Open Access

ARTICLE

MiR-30a-5p alleviates LPS-induced HPMEC injury through regulation of autophagy via Beclin-1

RAN PAN^1,#, JIAYAN MAO^2,#, YUELIANG ZHENG³, WEI CHEN², JUNPING GUO^1,*, LIJUN WANG^3,*

1 Rainbowfish Rehabilitation and Nursing School, Hangzhou Vocational & Technical College, Hangzhou, 310018, China
2 Cancer Institute of Integrated Traditional Chinese and Western Medicine, Key Laboratory of Cancer Prevention and Therapy Combining Traditional Chinese and Western Medicine, Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, 310012, China
3 Geriatric Medicine Center, Department of Endocrinology, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou, 310015, China

* Corresponding Authors: JUNPING GUO. Email: ; LIJUN WANG. Email:
# Contributed equally

(This article belongs to the Special Issue: MicroRNA as Biomarkers for Disease Diagnosis and Progression)

BIOCELL 2024, 48(3), 431-441. https://doi.org/10.32604/biocell.2023.046484

Received 03 October 2023; Accepted 12 December 2023; Issue published 15 March 2024

Abstract

Background: Sepsis, a type of systemic disease, can impact nearly all organs, tissues and cells. Among them, endothelial cells are amongst the first to be affected and respond to the insult. In this study, we investigated the protective effects of microRNA-30a-5p (miR-30a-5p) on human pulmonary microvascular endothelial cells (HPMECs) treated with lipolysaccharide (LPS). Methods: An in vitro model of sepsis was established in HPMECs with the use of LPS. Transfecting with different tools (mimetic and inhibitor) to modify miR-30a-5p expression. Cell viability, proliferation and apoptosis were detected by the CCK-8 assay, the EdU kit and fluorescence staining, respectively. The autophagy-related protein and mRNA expression, the number of autophagosomes were separately examined through Western blot analysis, qPT-PCR and confocal microscopy. TargetScan and the luciferase reporter assays were used to probe target genes interacting with miR-30a-5p. Results: LPS caused a reduction in the viability and proliferation of HPMECs, as well as an elevation in the number of apoptotic cells. Subsequently, we observed that miR-30a-5p might play a role in preventing LPS-induced inhibition of cell damage and decreasing HPMEC apoptosis, suggesting the potential function of miR-30a-5p in this injury process. Finally, we confirmed that miR-30a-5p exerts its protective effect by regulating cell autophagy, possibly by targeting Beclin-1. Conclusion: Our study provided evidence that autophagy is a crucial aspect in the protective role of miR-30a-5p against LPS-induced HPMEC injury, identifying a promising target for sepsis-related endothelial cell injury.

---

Keywords

---