Gene Transfer Of Extracellular Sod Protects Against Vascular Dysfuction With Aging
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This study examined the effects of gene transfer of extracellular superoxide dismutase (ECSOD) on vascular function in aged rats. The researchers found that aged rats had higher cholesterol levels and increased vascular superoxide levels compared to young rats. Gene transfer of ECSOD, but not a mutant form lacking the heparin-binding domain, reduced superoxide levels in aged rats and improved acetylcholine-induced vascular relaxation. This suggests that increased oxidative stress contributes to vascular dysfunction in aging, and ECSOD gene therapy has protective effects by reducing superoxide levels in the blood vessel wall.
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This study examined whether contractile activity in cardiomyocytes regulates inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production via focal adhesion kinase (FAK)-dependent signaling. The researchers treated spontaneously contracting neonatal rat ventricular myocytes with inhibitors of contraction and found they reduced iNOS expression and NO production by inhibiting FAK and AKT phosphorylation. Inhibiting FAK or PI3K also eliminated contraction-induced iNOS expression. Knockdown of FAK reduced AKT phosphorylation and iNOS expression, whereas overexpression of constitutively active FAK or AKT reversed the inhibitory effect of contraction inhibitors. Thus, contraction induces iNOS expression and NO production via a FAK-PI3K-AK
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178 vaccination against atherosclerosis
There is promising research into developing vaccines against atherosclerosis. Studies have found that vaccination against oxidized LDL and certain ApoB-100 peptides can reduce the development of atherosclerosis in animal models by up to 60%. A recent study immunized ApoE null mice with ApoB-100 peptide sequences and found a 60% reduction in atherosclerotic plaque in the aorta. Further research is still needed but vaccination shows potential as a way to prevent atherosclerosis and vulnerable plaques in humans. International collaboration could help advance this area towards developing heart attack prevention through immune modulation.
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This study examined whether contractile activity in cardiomyocytes regulates inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production via focal adhesion kinase (FAK)-dependent signaling. The researchers treated spontaneously contracting neonatal rat ventricular myocytes with inhibitors of contraction and found they reduced iNOS expression and NO production by inhibiting FAK and AKT phosphorylation. Inhibiting FAK or PI3K also eliminated contraction-induced iNOS expression. Knockdown of FAK reduced AKT phosphorylation and iNOS expression, whereas overexpression of constitutively active FAK or AKT reversed the inhibitory effect of contraction inhibitors. Thus, contraction induces iNOS expression and NO production via a FAK-PI3K-AK
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1) PGE2 produced in inflamed atherosclerotic plaques activates platelets through the EP3 receptor, similarly to how ADP activates platelets through P2Y12.
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2) The relaxation response is similar between arteries from CB1 receptor knockout mice and wild-type littermates, indicating it is not mediated by CB1 receptors.
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Nitric oxide(NO)-Physiological role
Nitric oxide was known as a toxic gas, as an air pollutant, as an agent causing ozone holes and acid rain till 1987 but this Nitric oxide (NO), a free radical, possesses various modulatory effects on biological systems. NO is synthesized from arginine by the action of nitric oxide synthase (NOS) enzymes.
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ROLE IN NERVOUS SYSTEM
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Background: We tried to understand some undetermined missions of cholesterol and triglycerides (TG) in the plasma in patients with the sickle cell diseases (SCD). Methods: All patients with the SCD and age and gender-matched control cases were included into the study. Results: We studied 363 patients with the SCD (194 males) and 255 control cases (136 males), totally. Mean ages of the SCD patients were similar in males and females (31.1 vs. 31.0 years, respectively, P > 0.05). Although the body weight and body mass index (BMI) were significantly suppressed in the SCD patients (59.9 vs. 71.5 kg and 21.9 vs. 25.6 kg/m2, respectively, P = 0.000 for both), the body heights were similar in both groups (164.9 vs. 167.0 cm, P > 0.05). Parallel to the suppressed mean body weight and BMI, fasting plasma glucose (92.8 vs. 97.6 mg/dL, P = 0.005), total cholesterol (121.4 vs. 165.0 mg/dL, P = 0.000), low-density lipoproteins (70.4 vs. 102.4 mg/dL, P = 0.000), and high-density lipoproteins (26.0 vs. 39.6 mg/dL, P = 0.000) values were all suppressed in the SCD patients, significantly. Similarly, both systolic (115.2 vs. 122.6 mmHg, P = 0.000) and diastolic blood pressure (73.0 vs. 86.6 mmHg, P = 0.000) were also suppressed in them, significantly. Interestingly, only the plasma TG were increased in the SCD patients (129.4 vs. 117.3 mg/dL, P = 0.000), significantly. Similarly, mean alanine aminotransferase value was not suppressed in them, too (27.4 vs. 27.3 U/L, P > 0.05). Conclusion: Cholesterol may be a negative whereas TG positive acute phase reactants in the plasma.
