An article published this year in “The International Journal of Biochemistry & Cell Biology” using our “ApoptosisDetection Kit FITC”, by our customers from Institute for Maternal
and Child Health, Trieste, Italy, in the analysis of how 25-Hydroxycholesterol and
inflammation in Lovastatin-deregulated mevalonate pathway. Congrats and Thanks.
Summay:
Mevalonate
pathway deregulation has been observed in several
diseases, including Mevalonate kinase deficiency
(MKD). MKD is a hereditary auto-inflammatory
disorder, due to mutations at mevalonate kinase gene (MVK), encoding
mevalonate kinase (MK) enzyme. MVK mutations
have been reported as associated with impairment of mevalonate pathway with
consequent decrease of protein prenylation levels, defective autophagy and increase of IL-1β secretion,
followed by cell death. Since 25-hydroxycholesterol (25-HC), a metabolite of cholesterol,
can suppress IL-1β
production, thus reducing inflammation, we evaluated the effect of 25-HC in an in
vitro model of mevalonate
pathway alteration, obtained using Lovastatin.
Human glioblastoma cell line (U87-MG) was chosen to mimic, at least in part,
the central nervous system impairment observed in MKD; 25-HC effects were
evaluated aimed at disclosing if this compound could be considered as novel
potential drug for MKD.
Our results
showed that 25-HC is able to reduce inflammation but it is ineffective to
restore autophagy flux and to decrease apoptosis levels,
both caused by lower protein prenylation; so, in spite of its anti-inflammatory
action it is not useful to rescue defective prenylation/autophagy
impairment-driven apoptosis in Lovastatin impaired mevalonate pathway.
We hypothesize
the presence in the mevalonate pathway of alternative mechanisms acting between
inflammation and apoptotic autophagy impairment.
Reference:
Product link:
Apoptosis Detection Kit FITC
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