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Updated: Jan 27, 2026
Isolation of Human Umbilical Vein Endothelial Cells HUVEC
Published on: April 28, 2007
miR-297 Protects Human Umbilical Vein Endothelial Cells against LPS-Induced Inflammatory Response and Apoptosis
Yanfen Yao1, Haiyan Jia1, Geng Wang2
1Department of Intensive Care Unit, Shandong Provincial Third Hospital, Jinan, China.
Background/Aims:
Recently, microRNA-297 (miR-297) and signal transducer and activator of transcription 3 (STAT3) have been demonstrated to be involved in dysfunction of vascular endothelial cells and inflammatory conditions, such as sepsis. The present study aimed to investigate the role of miR-297 and STAT3 in lipopolysaccharide (LPS)-induced inflammatory human umbilical vein endothelial cells (HUVECs).
Methods:
HUVECs were stimulated by different concentrations of LPS. miR-297 mimics were transfected into HUVECs to overexpress miR-297. The qRT-PCR was used to measure the expression level of miR-297. Western blot was used to detect the expressions of STAT3, inflammatory cytokines, adhesion molecules and apoptosis-related proteins. Cell apoptosis was determined by flow cytometry.
Results:
Compared with parental HUVECs, the expression of miR-297 was significantly down-regulated, while the expression of STAT3 was obviously up-regulated in LPS-induced HUVECs. The expressions of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin were also increased in LPS-induced HUVECs than those in parental HUVECs. In addition, LPS induced apoptosis of HUVECs through up-regulation of Bax and cleaved caspase 3 expressions. Conversely, miR-297 mimics inhibited LPS-activated expressions of STAT3, inflammatory cytokines, and adhesion molecules, and protected HUVECs against LPS-induced apoptosis through inhibition of Bax and cleaved caspase 3 expressions. Mechanistically, the 3'-untranslated region (3'-UTR) of STAT3 mRNA was validated as a direct target of miR-297. Over-expression of STAT3 partially abrogated protective effects of miR-297, whereas silencin g of STAT3 contributed to miR-297-mediated biological effects.
Conclusion:
miR-297 protects HUVECs against LPS-induced inflammatory response and apoptosis by targeting STAT3 pathway. Thus, miR-297 may be a promising therapeutic target for patients with sepsis.
Insights
MicroRNA-297 (miR-297) protects human umbilical vein endothelial cells from lipopolysaccharide (LPS)-induced inflammation and apoptosis by targeting the STAT3 pathway. This suggests miR-297 as a potential therapeutic target for sepsis.
Area of Science:
- Endothelial cell biology
- Molecular mechanisms of inflammation
- MicroRNA regulation
Background:
- MicroRNA-297 (miR-297) and signal transducer and activator of transcription 3 (STAT3) are implicated in endothelial cell dysfunction and sepsis.
- Lipopolysaccharide (LPS) induces inflammatory responses in vascular endothelial cells.
Purpose of the Study:
- To investigate the role of miR-297 and STAT3 in LPS-induced inflammatory human umbilical vein endothelial cells (HUVECs).
Main Methods:
- HUVECs were stimulated with LPS.
- miR-297 mimics were used to overexpress miR-297.
- qRT-PCR and Western blot analyzed gene and protein expression.
- Flow cytometry assessed cell apoptosis.
Main Results:
- LPS decreased miR-297 and increased STAT3 expression in HUVECs.
- LPS elevated inflammatory cytokines (IL-6, TNF-α), adhesion molecules (ICAM-1, VCAM-1, E-selectin), and apoptosis markers (Bax, cleaved caspase 3).
- miR-297 overexpression counteracted LPS effects, reducing inflammation and apoptosis by targeting STAT3 mRNA.
Conclusions:
- miR-297 confers protection against LPS-induced inflammation and apoptosis in HUVECs via the STAT3 pathway.
- miR-297 represents a potential therapeutic target for sepsis management.
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