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2018 ; 8
(1
): 4919
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Phosphatidylglycerol Incorporates into Cardiolipin to Improve Mitochondrial
Activity and Inhibits Inflammation
#MMPMID29559686
Chen WW
; Chao YJ
; Chang WH
; Chan JF
; Hsu YH
Sci Rep
2018[Mar]; 8
(1
): 4919
PMID29559686
show ga
Chronic inflammation and concomitant oxidative stress can induce mitochondrial
dysfunction due to cardiolipin (CL) abnormalities in the mitochondrial inner
membrane. To examine the responses of mitochondria to inflammation,
macrophage-like RAW264.7 cells were activated by Kdo2-Lipid A (KLA) in our
inflammation model, and then the mitochondrial CL profile, mitochondrial
activity, and the mRNA expression of CL metabolism-related genes were examined.
The results demonstrated that KLA activation caused CL desaturation and the
partial loss of mitochondrial activity. KLA activation also induced the gene
upregulation of cyclooxygenase (COX)-2 and phospholipid scramblase 3, and the
gene downregulation of COX-1, lipoxygenase 5, and ?-6 desaturase. We further
examined the phophatidylglycerol (PG) inhibition effects on inflammation. PG
supplementation resulted in a 358-fold inhibition of COX-2 mRNA expression.
PG(18:1)(2) and PG(18:2)(2) were incorporated into CLs to considerably alter the
CL profile. The decreased CL and increased monolysocardiolipin (MLCL) quantity
resulted in a reduced CL/MLCL ratio. KLA-activated macrophages responded
differentially to PG(18:1)(2) and PG(18:2)(2) supplementation. Specifically,
PG(18:1)(2) induced less changes in the CL/MLCL ratio than did PG(18:2)(2), which
resulted in a 50% reduction in the CL/MLCL ratio. However, both PG types rescued
20-30% of the mitochondrial activity that had been affected by KLA activation.