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1) PGE2 produced in inflamed atherosclerotic plaques activates platelets through the EP3 receptor, similarly to how ADP activates platelets through P2Y12.
2) A selective EP3 antagonist called DG-041 was developed that inhibits PGE2 facilitation of platelet aggregation in vitro and ex vivo without affecting bleeding time in rats, unlike
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1) Mesenteric branch arteries from mice relax in response to increasing extracellular calcium concentrations in a manner dependent on potassium channel activity.
2) The relaxation response is similar between arteries from CB1 receptor knockout mice and wild-type littermates, indicating it is not mediated by CB1 receptors.
3) The CB1 receptor antagonist SR141716A inhibits calcium-induced relaxation in arteries from both wild-type and CB1 receptor knockout mice, suggesting it acts through a non-CB1 receptor mechanism at higher concentrations.
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Nitric oxide is a molecule that plays an important role in various biological systems like the nervous, cardiovascular, and immune systems. It is involved in cellular signaling as a paracrine and autocrine molecule. Nitric oxide acts as a vasodilator by signaling smooth muscle in blood vessels to relax, increasing blood flow. Foods high in nitrates like beets, spinach, and watermelon can increase nitric oxide levels and lower blood pressure. Icariin supplements are effective natural boosters of nitric oxide that improve exercise performance and muscle recovery.
Cerebral Ischemia overview
Cerebral ischemia occurs when there is a decrease in blood flow to brain tissue, impairing metabolic functions and causing cell death. Animal models are used to study the cellular and molecular mechanisms of ischemic injury in the brain. During ischemia and reperfusion, there are excessive excitatory neurotransmitters, free radicals, acidosis, and inflammation which contribute to cell death through mechanisms like excitotoxicity, apoptosis, and necrosis. Hypothermia is neuroprotective by reducing metabolic demands and free radical production. Experimental therapies aim to reduce excitotoxicity, free radicals, inflammation and improve cell survival through neurotrophins or stem cells.
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Nitric oxide (NO) is an endogenous signaling molecule generated from L-arginine by nitric oxide synthase. It is a key signaling molecule in the cardiovascular, nervous, and immune systems. NO activates guanylate cyclase, increasing cyclic GMP levels to cause smooth muscle relaxation and inhibit platelet aggregation. The physiological role of NO was discovered in the vasculature, where it was shown that endothelium-derived relaxing factor causing vasodilation was NO. NO has diverse functions and is involved in processes like neurotransmission, host defense, and inflammation.
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This document provides an overview of the role of nitric oxide (NO) in the body. It discusses NO's structure as a lipid-soluble gas that is synthesized from L-arginine by nitric oxide synthase (NOS) enzymes. The three main types of NOS - neuronal, endothelial, and inducible - are described. The roles of NO in various body systems like the nervous, circulatory, immune and digestive systems are summarized. NO functions as a neurotransmitter, vasodilator, and plays roles in platelet inhibition and host defense. Abnormal NO production can contribute to conditions like hypertension. NO donors and inhibitors that are used experimentally are also listed.
