Mycoplasma pneumoniae (Mp) is the most frequently identified pathogen in the California Encephali... more Mycoplasma pneumoniae (Mp) is the most frequently identified pathogen in the California Encephalitis Project, but the role and mechanism of Mp is unclear. Since auto-antibodies to anti-galactocerebroside (anti-GalC) have been reported in patients with evidence of acute Mp infection of the central nervous system (CNS), serum and cerebrospinal fluid (CSF) samples from 26 patients with evidence of Mp were tested for anti-GalC antibodies. Anti-GalC antibody was found in the CSF of only eight (31%) of 21 Mp patients indicating that CSF anti-GalC antibody is not a specific marker for Mp CNS disease.
NADPH oxidase (Nox)-derived reactive oxygen species (ROS) are known to be involved in angiotensin... more NADPH oxidase (Nox)-derived reactive oxygen species (ROS) are known to be involved in angiotensin II-induced hypertension and endothelial dysfunction. Several Nox isoforms are expressed in the vessel wall, among which Nox2 is especially abundant in the endothelium. Endothelial Nox2 levels rise during hypertension but little is known about the cell-specific role of endothelial Nox2 in vivo. To address this question, we generated transgenic mice with endothelial-specific overexpression of Nox2 (Tg) and studied the effects on endothelial function and blood pressure. Tg had an about twofold increase in endothelial Nox2 levels which was accompanied by an increase in p22phox levels but no change in levels of other Nox isoforms or endothelial nitric oxide synthase (eNOS). Basal NADPH oxidase activity, endothelial function and blood pressure were unaltered in Tg compared to wild-type littermates. Angiotensin II caused a greater increase in ROS production in Tg compared to wild-type aorta and attenuated acetylcholine-induced vasorelaxation. Both low and high dose chronic angiotensin II infusion increased telemetric ambulatory blood pressure more in Tg compared to wild-type, but with different patterns of BP change and aortic remodeling depending upon the dose of angiotensin II dose. These results indicate that an increase in endothelial Nox2 levels contributes to angiotensin II-induced endothelial dysfunction, vascular remodeling and hypertension.
Endothelial activation refers to a specific change in endothelial phenotype, characterized most n... more Endothelial activation refers to a specific change in endothelial phenotype, characterized most notably by an increase in endothelial-leukocyte interactions and permeability, which is pivotal to inflammatory responses in both physiologic and pathologic settings. An increasing body of evidence indicates an important role for reactive oxygen species (ROS)-mediated modulation of signal-transduction pathways in many of the processes involved in endothelial activation. ROS generated by the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes may be especially important in this regard. We discuss the evidence implicating redox signaling pathways in the molecular and cellular processes underlying endothelial activation and the role in cardiovascular diseases, and also provide a detailed description of NADPH oxidase regulation in endothelial cells, in view of its likely importance in this context.
Mycoplasma pneumoniae (Mp) is the most frequently identified pathogen in the California Encephali... more Mycoplasma pneumoniae (Mp) is the most frequently identified pathogen in the California Encephalitis Project, but the role and mechanism of Mp is unclear. Since auto-antibodies to anti-galactocerebroside (anti-GalC) have been reported in patients with evidence of acute Mp infection of the central nervous system (CNS), serum and cerebrospinal fluid (CSF) samples from 26 patients with evidence of Mp were tested for anti-GalC antibodies. Anti-GalC antibody was found in the CSF of only eight (31%) of 21 Mp patients indicating that CSF anti-GalC antibody is not a specific marker for Mp CNS disease.
NADPH oxidase (Nox)-derived reactive oxygen species (ROS) are known to be involved in angiotensin... more NADPH oxidase (Nox)-derived reactive oxygen species (ROS) are known to be involved in angiotensin II-induced hypertension and endothelial dysfunction. Several Nox isoforms are expressed in the vessel wall, among which Nox2 is especially abundant in the endothelium. Endothelial Nox2 levels rise during hypertension but little is known about the cell-specific role of endothelial Nox2 in vivo. To address this question, we generated transgenic mice with endothelial-specific overexpression of Nox2 (Tg) and studied the effects on endothelial function and blood pressure. Tg had an about twofold increase in endothelial Nox2 levels which was accompanied by an increase in p22phox levels but no change in levels of other Nox isoforms or endothelial nitric oxide synthase (eNOS). Basal NADPH oxidase activity, endothelial function and blood pressure were unaltered in Tg compared to wild-type littermates. Angiotensin II caused a greater increase in ROS production in Tg compared to wild-type aorta and attenuated acetylcholine-induced vasorelaxation. Both low and high dose chronic angiotensin II infusion increased telemetric ambulatory blood pressure more in Tg compared to wild-type, but with different patterns of BP change and aortic remodeling depending upon the dose of angiotensin II dose. These results indicate that an increase in endothelial Nox2 levels contributes to angiotensin II-induced endothelial dysfunction, vascular remodeling and hypertension.
Endothelial activation refers to a specific change in endothelial phenotype, characterized most n... more Endothelial activation refers to a specific change in endothelial phenotype, characterized most notably by an increase in endothelial-leukocyte interactions and permeability, which is pivotal to inflammatory responses in both physiologic and pathologic settings. An increasing body of evidence indicates an important role for reactive oxygen species (ROS)-mediated modulation of signal-transduction pathways in many of the processes involved in endothelial activation. ROS generated by the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes may be especially important in this regard. We discuss the evidence implicating redox signaling pathways in the molecular and cellular processes underlying endothelial activation and the role in cardiovascular diseases, and also provide a detailed description of NADPH oxidase regulation in endothelial cells, in view of its likely importance in this context.
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Papers by Sara Ruiz