Key result
Cardiac hemangioma exhibits lower miR-503-5p and higher BMPR1A levels versus healthy controls.
Why the study?
Although miR-503-5p has been suggested as key for the future diagnosis and treatment of cardiac hemangioma, the relationship between the two had not been fully validated.
Case-Control
p-value: p=<0.05
miR-503-5p participates in cardiac hemangioma growth by targeted sponging of BMPR1A, highlighting a potential mechanism for future diagnosis and treatment.
miR-503-5p/BMPR1A axis may influence CH cells; hypothesis-generating in vitro data leave clinical translation open.
It has been claimed that microRNA 503-5p (miR-503-5p) is the key to the future diagnosis and treatment of cardiac hemangioma (CH), but the relationship between the two has not been fully validated. In this study, we analyzed the effect of miR-503-5p targeting type IA bone morphogenetic protein receptor (BMPR1A) on CH to inform future diagnosis and treatment of CH. First, miR-503-5p and BMPR1A abnormal expression sequences (vectors) were transfected into human hemangioma-derived endothelial cells (HemECs) and human umbilical vein endothelial cells (HUVECs) to observe alterations in cell biological behavior, adhesion, and epithelial mesenchymal transition (EMT). We found enhanced proliferative, invasive and migrating abilities of HemECs and HUVECs after silencing miR-503-5p or increasing BMPR1A, accompanied by reduced apoptosis, elevated intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and accelerated EMT; after increasing miR-503-5p or silencing BMPR1A, the cells exhibited reduced apoptosis, elevated ICAM-1 and VCAM-1, and accelerated EMT (P<0.05). Subsequently, a dual-luciferase reporter assay was performed to analyze the targeting relationship between miR-503-5p and BMPR1A. The results showed that miR-503-5p inhibited BMPR1A-wild type (WT) fluorescence activity (P<0.05). Through the rescue experiment, it was observed that the biological behavior of the cells with simultaneous elevation or simultaneous silencing of miR-503-5p and BMPR1A was not different from that of cells transfected with BMPR1A empty vector (P>0.05), indicating that the effect of BMPR1A on cells was reversed by miR-503-5p. Finally, in the analysis of clinical records, we found that CH cases exhibited lower miR-503-5p and higher BMPR1A levels than healthy controls (P<0.05). The expression of the two genes was negatively correlated (P<0.05). These results suggest that miR-503-5p participates in CH growth by targeted sponging of BMPR1A.
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Kai Lu (2024) conducted a case-control in Cardiac hemangioma. miR-503-5p and BMPR1A levels vs. Healthy controls was evaluated on miR-503-5p and BMPR1A expression levels (p=<0.05). Cardiac hemangioma cases exhibited significantly lower miR-503-5p and higher BMPR1A levels compared to healthy controls (P<0.05).
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