Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
- |
- |
Mus musculus C57BL/6J | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
heart | - |
Mus musculus | - |
leukocyte | - |
Mus musculus | - |
macrophage | - |
Mus musculus | - |
neutrophil | - |
Mus musculus | - |
Synonyms | Comment | Organism |
---|---|---|
12/15-lipoxygenase | - |
Mus musculus |
12/15-LOX | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
malfunction | deletion of 12/15-LOX in mice leads to increased cytochrome P450-derived bioactive lipid mediator epoxyeicosatrienoic acids, i.e. 11,12-EpETrE and 14,15-EpETrE, which are further enhanced by acute PUFA intake post-MI. Macrophage density is decreased in wild-type + PUFA and 12/15-LOX-/- mice compared with their respective standard diet-fed wild-type controls at day 5 post-MI. 12/15-LOX-/- + PUFA mice display an increased expression of chemokine (C-C motif) ligand 2 and reparative macrophages markers (Ym-1, Mrc-1, and Arg-1) in the infarcted area. Furthermore, 12/15-LOX-/- mice, with or without PUFA, show reduced collagen deposition at day 5 post-MI compared with wild-type mice. In conclusion, deletion of 12/15-LOX and short-term exposure of PUFA promote leukocyte clearance, thereby limiting cardiac remodeling and promoting an effective resolution of inflammation | Mus musculus |
physiological function | the metabolic transformation of fatty acids to form oxylipids using 12/15-lipoxygenase (LOX) can promote either resolving or nonresolving inflammation. 12/15-LOX interacts with polyunsaturated fatty acids (PUFA) in postmyocardial infarction (post-MI) healing, mechanism, overview | Mus musculus |