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Updated: May 6, 2026
Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization
Published on: September 15, 2018
Expression of Cx43-related microRNAs in patients with tetralogy of Fallot
Yao Wu1, Xiao-Jing Ma, Hui-Jun Wang
1Children's Hospital of Fudan University, Shanghai, 200032, China.
Background:
Abnormal expression of connexin 43 (Cx43) has been reported to play an important role in the development of conotrunccal anomalies. However, less is known about the underlying reason for its abnormal expression. MicroRNAs (miRNAs), as an important part of gene expression regulation, have been implicated in some cardiac diseases. This study aimed to investigate the expression of Cx43 and its related miRNAs in patients with tetralogy of Fallot (TOF), and illustrate the potential role of abnormal miRNAs regulation to Cx43 expression in the pathology of TOF.
Methods:
Real-time polymerase chain reaction (PCR) was used to detect the expression of Cx43 and 10 Cx43-related miRNAs in the myocardium from 30 TOF patients and 10 normal controls. Immunohistochemistry was used to detect Cx43 protein expression. Putative miRNA binding sites in the 3'UTR of Cx43 were examined in 200 TOF patients and 200 healthy individuals, using Sanger sequencing, to exclude sequence variations resulting in binding difficulties of miRNAs.
Results:
Cx43 mRNA and protein expression in the myocardium tissue was significantly increased in TOF patients. The expression of MiR-1 and 206 was significantly decreased in the TOF patients as compared with the controls (P<0.05). No obvious difference was observed in the expression of the other 7 miRNAs between the TOF patients and controls (P>0.05). No meaningful sequence variation was detected in the putative miR1/206 binding sites in the 3'UTR of Cx43.
Conclusions:
This study indicated that miR-1 and 206 is down-regulated in TOF patients, which may cause an up-regulation of Cx43 protein's synthesis. It provided a clue that miR-1 and 206 might be involved in the pathogenesis of TOF, additional experiments are needed to determine if in fact, miR-1 and 206 contribute substantially to TOF.
Insights
In tetralogy of Fallot (TOF) patients, miR-1 and miR-206 are decreased, potentially increasing connexin 43 (Cx43) expression and contributing to the disease. Further research is needed to confirm this link.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- Developmental Biology
Background:
- Abnormal connexin 43 (Cx43) expression is linked to conotruncal anomalies.
- The regulatory mechanisms behind Cx43 dysregulation in cardiac diseases remain unclear.
- MicroRNAs (miRNAs) are key regulators of gene expression implicated in cardiac pathology.
Purpose of the Study:
- To investigate Cx43 and related miRNA expression in tetralogy of Fallot (TOF) patients.
- To explore the role of aberrant miRNA regulation in Cx43 expression within TOF pathogenesis.
- To identify specific miRNAs potentially involved in TOF development.
Main Methods:
- Real-time PCR to quantify Cx43 mRNA and 10 related miRNAs in myocardial tissue from TOF patients and controls.
- Immunohistochemistry to assess Cx43 protein levels.
- Sanger sequencing to analyze miRNA binding sites in the Cx43 3'UTR.
Main Results:
- Cx43 mRNA and protein levels were significantly elevated in TOF myocardium.
- Expression of miR-1 and miR-206 was significantly reduced in TOF patients compared to controls.
- No significant sequence variations were found in the miR-1/206 binding sites of Cx43.
Conclusions:
- Down-regulation of miR-1 and miR-206 in TOF may lead to increased Cx43 synthesis.
- miR-1 and miR-206 are potential contributors to TOF pathogenesis.
- Further investigation is warranted to establish the substantial role of miR-1 and miR-206 in TOF.
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