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Apomimetic peptides
This presentation discusses a newer approach to treating vascular dysfunction diseases using apomimetic peptides that mimic apolipoproteins. It provides background on lipoproteins, HDL, and apolipoproteins before discussing how short synthetic peptides called apomimetic peptides can mimic apolipoprotein functions. Several apomimetic peptides are presented that show promise in reducing atherosclerosis and improving cholesterol efflux in animal models. The presentation concludes that apomimetic peptides may prove useful as diagnostic and therapeutic agents for vascular diseases.
Anti adamts2 monoclonal antibody
This document provides information about an anti-ADAMTS2 monoclonal antibody that targets the ADAMTS2 protein. It summarizes that ADAMTS2 is a protein coding gene involved in the degradation of the extracellular matrix. Mutations in ADAMTS2 cause Ehlers-Danlos syndrome type VIIC, a connective tissue disorder characterized by fragile tissues and joint hypermobility. The monoclonal antibody in this document targets a region of the ADAMTS2 protein and can be used for applications like western blotting and ELISA.
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Nitric oxide (NO) is an important signalling molecule in the body that regulates many physiological processes. It is synthesized by nitric oxide synthase enzymes from L-arginine and oxygen. NO signals through activation of soluble guanylate cyclase and production of cyclic GMP. It has diverse effects in the cardiovascular, immune, and nervous systems and is involved in processes like vasodilation, neurotransmission, and inflammation. Both insufficient and excessive NO production can contribute to disease.
Nitric oxide(NO)-Physiological role
Nitric oxide was known as a toxic gas, as an air pollutant, as an agent causing ozone holes and acid rain till 1987 but this Nitric oxide (NO), a free radical, possesses various modulatory effects on biological systems. NO is synthesized from arginine by the action of nitric oxide synthase (NOS) enzymes.
ROLE IN CARDIOVASCULAR SYSTEM
ROLE IN IMMUNE SYSTEM
ROLE IN NERVOUS SYSTEM
ROLE IN REPRODUCTIVE SYSTEM
ROLE IN RESPIRATORY SYSTEM
ROLE IN RENAL SYSTEM
ROLE IN ENDOCRINE SYSTEM
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ROLE IN HAIR GROWTH
Pharmacology of Nitric oxide
The endothelium is the thin layer of cells that lines the interior surface of blood vessels. Endothelial cells release nitric oxide (NO), which acts as a vasodilator and modulates vessel tone. NO is synthesized from L-arginine by the enzyme nitric oxide synthase. It binds to guanylate cyclase, increasing cGMP levels and causing smooth muscle relaxation through various mechanisms. NO has many roles in the nervous, circulatory, immune and other body systems. It is involved in processes like vasodilation, neurotransmission, and host defense. NO synthesis can be inhibited by L-arginine analogs, while NO donors are used therapeutically to elicit smooth muscle relaxation.
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This document discusses reactive oxygen species (ROS), specifically hydrogen peroxide (H2O2), in physiological and pathological conditions related to vascular diseases. It provides background on ROS, describing them as molecules containing unpaired electrons that are either free radicals like superoxide or non-radicals like H2O2. H2O2 is produced during normal cell metabolism and can act as a signaling molecule by oxidizing proteins, but also needs to be carefully regulated to prevent oxidative damage. The document then focuses on the roles and mechanisms of H2O2 in vasoconstriction and vasodilation, explaining it can cause both effects depending on conditions through pathways like activating potassium channels or the cyclooxygenase pathway.
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Cholesterol May be a Negative Whereas Triglycerides Positive Acute Phase Reac...
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222 animal models of heart attack
This document summarizes various animal models that have been used to study atherosclerosis and heart attacks, including quail, pigeons, chickens, dogs, monkeys, pigs, rats, rabbits, and mice. It provides details on the types of lesions each animal can develop and how closely they resemble human coronary artery disease. It highlights that double knockout LDL/apoE mice may offer an improved model for studying clinical complications of atherosclerosis like human ischemic heart disease, though it is unclear how closely they mimic vulnerable human plaques.
222 animal models of heart attack
I. The double knockout LDL/apoE mice model of atherosclerosis more closely resembles human coronary artery disease than other animal models as it exhibits morphological and functional defects similar to those seen in humans, including extensive coronary artery lesions, fibrin deposition, and spontaneous myocardial infarctions at a young age.
