PMID- 24077843
OWN - NLM
STAT- MEDLINE
DCOM- 20140619
LR  - 20211021
IS  - 1420-908X (Electronic)
IS  - 1023-3830 (Print)
IS  - 1023-3830 (Linking)
VI  - 62
IP  - 12
DP  - 2013 Dec
TI  - The effect of 7-ketocholesterol and 25-hydroxycholesterol on the integrity of the 
      human aortic endothelial and intestinal epithelial barriers.
PG  - 1015-23
AB  - OBJECTIVE AND DESIGN: The damage of barrtier tissues, such as the vascular 
      endothelium and intestinal epithelium, may lead to disturbances of local immune 
      homeostasis. The aim of the study was to assess and compare the effect of 
      oxidized cholesterols (7-ketocholesterol and 25-hydroxycholesterol) on the 
      barrier properties of human primary aortic endothelium (HAEC) and intestinal 
      epithelium Caco-2 cells using a realtime cell electric impedance sensing system 
      (RTCA-DP). MATERIALS AND METHODS: HAEC and Caco-2 cells were stimulated with 
      7-ketocholesterol and 25-hydroxycholesterol by the RTCA-DP system. Apoptosis was 
      assessed by flow cytometry and cell monolayer morphology was assessed under a 
      light microscope. RESULTS: 7-ketocholesterol decreased impedance (nCI) in both 
      the endothelium and epithelium. However, the decrease was more profound in the 
      endothelium. Similarly, although 25-hydroxycholesterol decreased nCI in both the 
      endothelium and epithelium, the effect was weaker than that of 7-ketocholesterol, 
      which caused extensive damage to the endothelial monolayer, while 
      25-hydroxycholesterol caused partial damage and did not affect the epithelial 
      monolayer. 7-ketocholesterol, but not 25-hydroxycholesterol, increased 
      endothelial cell apoptosis and decreased the viability of endothelial cells. 
      However, 7-ketocholesterol and 25-hydroxycholesterol decreased epithelial cell 
      apoptosis and increased viability. CONCLUSION: Oxidized cholesterols destroy the 
      HAEC, but not the Caco-2 epithelial barrier, via cell apoptosis dependent on the 
      site of oxidation. Damage to the endothelium by oxidized cholesterol may disrupt 
      local homeostasis and provide open access to inner parts of the vascular wall for 
      lipids, other peripheral blood-derived agents, and immune cells, leading to 
      inflammation and atherogenesis.
FAU - Chalubinski, Maciej
AU  - Chalubinski M
FAU - Zemanek, Katarzyna
AU  - Zemanek K
FAU - Skowron, Wojciech
AU  - Skowron W
FAU - Wojdan, Katarzyna
AU  - Wojdan K
FAU - Gorzelak, Paulina
AU  - Gorzelak P
FAU - Broncel, Marlena
AU  - Broncel M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Hydroxycholesterols)
RN  - 0 (Ketocholesterols)
RN  - 767JTD2N31 (25-hydroxycholesterol)
RN  - O7676FE78M (7-ketocholesterol)
SB  - IM
MH  - Aorta/cytology
MH  - Apoptosis/drug effects
MH  - Caco-2 Cells
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Endothelial Cells/*drug effects
MH  - Epithelial Cells/*drug effects
MH  - Humans
MH  - Hydroxycholesterols/*pharmacology
MH  - Intestinal Mucosa/cytology
MH  - Ketocholesterols/*pharmacology
PMC - PMC3826051
EDAT- 2013/10/01 06:00
MHDA- 2014/06/20 06:00
PMCR- 2013/09/28
CRDT- 2013/10/01 06:00
PHST- 2013/03/19 00:00 [received]
PHST- 2013/08/16 00:00 [accepted]
PHST- 2013/10/01 06:00 [entrez]
PHST- 2013/10/01 06:00 [pubmed]
PHST- 2014/06/20 06:00 [medline]
PHST- 2013/09/28 00:00 [pmc-release]
AID - 660 [pii]
AID - 10.1007/s00011-013-0660-x [doi]
PST - ppublish
SO  - Inflamm Res. 2013 Dec;62(12):1015-23. doi: 10.1007/s00011-013-0660-x.