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The activity of 15-Lipoxygenase expression levels were increased in patients with multiple sclerosis compared to healthy controls.
5-LOX does not react with 5,15-diHpETE, although it can produce lipoxin A4 when 15-HpETE is the substrate. In contrast, both 12-LOX and 15-LOX-1 react with 5,15-diHpETE, forming specifically lipoxin B4.
ALOX15 expression was positive in pauci-eosinophilic biopsies from children with eosinophilic esophagitis and negative in healthy controls.
This review summarizes our current knowledge on the role of 12/15-LOX in inflammation and various human diseases. [Review]
MAO-A expression is co-induced with 15-lipoxygenase (15-LO) in interleukin 13 (IL-13)-activated primary human monocytes and A549 non-small cell lung carcinoma cells.
Results demonstrate the expression of ALOX15 and ALOX15B in failing as well as in donor hearts. ALOX15/B signaling may play an important role in heart disease, including heart failure. Isolated fibroblasts from all four chambers of the heart expressed ALOX15 as well as ALOX15B, and gene expression levels were further increased under hypoxia.
ALOX15 orthologs, commonly known as 12/15-lipoxygenases, were suggested to exhibit mainly arachidonic acid 12-lipoxygenating specificity in mammals ranked in evolution lower than gibbons and 15-lipoxygenating specificity in the higher ranking primates [Review].
Study in the dextran sulfate sodium colitis model utilizing transgenic mice overexpressing human ALOX15 suggests a pro-inflammatory activity of human 15-LOX1.
Pinosylvin enhances the apoptosis of LPS preconditioned leukocytes by up-regulating ALOX 15 expression through ERK and JNK.
indicate regulation of Alox15 mRNA expression in neuroblastoma cells by histone modifications, and increasing Alox15 expression in differentiating neurons
The present study shows that rs7217186:C > T and rs2619112:G > A of ALOX15 are associated with increased risk of CAD in the North Indian population.
Results identify ALOX15, which was upregulated under low oxygen conditions and is associated with an increase in the rate of phagocytosis of apoptotic cells.
the results indicate that 15-LO-1 has an important role in the disease progression of osteoarthritis. Thus 15-LO-1 may be a good target for developing drugs in the treatment of osteoarthritis.
15-LOX-1 expression in colon and prostate cancer cells leads to reduced angiogenesis. These changes could be mediated by an increase in the expression of both ICAM-1 and the anti-angiogenic protein TSP-1.
Polymorphisms in the ALOX15 gene may influence periodontal disease pathogenesis. Hence, investigation of such polymorphisms could benefit the evaluation of lipoxins role in periodontal disease
Results suggest an evolution of ALOX15 (12/15-lipoxygenase)specificity.
Compound heterozygous mutations in DYNC2H1 and ALOX15 were identified in miscarriages from two families with RPL. DYNC2H1 is involved in cilia biogenesis and has been associated with fetal lethality in humans. ALOX15 is expressed in placenta and its dysregulation has been associated with inflammation, placental, dysfunction, abnormal oxidative stress response and angiogenesis.
Immunofluorescence analyses revealed that the ALOX15 protein consistently localizes to cell membrane during the course of ferroptosis. Importantly, treatments of cells with ALOX15-activating compounds accelerated cell death at low, but not high doses of erastin and RSL3
present in late-stage germ cells of the testis
Studied human umbilical cord mesenchymal stem cell (hucMSCs) transplantation in DSS-induced inflammatory bowel disease (IBD); hucMSC transplantation significantly relieved IBD symptoms thru the regulation of 15-LOX-1 expression and modulation of inflammatory responses in macrophages.
The authors show that Alox15 mediates production of resolvin D2 that is required to maintain skin integrity by suppressing dermal inflammation.
12/15-LOX is overexpressed in macrophages after SAH in mice, and inhibition of the 12/15-LOX pathway decreases brain injury and improves neurological outcome. This study suggests 12/15-LOX as a novel therapeutic target to limit brain injury after SAH.
these results indicate that Alox12 loss activates a compensatory increase in Alox15 that sensitizes mouse beta cells to oxidative stress.
Our study demonstrated that hypoxia increases the expression of MMP-2 and MMP-9 through the 15-lipoxygenase/15-HETE pathway, and that MMP-2 and MMP-9 promote PAEC angiogenesis. These findings suggest that MMP-2 and MMP-9 may serve as new potential therapeutic targets for the treatment of pulmonary arterial hypertension (PAH).