II. However, it is unclear how well this new model simulates the specific pathophysiology and pathology of vulnerable human atherosclerotic plaques, such as thin fibrous caps.
III. Further research is still needed to determine how the coagulation systems of animal models compare to humans and whether any can accurately model repeated plaque ruptures over time as occurs naturally in human disease.
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Hydrogen sulphide as a gasotransmitter loading
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Gene Transfer Of Extracellular Sod Protects Against Vascular Dysfuction With Aging
- 1. Gene transfer of extracellular superoxide dismutase protects against vascular dysfunction with aging Am J Physiol Heart Circ Physiol 290: H2600–H2605, 2006. Kathryn A. Brown, Yi Chu,Donald D. Lund, Donald D. Heistad, and Frank M. Faraci Speaker: 賴小婷 Date:97/08/13
- 2. Introduction
- 4. O 2 ． ¯ H 2 0 2 H 2 O+O 2 NO + O 2 ． ¯ ONOO¯ Oxidative stress (Peroxynitrite) DNA damage (Endothelial dysfunction) SOD Calatase GPx SOD ONOO ¯ can induce protein modifications and DNA damage
- 7. Methods
- 8. Male Fischer 344 rats ages 4–6 months ( n = 23) Young 29–31 months ( n = 37) Old Plasma analysis ( glucose 、 cholesterol ) Gene transfer of ECSOD and ECSOD△HBD Thoracic aortas ( 95% O2-5% CO2 .37℃) ＊ Vasomotor function (ACh 、 SNP 、 5-HT 、 PE ) ＊ SOD protein expression ＊ Superoxide levels ( O2 ． ¯ )
- 9. ECSODHBD is identical to ECSOD except that the carboxy-terminal 13-amino-acid segment containing the HBD is deleted . ECSOD is a homotetrameric glycosylated protein (155 kDa) CuZnSOD is a 32-kDa homodimer without glycosylation ( Circ Res . 2003;92:461-468.)
- 10. Results
- 11. Fig 1 * Old rats had significantly higher plasma levels of cholesterol than young rats, although the levels of cholesterol were still relatively low There was no significant difference in body weight or plasma glucose (nonfasting) between young and old Fischer 344 rats
- 12. Acetylcholine Relaxation Vasomotor function ◎ Acetylcholine (ACh) stimulates the endothelial cells to produce a factor, NO, which penetrates into and activates the muscle cells causing relaxation
- 13. Fig 2 Responses to ACh were significantly improved after adenoviral-mediated gene transfer of human ECSOD Transfection with ECSOD lacking the HBD had no significant effect on responses to ACh in vessels from old rats ACh:Acetylcholine ＊ ACh was used to assess NO-mediated endothelial function
- 14. Fig 3 Responses to SNP were similar in aortas from young and old rats and were not altered by gene transfer of either form of ECSOD ◎ SNP (sodium nitroprusside) : activates the vessel causing relaxation
- 15. Fig 4 There were no significant differences in response to serotonin in aortas from young and old rats ◎ 5-HT (5-hydroxytryptamine 、 serotonin) : stimulates smooth muscle cell contraction
- 16. Fig 5 Gene transfer of either form of ECSOD had no significant effect on the response to phenylephrine ◎ PE (Phenylephrine): stimulates the vessel causing contraction
- 17. Fig 6 There were no significant differences in the levels of MnSOD and CuZnSOD between groups There was a tendency for MnSOD to be increased in the old rats
- 18. Fig 7 After gene transfer of ECSOD, superoxide levels from old rats were similar to those in aorta from young rats Superoxide levels
- 19. Discussion
- 20. These results suggest : 1 . Vascular dysfunction associated with aging is mediated in part by increased levels of superoxide 2 . Gene transfer of ECSOD reduces vascular superoxide and dysfunction in old rats 3 .Beneficial effects of ECSOD in old rats require the heparin-binding domain (HBD) of ECSOD.
- 22. ☆ Thanks for your attention