Related Experiment Video

Updated: Sep 21, 2025

TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing
07:05

TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

5.3K

MiR-130a-5p contributed to the progression of endothelial cell injury by regulating FAS

Wei Wang1, Wenbo Tang2, Erbo Shan3

  • 1The First Clinical College of Jinan University, Guangzhou, and Surgical Oncology Department, the Second Affiliated Hospital of Bengbu Medical College, Bengbu. wangwei@bbmc.edu.cn.

European Journal of Histochemistry : EJH
|May 31, 2022
PubMed

Insights

MicroRNA miR-130a-5p regulates FAS to impact endothelial cell injury in atherosclerosis. Downregulation of miR-130a-5p exacerbates oxidized low-density lipoprotein-induced damage, suggesting a therapeutic target for vascular disease.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Cell Biology

Background:

  • MicroRNAs (miRNAs) are crucial in vascular disease development.
  • The specific role of miR-130a-5p and its targets in atherosclerosis (AS) remains unclear.
  • Endothelial cell injury is a key factor in AS pathogenesis.

Purpose of the Study:

  • To investigate the role of miR-130a-5p and its target gene in endothelial cell injury.
  • To elucidate the mechanism by which miR-130a-5p influences atherosclerosis progression.

Main Methods:

  • Oxidized low-density lipoprotein (ox-LDL) was used to induce injury in human umbilical vein endothelial cells (HUVECs).
  • Expression levels of miR-130a-5p and FAS were measured.
  • Cell viability, apoptosis, cell cycle, proliferation, migration, and invasion assays were performed.
  • FAS knockdown and miR-130a-5p overexpression were utilized.

Main Results:

  • Ox-LDL induced FAS expression and apoptosis in HUVECs.
  • miR-130a-5p expression decreased following ox-LDL treatment and was negatively correlated with FAS.
  • FAS expression was upregulated in ox-LDL-treated HUVECs.
  • Combined knockdown of FAS and overexpression of miR-130a-5p aggravated ox-LDL-induced detrimental effects on endothelial cells.

Conclusions:

  • miR-130a-5p contributes to endothelial cell injury by regulating FAS.
  • This miR-130a-5p/FAS pathway presents a potential therapeutic target for atherosclerosis.

More Related Videos

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

11.4K
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

7.7K

Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

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
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
2.8K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
6.3K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.7K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.7K