Lipid peroxidation product 4-hydroxynonenal as factor of oxidative homeostasis supporting bone regeneration with bioactive glasses.
Author(s) -
Lidija Mrakovčić,
Renate Wildburger,
Morana Jaganjac,
Marina Cindrić,
Ana Čipak Gašparović,
Suzana Borović-Šunjić,
Georg Waeg,
Andrea Moguš Milanković,
Neven Žarković
Publication year - 2010
Publication title -
acta biochimica polonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.452
H-Index - 78
eISSN - 1734-154X
pISSN - 0001-527X
DOI - 10.18388/abp.2010_2391
Subject(s) - 4 hydroxynonenal , lipid peroxidation , chemistry , regeneration (biology) , oxidative stress , microbiology and biotechnology , homeostasis , bioactive glass , mapk/erk pathway , oxidative phosphorylation , biochemistry , kinase , biology , medicine , dentistry
Bone regeneration is a process of vital importance since fractures of long bones and large joints have a highly deleterious impact on both, individuals and society. Numerous attempts have been undertaken to alleviate this severe medical and social problem by development of novel bioactive materials, among which bioactive glass is the most attractive because of its osteoconductive and osteostimulative properties. Since lipid peroxidation is an important component of systematic stress response in patients with traumatic brain injuries and bone fractures, studies have been undertaken of the molecular mechanisms of the involvement of 4-hydroxynonenal (HNE), an end product of lipid peroxidation, in cellular growth regulation. We found that HNE generated in bone cells grown in vitro on the surfaces of bioactive glasses 45S5 and 13-93. This raises an interesting possibility of combined action of HNE and ionic bioglass dissolution products in enhanced osteogenesis probably through a mitogen-activated protein kinase (MAPK) pathway. While the proposed mechanism still has to be elucidated, the finding of HNE generation on bioglass offers a new interpretation of the osteoinducting mechanisms of bioglass and suggests the possibility of tissue engineering based on manipulations of oxidative homeostasis.
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