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Updated: Nov 9, 2025

In Silico Identification and Characterization of circRNAs During Host-Pathogen Interactions
Published on: October 21, 2022
Circular RNA circ_HECTD1 regulates cell injury after cerebral infarction by miR-27a-3p/FSTL1 axis
Zhenduo Zhang1, Jinbo He2, Baoliang Wang1
1Department of Encephalopathy Third Ward, The First Affiliated Hospital of Henan University of CM, Zhengzhou, Henan, China.
Insights
Circular RNAs HECTD1 (circ_HECTD1) protects against cerebral infarction by regulating the microRNA-27a-3p/FSTL1 axis. This finding offers a potential therapeutic strategy for cerebral infarction, a condition with high mortality.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Cerebral infarction, a leading cause of mortality, involves neural cell injury.
- Oxygen-glucose deprivation/reperfusion (OGD/R) models are crucial for studying cerebral ischemia.
- Circular RNAs are increasingly recognized for their roles in cellular processes and disease.
Purpose of the Study:
- To investigate the role and mechanism of circ_HECTD1 in OGD/R-induced neuronal injury.
- To explore the potential of circ_HECTD1 as a therapeutic target for cerebral infarction.
Main Methods:
- Real-time quantitative PCR (RT-qPCR) for gene expression analysis.
- Cell viability, proliferation (EdU, MTT), and apoptosis assays (flow cytometry).
- Western blot for protein expression and dual-luciferase reporter assay for molecular interactions.
Main Results:
- Circ_HECTD1 and FSTL1 expression increased, while miR-27a-3p decreased in OGD/R-treated cells.
- Knockdown of circ_HECTD1 enhanced cell proliferation and reduced apoptosis in OGD/R conditions.
- Circ_HECTD1 acts as a molecular sponge for miR-27a-3p, regulating FSTL1 expression.
Conclusions:
- Circ_HECTD1 deficiency mitigates OGD/R-induced neuronal damage by modulating the miR-27a-3p/FSTL1 axis.
- The circ_HECTD1/miR-27a-3p/FSTL1 pathway represents a promising therapeutic target for cerebral infarction.
Abstract:
Cerebral infarction is a common cerebrovascular disease caused by neural cell injury, with high mortality worldwide. Circular RNAs HECT domain E3 ubiquitin-protein ligase 1 (circ_HECTD1) has been reported to be related to the oxygen-glucose deprivation/reperfusion (OGD/R)-caused neuronal damage in cerebral ischemia. This study is designed to explore the role and mechanism of circ_HECTD1 in OGD/R-induced cell injury in cerebral ischemia. Circ_HECTD1, microRNA-27a-3p (miR-27a-3p), and Follistatin-like 1 (FSTL1) level were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The localization of circ_HECTD1 was analyzed by subcellular fractionation assay. Cell proliferative ability and apoptosis were assessed by 5-ethynyl-2'-deoxyuridine (EdU), 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), and flow cytometry assays. The protein levels of proliferating cell nuclear antigen (PCNA), B-cell lymphoma-2 (Bcl-2), Bcl-2 related X protein (Bax), Cleaved poly-ADP-ribose polymerase (PARP), and FSTL1 were examined by western blot assay. The binding relationship between miR-27a-3p and circ_HECTD1 or FSTL1 was predicted by starbase 3.0 then verified by a dual-luciferase reporter assay. Circ_HECTD1 and FSTL1 were highly expressed, and miR-27a-3p was decreased in OGD/R-treated HT22 cells. Moreover, circ_HECTD1 knockdown could boost cell proliferative ability and repress apoptosis in OGD/R-triggered HT22 cells in vitro. Mechanical analysis discovered that circ_HECTD1 could regulate FSTL1 expression by sponging miR-27a-3p. Circ_HECTD1 deficiency could mitigate OGD/R-induced HT22 cell damage by modulating the miR-27a-3p/FSTL1 axis, providing a promising therapeutic target for cerebral infarction treatment.
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