Intralipid Increases Nitric Oxide Release from Human Endothelial Cells During Oxidative Stress.
Dorothee WeihrauchStephen D ShumpertMichael E LarsonNatalie McVeyJohn G KrolikowskiOmoshalewa BamkoleMatthias L RiessPublished in: JPEN. Journal of parenteral and enteral nutrition (2020)
ILP enters ECs via endocytosis by a CD36/caveolin-1 cell membrane receptor complex, which in turn is pulled into the cell by dynamin-2 activity. Upregulation of src-kinase-1 and eNOS phosphorylation suggest downstream mediators. Subsequent NO release from ECs serve as a paracrine signal to neighboring cells for protection against IR injury. Student t-test was utilized for single comparisons and analysis of variance with Bonferroni-Dunn post hoc modification for multiple comparisons; P < .05 was considered statistically significant.
Keyphrases
- endothelial cells
- induced apoptosis
- nitric oxide
- oxidative stress
- high glucose
- tyrosine kinase
- signaling pathway
- protein kinase
- nitric oxide synthase
- cell cycle arrest
- endoplasmic reticulum stress
- single cell
- vascular endothelial growth factor
- cell therapy
- cell proliferation
- poor prognosis
- pi k akt
- dna damage
- living cells
- fluorescent probe
- medical students
- cell death
- stem cells
- diabetic rats
- bone marrow
- pluripotent stem cells
- nk cells
- heat shock protein
- quantum dots