ArticleMolecular medicine reports2022
SESN1 attenuates the Ox‑LDL‑induced inflammation, apoptosis and endothelial‑mesenchymal transition of human umbilical vein endothelial cells by regulating AMPK/SIRT1/LOX1 signaling.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 14 citations in OpenAlex.
- Review
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- Unraveling the role and mechanism of mitochondria in postoperative cognitive dysfunction: a narrative review.Journal of neuroinflammation · 2024Review
- IGFBP7 mediates oxLDL-induced human vascular endothelial cell injury by suppressing the expression of SIRT1.Heliyon · 2024Article
- Regulation of endothelial ferroptosis by SESN1 in atherosclerosis and its related mechanism.Aging · 2023Article
- E prostanoid receptor-3 promotes oxidized low-density lipoprotein-induced human aortic smooth muscle cells inflammation.ESC heart failure · 2023Article
- G0S2 ameliorates oxidized low-density lipoprotein-induced vascular endothelial cell injury by regulating mitochondrial apoptosis.Annals of translational medicine · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Endothelial cells are an important component of the heart and vasculature and form a crucial link between the cardiovascular system and the immune system. Sestrin 1 (SESN1) has an important role in atherosclerosis by inhibiting NOD‑like receptor family pyrin domain containing 3 inflammasome activation. However, whether SESN1 is involved in human umbilical vein endothelial cell (HUVEC) injury caused by atherosclerosis has remained to be elucidated. The present study aimed to investigate the functions of SESN1 in the inflammatory response, apoptosis and endothelial‑mesenchymal transition (EndMT) of HUVECs following stimulation with oxidized low‑density lipoprotein (Ox‑LDL). SESN1 expression at the mRNA and protein levels was detected using reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analysis. Following SESN1 overexpression in Ox‑LDL‑stimulated HUVECs, cell viability was determined using a Cell Counting Kit‑8 assay. Terminal deoxynucleotidyl transferase‑mediated nick‑end labeling staining was employed to detect cell apoptosis and western blot analysis was used to determine the levels of apoptosis‑related proteins. RT‑qPCR, ELISA and western blot were utilized to determine the levels of inflammatory factors. Immunofluorescence staining, RT‑qPCR and western blot analysis were employed to assess the EndMT of Ox‑LDL‑stimulated HUVECs. The results revealed that SESN1 exhibited a low expression in HUVECs following Ox‑LDL stimulation. SESN1 overexpression suppressed inflammation, apoptosis and EndMT in Ox‑LDL‑induced HUVECs. In addition, SESN1 stimulated adenosine monophosphate‑activated protein kinase catalytic subunit α1/sirtuin 1 signaling to suppress Ox‑LDL receptor‑1 expression. An AMPK and SIRT1 inhibitor reversed the effects of SESN1 overexpression on the inflammatory response, apoptosis and EndMT of HUVECs exposed to Ox‑LDL. Taken together, the present study demonstrated that SENS1 exerts a suppressive effect on Ox‑LDL‑induced inflammation, apoptosis and EndMT of HUVECs, suggesting that SENS1 may be used as a novel biomarker for endothelial injury‑related disorders.
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