CircDiaph3 aggravates H/R-induced cardiomyocyte apoptosis and inflammation through miR-338-3p/SRSF1 axis DOI Creative Commons
Lin Lin, Li Wang, Aimin Li

et al.

Journal of Bioenergetics and Biomembranes, Journal Year: 2024, Volume and Issue: 56(3), P. 235 - 245

Published: April 13, 2024

Acute myocardial infarction (AMI) is one of the most prevalent cardiovascular diseases, accounting for a high incidence rate and mortality worldwide. Hypoxia/reoxygenation (H/R)-induced cell injury main cause AMI. Several studies have shown that circular RNA contributes significantly to pathogenesis Here, we established an AMI mouse model investigate effect circDiaph3 in cardiac function explore functional role H/R-induced cardiomyocyte its molecular mechanism. Bioinformatics tool RT-qPCR techniques were applied detect expression human patient samples, heart tissues mice, H9C2 cells. CCK-8 was used examine viability, while annexin-V/PI staining assess apoptosis. Myocardial reactive oxygen species (ROS) levels detected by immunofluorescence. Western blot protein anti-apoptotic Bcl-2 pro-apoptotic Bax cleaved-Caspase-3. Furthermore, ELISA inflammatory cytokines production. While bioinformatics pull-down assay verify interaction between miR-338-3p. We found patients as well H/R-treated CircDiaph3 silencing ameliorated apoptosis response cardiomyocytes vivo. Moreover, knockdown cirDiaph3 mitigated release mediators like IL-1β, IL-6, TNF-α Mechanistically, induced responses cells sponging Overexpressing miR-338-3p prominently reversed circDiaph3-induced effects. Notably, inhibited SRSF1 overexpressing abrogated miR-338-3p-mediated alleviation inflammation after H/R treatment. To summarize, aggravates through miR-338-3p/SRSF1 axis. These findings suggest circDiaph3/miR-338-3pp/SRSF1 axis could be potential therapeutic target treating injury.

Language: Английский

Regulation of inflammatory response by LINC00346 via miR-25-3p-mediated modulation of the PTEN/PI3K/AKT/NF-κB pathway DOI
Min-Ji Kim, Su‐Geun Lim, Dong‐Hyung Cho

et al.

Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 709, P. 149828 - 149828

Published: March 25, 2024

Language: Английский

Citations

7
Circulating microRNA Profiles Identify a Patient Subgroup with High Inflammation and Severe Symptoms in Schizophrenia Experiencing Acute Psychosis DOI Open Access
Takuya Miyano, Tsuyoshi Mikkaichi, Kouichi Nakamura

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(8), P. 4291 - 4291

Published: April 12, 2024

Schizophrenia is a complex and heterogenous psychiatric disorder. This study aimed to demonstrate the potential of circulating microRNAs (miRNAs) as clinical biomarker stratify schizophrenia patients enhance understandings their pathophysiology. We measured levels 179 miRNA 378 proteins in plasma samples experiencing acute psychosis obtained Positive Negative Syndrome Scale (PANSS) scores. The profile revealed three subgroups patients, where one subgroup tended have higher scores all PANSS subscales compared other subgroups. with high had four distinctively downregulated miRNAs, which enriched ‘Immune Response’ according set enrichment analysis were reported negatively regulate IL-1β, IL-6, TNFα. same 22 upregulated proteins, ‘Cytokine-cytokine receptor interaction’ protein analysis, mapped pro-inflammatory cytokines. Hence, inferred comparatively inflammation within schizophrenia. In conclusion, miRNAs are that reflects both disease symptoms molecular pathophysiology, identify patient inflammation. These findings provide insights for precision medicinal strategies anti-inflammatory treatments high-inflammation

Language: Английский

Citations

5
Apoptosis and long non-coding RNAs: Focus on their roles in Heart diseases DOI
Abeer A. Al‐Masri

Pathology - Research and Practice, Journal Year: 2023, Volume and Issue: 251, P. 154889 - 154889

Published: Oct. 16, 2023

Language: Английский

Citations

6
The Clinical Significance and the Potential Regulatory Mechanism of the LncRNA OIP5-AS1 in Paediatric Severe Community-Acquired Pneumonia Blood Through the MiR-150-5p/PDCD4 Axis DOI
Juan Lu, Qingguo Ren, Weiwei Qi

et al.

Immunological Investigations, Journal Year: 2024, Volume and Issue: 53(4), P. 541 - 558

Published: Jan. 31, 2024

This study aimed to elucidate the clinical significance and regulatory mechanism of long non-coding RNA OIP5-AS1 in severe community-acquired pneumonia (SCAP) among paediatric patients.

Language: Английский

Citations

2
Sevoflurane preconditioning attenuates myocardial cell damage caused by hypoxia and reoxygenation via regulating the NORAD/miR-144-3p axis DOI Creative Commons
Duo Qian, Jie Wen,

Yawei Yuan

et al.

Human & Experimental Toxicology, Journal Year: 2024, Volume and Issue: 43

Published: Jan. 1, 2024

This study aimed to investigate the function and mechanism of lncRNA NORAD in Sevoflurane (Sev) protection against myocardial hypoxia-reoxygenation (H/R).

Language: Английский

Citations

2
CircDiaph3 aggravates H/R-induced cardiomyocyte apoptosis and inflammation through miR-338-3p/SRSF1 axis DOI Creative Commons
Lin Lin, Li Wang, Aimin Li

et al.

Journal of Bioenergetics and Biomembranes, Journal Year: 2024, Volume and Issue: 56(3), P. 235 - 245

Published: April 13, 2024

Acute myocardial infarction (AMI) is one of the most prevalent cardiovascular diseases, accounting for a high incidence rate and mortality worldwide. Hypoxia/reoxygenation (H/R)-induced cell injury main cause AMI. Several studies have shown that circular RNA contributes significantly to pathogenesis Here, we established an AMI mouse model investigate effect circDiaph3 in cardiac function explore functional role H/R-induced cardiomyocyte its molecular mechanism. Bioinformatics tool RT-qPCR techniques were applied detect expression human patient samples, heart tissues mice, H9C2 cells. CCK-8 was used examine viability, while annexin-V/PI staining assess apoptosis. Myocardial reactive oxygen species (ROS) levels detected by immunofluorescence. Western blot protein anti-apoptotic Bcl-2 pro-apoptotic Bax cleaved-Caspase-3. Furthermore, ELISA inflammatory cytokines production. While bioinformatics pull-down assay verify interaction between miR-338-3p. We found patients as well H/R-treated CircDiaph3 silencing ameliorated apoptosis response cardiomyocytes vivo. Moreover, knockdown cirDiaph3 mitigated release mediators like IL-1β, IL-6, TNF-α Mechanistically, induced responses cells sponging Overexpressing miR-338-3p prominently reversed circDiaph3-induced effects. Notably, inhibited SRSF1 overexpressing abrogated miR-338-3p-mediated alleviation inflammation after H/R treatment. To summarize, aggravates through miR-338-3p/SRSF1 axis. These findings suggest circDiaph3/miR-338-3pp/SRSF1 axis could be potential therapeutic target treating injury.

Language: Английский

Citations

1