PMID- 37507971
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230731
IS  - 2076-3921 (Print)
IS  - 2076-3921 (Electronic)
IS  - 2076-3921 (Linking)
VI  - 12
IP  - 7
DP  - 2023 Jul 16
TI  - Differential Effects of High Fat Diets on Resilience to H(2)O(2)-Induced Cell 
      Death in Mouse Cerebral Arteries: Role for Processed Carbohydrates.
LID - 10.3390/antiox12071433 [doi]
LID - 1433
AB  - High fat, western-style diets increase vascular oxidative stress. We hypothesized 
      that smooth muscle cells and endothelial cells adapt during the consumption of 
      high fat diets to become more resilient to acute oxidative stress. Male C57Bl/6J 
      mice were fed a western-style diet high in fat and processed carbohydrates (WD), 
      a high fat diet that induces obesity (DIO), or their respective control (CD) and 
      standard (SD) diets for 16 weeks. Posterior cerebral arteries (PCAs) were 
      isolated and pressurized for study. During acute exposure to H(2)O(2) (200 microM), 
      smooth muscle cell and endothelial cell death were reduced in PCAs from WD, but 
      not DIO mice. WD selectively attenuated mitochondrial membrane potential 
      depolarization and vessel wall Ca(2+) influx during H(2)O(2) exposure. Selective 
      inhibition of transient receptor potential (TRP) V4 or TRPC3 channels reduced 
      smooth muscle cell and endothelial cell death in concert with the vessel wall 
      [Ca(2+)](i) response to H(2)O(2) for PCAs from CD mice and eliminated differences 
      between CD and WD. Inhibiting Src kinases reduced smooth muscle cell death along 
      with [Ca(2+)](i) response to H(2)O(2) only in PCAs from CD mice and eliminated 
      differences between diets. However, Src kinase inhibition did not alter 
      endothelial cell death. These findings indicate that consuming a WD, but not high 
      fat alone, leads to adaptations that limit Ca(2+) influx and vascular cell death 
      during exposure to acute oxidative stress.
FAU - Norton, Charles E
AU  - Norton CE
AUID- ORCID: 0000-0001-9442-4039
AD  - Department of Medical Pharmacology and Physiology, University of Missouri, 
      Columbia, MO 65212, USA.
FAU - Shaw, Rebecca L
AU  - Shaw RL
AD  - Department of Medical Pharmacology and Physiology, University of Missouri, 
      Columbia, MO 65212, USA.
FAU - Segal, Steven S
AU  - Segal SS
AUID- ORCID: 0000-0001-5667-2154
AD  - Department of Medical Pharmacology and Physiology, University of Missouri, 
      Columbia, MO 65212, USA.
AD  - Dalton Cardiovascular Research Center, Columbia, MO 65211, USA.
AD  - Department of Biomedical Sciences, University of Missouri, Columbia, MO 65201, 
      USA.
AD  - Department of Biomedical, Biological and Chemical Engineering, University of 
      Missouri, Columbia, MO 65211, USA.
AD  - Department of Nutrition and Exercise Physiology, University of Missouri, 
      Columbia, MO 65211, USA.
LA  - eng
GR  - 19TPA34850102/American Heart Association/
PT  - Journal Article
DEP - 20230716
PL  - Switzerland
TA  - Antioxidants (Basel)
JT  - Antioxidants (Basel, Switzerland)
JID - 101668981
PMC - PMC10376469
OTO - NOTNLM
OT  - Src family kinases
OT  - endothelial cells
OT  - mitochondrial membrane potential
OT  - smooth muscle cells
OT  - transient receptor potential (TRP) channels
COIS- The authors declare no conflict of interest.
EDAT- 2023/07/29 11:53
MHDA- 2023/07/29 11:54
PMCR- 2023/07/16
CRDT- 2023/07/29 01:04
PHST- 2023/06/06 00:00 [received]
PHST- 2023/06/30 00:00 [revised]
PHST- 2023/07/11 00:00 [accepted]
PHST- 2023/07/29 11:54 [medline]
PHST- 2023/07/29 11:53 [pubmed]
PHST- 2023/07/29 01:04 [entrez]
PHST- 2023/07/16 00:00 [pmc-release]
AID - antiox12071433 [pii]
AID - antioxidants-12-01433 [pii]
AID - 10.3390/antiox12071433 [doi]
PST - epublish
SO  - Antioxidants (Basel). 2023 Jul 16;12(7):1433. doi: 10.3390/antiox12071433.