Related Experiment Video
Updated: Sep 8, 2025

07:49
Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
11.4K
Human cathelicidin peptide LL-37 induces endothelial-to-mesenchymal transition
Kaori Suzuki1,2, Mari Ohkuma1, Isao Nagaoka1,2,3
1Department of Host Defense and Biochemical Research, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Bioscience, Biotechnology, and Biochemistry
|July 21, 2025
Summary
The antimicrobial peptide LL-37 promotes endothelial-to-mesenchymal transition (EndMT) in human cells. This process, implicated in atherosclerosis, involves LL-37 activating Akt and NF-κB signaling pathways.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Immunology
Background:
- Endothelial-to-mesenchymal transition (EndMT) is a cellular process implicated in atherosclerosis pathogenesis.
- LL-37, an antimicrobial peptide, is found in atherosclerotic plaques, suggesting a potential role in the disease.
Purpose of the Study:
- To investigate the potential of LL-37 to induce EndMT in human umbilical vein endothelial cells (ECs).
- To elucidate the signaling pathways involved in LL-37-mediated EndMT.
Main Methods:
- Treatment of human umbilical vein ECs with LL-37.
- Assessment of EC and mesenchymal cell markers.
- Evaluation of vascular network formation and cell migration.
- Inhibition studies using Akt and NF-κB pathway inhibitors.
Main Results:
- LL-37 treatment decreased endothelial cell markers and increased mesenchymal cell markers.
- LL-37 reduced vascular network formation but enhanced cell migration.
- LL-37-induced EndMT was significantly inhibited by Akt and NF-κB pathway inhibitors.
Conclusions:
- LL-37 acts as an inducer of EndMT in human ECs.
- LL-37 likely promotes EndMT by activating the Akt and NF-κB signaling pathways.
- LL-37 may play a role in the pathogenesis of atherosclerosis through EndMT induction.
Related Concept Videos
Metastasis
5.7K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.7K
Regulation of Angiogenesis and Blood Supply
2.7K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.7K

