interactions between them. The role of MFACR in regulating the methylation of miR-125b gene was analyzed by methylation-specific PCR. Cell apoptosis after transfections was analyzed by cell apoptosis assay.Result ：MFACR was overexpressed in MI and inversely correlated with miR-125b. In AC16 cells, hypoxia treatment increased MFACR expression and decreased miR-125b expression. In AC16 cells, MFACR overexpression decreased miR-125b expression and increased the methylation of miR-125b gene. Under hypoxia, MFACR overexpression increased AC16 cell apoptosis, and miR-125b overexpression decreased cell apoptosis. In addition, miR-125b overexpression reversed the effects of MFACR overexpression on cell apoptosis.Conclusions： MFACR may downregulate miR-125b through methylation to promote the apoptosis of cardiomyocytes in MI.

scholarly journals CircRNA circFADS2 is Under-expressed in Sepsis and Protects Lung Cell From LPS-induced Apoptosis by Downregulating miR-133a

2020 ◽  
Author(s):  
Fang Niu ◽  
Xiaofeng Liang ◽  
Jindi Ni ◽  
Zhuye Xia ◽  
Lijing Jiang ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Inverse Correlation ◽  
Lung Cells ◽  
Healthy Controls ◽  
Apoptosis Assay ◽  
Induced Apoptosis ◽  
Lps Treatment

Abstract Background: It has been reported that circFADS2 and miR-133a play opposite roles in LPS-induced cell apoptosis, which contributes to the development of sepsis. This study was carried out to explore the interaction between circFADS2 and miR-133a in sepsis. Methods: Expression of circFADS2 and miR-133a in plasma from both sepsis patients (n=62) and healthy controls (n=62) was studied by RT-qPCR. The effects of LPS on the expression of circFADS2 and miR-133a were also analyzed by RT-qPCR. The crosstalk between circFADS2 and miR-133a was analyzed by overexpression, followed by RT-qPCR. The role of circFADS2 and miR-133a in regulating the apoptosis of lung cells induced by LPS was analyzed by cell apoptosis assay.Results: We found that circFADS2 was under-expressed in sepsis and miR-133a was overexpressed in sepsis. An inverse correlation between circFADS2 and miR-133a was observed across sepsis samples. In lung cells, LPS treatment decreased the expression of circFADS2 and increased the expression of miR-133a. In lung cells, circFADS2 overexpression decreased the expression of miR-133a. Moreover, circFADS2 overexpression reduced the enhancing effects of miR-133a overexpression on cell apoptosis induced by LPS. Conclusion: Therefore, circFADS2 is under-expressed in sepsis and may protect lung cell from LPS-induced apoptosis by downregulating miR-133a.

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