Nouvelle gamme de réactifs pour la Cytométrie en Flux Retour



Anticorps pour la cytométrie en flux : IREM2/CD303, Kappa, Lambda, F(ab)'2, CD19

Voir les produits

Kits Apoptose

Voir les produits

Kit d'analyse des cellules souches

Voir les produits


Kits Apoptose :

Références bibliographiques :


An article published this year in “The International Journal of Biochemistry & Cell Biology" using our “Apoptosis Detection 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.

Summary :

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.