Disease relevance of 2010317E24Rik

• This study shows that 12/15-LOX(-/-) mice have increased NO biosynthesis and impaired ang II-dependent vascular responses in vitro and in vivo, suggesting that 12/15-LOX signaling contributes to impaired NO bioactivity in vascular disease in vivo [1].

High impact information on 2010317E24Rik

• To characterize whether 12/15-LOX also contributes to endothelial dysfunction and hypertension, regulation of vessel tone and angiotensin II (ang II) responses were characterized in mice deficient in 12/15-LOX [1].
• Angiotensin II failed to vasoconstrict 12/15-LOX(-/-) aortic rings in the absence of L-nitroarginine-methyl ester, and ang II impaired acetylcholine-induced relaxation in wild-type, but not 12/15-LOX(-/-) rings [1].
• In vivo, 12/15-LOX(-/-) mice had similar basal systolic blood pressure measurements to wild type, however, blood pressure elevations in response to ang II infusion (1.1 mg/kg/day) were significantly attenuated (maximal pressure, 143.4 +/- 4 mmHg versus 122.1 +/- 5.3 mmHg for wild type and 12/15-LOX(-/-), respectively) [1].
• The ability of angiotensin II (ang II) to produce apoptosis is controversial [2].
• The absence of ang II-induced cell death was also demonstrated in neonatal mouse cardiomyocytes in culture [2].

Biological context of 2010317E24Rik

• ang is a novel gene expressed in early neuroectoderm, but its null mutant exhibits no obvious phenotype [3].
• Rather ang II prevented serum deprivation-induced apoptosis [2].

Anatomical context of 2010317E24Rik

• The 10.0 and 11.5 hr for oesophagus ang tongue epithelium respectively made experimental design for chalone assay difficult when pinna epidermis was the target tissue [4].

Associations of 2010317E24Rik with chemical compounds

• There was no evidence of ang II-induced apoptosis in the presence of the ang II Type 1 receptor antagonist losartan in embryonic chick cardiomyocytes [2].

References