Inactivation of Foxo3a and Subsequent Downregulation of PGC-1alpha Mediate Nitric Oxide-Induced Endothelial Cell Migration.

Background: FOXO3a is a protein that is an important regulator of oxidative stress by modulating antioxidants like catalase, influences aging, is a tumor repressor, reduced in Nrf2 animals and may contribute to fertility problems. It is found in higher amounts in centenarians, meaning those that live to a hundred years or more. Its activity can be effected by methylation and acetylation. (Wipedia-FOXO3a)

"Borniquel, S., García-Quintáns, N., Valle, I., Olmos, Y., Wild, B., Martínez-Granero, F., Soria, E., Lamas, S., and Monsalve, M. (2010). Inactivation of foxo3a and subsequent downregulation of pgc-1alpha mediate nitric oxide-induced endothelial cell migration. Molecular and cellular biology, 30(16):4035-4044."

CiteULike: Inactivation of Foxo3a and Subsequent Downregulation of PGC-1alpha Mediate Nitric Oxide-Induced Endothelial Cell Migration.:

Endotoxemia Causes A Decrease in eNOS-Dependant Vasodilation in Microvasculature~!

"experimental endotoxemia in humans causes a specific decrease in endothelial NO-dependent vasodilation in the microcirculation which cannot be explained by a change of ADMA levels. Microvascular NO deficiency might be responsible for the heterogeneity of tissue perfusion observed in sepsis and could be a therapeutic target" Link: ACUTE ENDOTOXEMIA INHIBITS MICROVASCULAR NITRIC OX... [Shock. 2010] - PubMed result:

Study of the nitric oxide system in the rat cerebellum during aging

CiteULike: Study of the nitric oxide system in the rat cerebellum during aging: "Blanco, S., Molina, F. J., Castro, L., Del Moral, M. L., Hernandez, R., Jimenez, A., Rus, A., Martinez-Lara, E., Siles, E., and Peinado, M. A. (2010). Study of the nitric oxide system in the rat cerebellum during aging. BMC Neuroscience, 11(78):1-33."

Role of CO in cardiac mitochondrial biogenesis

"Mitochondrial biogenesis is activated by gene and protein expression of the nuclear respiratory factor 1 (NRF1) and NRF2, of peroxisome proliferator-activated receptor gamma co-activator-1, and of mitochondrial transcription factor A (TFAM), which augmented the copy number of mitochondrial DNA (mtDNA). This is independent of nitric oxide synthase (NOS), as demonstrated by the identical responses in wild-type and endothelial NOS (eNOS)-deficient mice, and by the inhibition of inducible NOS (iNOS)."

A new activating role for CO in cardiac mitochondrial biogenesis -- Suliman et al. 120 (2): 299 -- Journal of Cell Science:

Resistin decreases eNOS and May Play Major Role in Oxidative Stress and Mitochondrial Dysfuntion!

Resistin: Resistin is a protein secreted by immune and epithelial cells in some mammals including primates and dogs and secreted in adipocytes in mice and rats. Recent discoveries of its role include inflammation and energy regulation as well as, observations in playing a part in insulin resistance. (Wipedia)

Three antioxidants, seleno-L-methionine, ginsenoside Rb1, and MnTBAP (superoxide dismutase mimetic), effectively blocked resistin-induced eNOS downregulation....Thus resistin directly induces eNOS downregulation through overproduction of ROS and activation of p38 and JNK in HCAECs. Resistin-induced mitochondrial dysfunction and imbalance in cellular redox enzymes may be the underlying mechanisms of oxidative stress.

HEIRS Library Tags: Resistin

CiteULike: Resistin decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells: "Chen, C., Jiang, J., Lu, J.-M., Chai, H., Wang, X., Lin, P. H., and Yao, Q. (2010). Resistin decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells. Am J Physiol Heart Circ Physiol, 299(1):H193-201."