Monoglyceride Lipase Deficiency Is Associated with Altered Thrombogenesis in Mice

Madeleine Goeritzer, Katharina B Kuentzel, Sarah Beck, Melanie Korbelius, Silvia Rainer, Ivan Bradić, Dagmar Kolb, Marion Mussbacher, Waltraud C Schrottmaier, Alice Assinger, Axel Schlagenhauf, René Rost, Benjamin Gottschalk, Thomas O Eichmann, Wolfgang F Graier, Nemanja Vujić, Dagmar Kratky

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskriftPeer review


Monoglyceride lipase (MGL) hydrolyzes monoacylglycerols (MG) to glycerol and one fatty acid. Among the various MG species, MGL also degrades 2-arachidonoylglycerol, the most abundant endocannabinoid and potent activator of the cannabinoid receptors 1 and 2. We investigated the consequences of MGL deficiency on platelet function using systemic (Mgl-/-) and platelet-specific Mgl-deficient (platMgl-/-) mice. Despite comparable platelet morphology, loss of MGL was associated with decreased platelet aggregation and reduced response to collagen activation. This was reflected by reduced thrombus formation in vitro, accompanied by a longer bleeding time and a higher blood volume loss. Occlusion time after FeCl3-induced injury was markedly reduced in Mgl-/- mice, which is consistent with contraction of large aggregates and fewer small aggregates in vitro. The absence of any functional changes in platelets from platMgl-/- mice is in accordance with lipid degradation products or other molecules in the circulation, rather than platelet-specific effects, being responsible for the observed alterations in Mgl-/- mice. We conclude that genetic deletion of MGL is associated with altered thrombogenesis.

TidskriftInternational Journal of Molecular Sciences
StatusPublished - 2023 feb. 4
Externt publiceradJa


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