Trial lecture - time and place
14.02.2025,10.15, Auditoriet, Gydas vei 8
Role of legumain in cancer, cardiovascular and neurodegenerative diseases: biological mechanisms and pharmacological targets
Conferral summary
Master i farmasi Karl Martin Forbord har studert enzymet legumain som hemmer kroppens beinbyggende celler. I sine studier har Forbord vist at legumain påvirker naboceller direkte som et signalmolekyl, og indirekte ved å endre cellenes omgivelser. Videre har han vist hvordan legumain spiller en rolle i omsetningen av vitamin D som er et essensielt næringsstoff for beinbygging, mens vitamin D på sin side påvirker produksjonen av legumain i beinbyggende celler i kultur og i mus.
Main research findings
Strong and healthy bones depend on the proper function of osteoblasts, the bone-forming cells. High level of the enzyme legumain are linked to reduced osteoblast activity and impaired bone mineralization, which can lead to bone diseases like osteoporosis.
This thesis has demonstrated that legumain acts as a paracrine regulator, influencing osteoblast maturation both directly and indirectly. On one hand, legumain can be internalized and activated by osteoblasts which suppress the ability to form mineralized bone. On the other, legumain in osteoblasts modifies the extracellular environment, which further alter the activity in the bone-forming cells. Notably, the negative effect of internalized legumain was reversed when the activity of legumain was pharmacologically inhibited. Furthermore, transforming growth factor beta 1 and vitamin D3, both crucial regulators of bone health, was shown to impact legumain activity, deepening our understanding of the role of legumain in bone metabolism.
These findings highlight legumain as a promising target for treatment strategies aimed at enhancing bone formation. Legumain inhibitors could represent a valuable addition to the limited range of anabolic therapies available to improve bone health in the treatment of osteoporosis.
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