Data show that middle cerebral artery occlusion (MCAO) upregulates 15-lipoxygenase expression in a time-dependent manner, especially in later stages of post-stroke.
genetic deletion of 12/15LOX reduces 12-(S)-hydroperoxyeicosatetraenoic acid and activates CYP2J-derived epoxyeicosatrienoic acids to promote effective resolution of inflammation post-myocardial infarction.
These results demonstrated that activation of ALOX15/13-HODE circuit critically mediates the pathogenesis of alcoholic liver disease.
The data demonstrate that the db/db mouse is a suitable model for investigation of 12/15LO inhibitors in the development of inflammatory mediated type 2 diabetes, with a narrow window of therapeutic intervention prior to 8 weeks of age.
a specific endogenous metabolite of vitamin E, alpha-tocopherol hydroquinone, was a dramatically more potent inhibitor of ferroptosis than its parent compound, and inhibits 15-lipoxygenase via reduction of the enzyme's non-heme iron from its active Fe3+ state to an inactive Fe2+ state.
Alox15 exhibits pro-inflammatory activity in the dextran sulfate sodium mouse colitis model as indicated by genetic loss- and gain-of-function strategies.
Deletion of 12/15-lipoxygenase accelerates the development of aging-associated and instability-induced osteoarthritis.
upregulation of ALOX15 occurring in response to oxidative stress in germ cells of the male mouse leads to enhanced 4-hydroxynonenal production and subsequent pathways of deleterious protein modification
The data provide the first evidence to date that small molecules that target 12/15-LOX can prevent progression of beta-cell dysfunction and glycemic deterioration in models of type 1 diabetes.
Findings suggest a pivotal role for 12/15-lipoxygenase (12/15-LOX) in both caspase-dependent and caspase-independent apoptotic pathways following global cerebral ischemia and suggest a novel therapeutic approach to reduce brain injury following cardiac arrest.
The present study investigated the roles of arachidonate 15-lipoxygenase (Alox15) in the clearance of dying adipocytes by adipose tissue macrophages.
Findings suggest that 12/15-lipoxygenase (12/15-LO)-mediated enzymatic lipid oxidation serves as a key mechanism controlling eosinophil-directed coagulation and physiological hemostasis.
data support that endothelial, rather than monocytic/macrophagic, 12/15-LO has a critical role in hyperglycemia-induced ICAM-1 expression, leukocyte adhesion, and subsequent local retinal barrier dysfunction.
This study determined that 1) deletion of 12/15-lipoxygenase (LOX) promotes the generation of epoxyeicosatrienoic acids, the cytochrome P-450-derived metabolites in postmyocardial infarction (post-MI) healing; 2) acute exposure of fatty acids to 12/15-LOX(-/-) mice drives leukocyte (neutrophils and macrophages) clearance post-MI; and 3) metabolic transformation of fats is the significant contributor in leukocyte clearance
These data suggest that systemic inactivation of the Alox15 gene normalizes the reduced fertility of male Sec46Ala-Gpx4(+/-) mice by improving the motility of their sperm. If these data can be confirmed in humans, ALOX15 inhibitors might counteract male infertility related to GPX4 deficiency.
The crystal structure of a mammalian 12-lipoxygenase reveals a plausible substrate access channel for oxygen.
12/15-Lipoxygenase activity increases the degradation of macrophage ATP-binding cassette transporter G1.
EPR spectroscopy and electrospray mass spectroscopy reveal distinctive features of the iron site in leukocyte arachidonate 12-lipoxygenase.
The conserved residue Leu597 actually drives the regiospecific hydroperoxidation of linoleic acid catalyzed by 15-lipoxygenase enzyme.
The study presents an atomic-level study of catalytically competent binding modes for linoleic acid to rabbit 15-lipoxygenase and compare the results to our previous work on arachidonic acid.
Results indicate 15-lipoxygenase modified LDL as a new inducer for LOX-1 expression and as a new ligand for LOX-1.
15-Lipoxygenase metabolites contribute to age-related reduction in acetylcholine-induced hypotension in rabbits.
demonstrates 12-lipoxygenase and some 15-lipoxygenase enzyme activity
, arachidonate omega-6 lipoxygenase
, arachidonate 15-lipoxygenase
, arachidonate 12-lipoxygenase, leukocyte-type
, arachidonate 12-lipoxygenase, 12S-type
, Arachidonate 15-lipoxygenase
, erythroid cell-specific 15-lipoxygenase
, omega-6 lipoxygenase
, arachidonate lipoxygenase, epidermal