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Article ; Online: Amiodarone improves anemia in a murine model of sickle cell disease and is associated with increased erythrocyte bis(monoacylglycerol) phosphate.

Venugopal, Jessica / Wang, Jintao / Guo, Chiao / Eitzman, Daniel T

2022 Volume 12, Issue 1, Page(s) 16437

Abstract: Sickle cell disease (SCD) is associated with altered plasma and erythrocyte lipid profiles. In a previous study, SCD mice with deficiency of proprotein convertase subtilisin/kexin type 9 (PCSK9) were observed to have more severe anemia and increased ... ...

Abstract	Sickle cell disease (SCD) is associated with altered plasma and erythrocyte lipid profiles. In a previous study, SCD mice with deficiency of proprotein convertase subtilisin/kexin type 9 (PCSK9) were observed to have more severe anemia and increased sickling compared to control SCD mice. Although PCSK9 affects circulating low density lipoprotein (LDL) by regulation of the LDL receptor, the effect of PCSK9 on anemia was independent of LDL receptor expression. In the current study, erythrocyte metabolomics were performed and revealed altered erythrocyte lipid species between SCD mice with and without PCSK9. Of particular interest, the late endosome-specific lipid bis(mono)acylglycerol phosphate (BMP) 44:12 was markedly decreased in erythrocytes from SCD mice deficient in PCSK9 mice relative to control SCD mice. Incubation of sickle erythrocytes with a neutralizing antibody to BMP increased erythrocyte sickling in vitro. In vitro treatment of SCD erythrocytes with amiodarone (1.5 μM) or medroxyprogesterone (6.75 μM), two pharmacologic compounds known to increase BMP, resulted in reduced erythrocyte sickling. Treatment of SCD mice with amiodarone (10 mg/kg) for 2 weeks resulted in increased BMP, improvement in anemia with reduced reticulocytosis, and decreased ex vivo sickling. In conclusion, severity of anemia in SCD is improved with amiodarone treatment, an effect which may be mediated through increased erythrocyte BMP.
MeSH term(s)	Amiodarone/pharmacology ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/drug therapy ; Animals ; Antibodies, Neutralizing/pharmacology ; Disease Models, Animal ; Erythrocytes/metabolism ; Lipoproteins, LDL/metabolism ; Medroxyprogesterone/pharmacology ; Mice ; Monoglycerides/metabolism ; Phosphates/metabolism ; Proprotein Convertase 9/metabolism ; Receptors, LDL/metabolism ; Subtilisins/metabolism
Chemical Substances	Antibodies, Neutralizing ; Lipoproteins, LDL ; Monoglycerides ; Phosphates ; Receptors, LDL ; PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-) ; Subtilisins (EC 3.4.21.-) ; Medroxyprogesterone (HSU1C9YRES) ; Amiodarone (N3RQ532IUT)
Language	English
Publishing date	2022-09-30
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-20955-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Interleukin-1 receptor inhibition reduces stroke size in a murine model of sickle cell disease.

Venugopal, Jessica / Wang, Jintao / Mawri, Jalal / Guo, Chiao / Eitzman, Daniel

Haematologica

2021 Volume 106, Issue 9, Page(s) 2469–2477

Abstract: Sickle cell disease (SCD) is associated with chronic hemolytic anemia and a heightened inflammatory state. The causal role of inflammatory pathways in stroke associated with SCD is unclear. Therefore, the hypothesis that deletion of the non-hematopoietic ...

Abstract	Sickle cell disease (SCD) is associated with chronic hemolytic anemia and a heightened inflammatory state. The causal role of inflammatory pathways in stroke associated with SCD is unclear. Therefore, the hypothesis that deletion of the non-hematopoietic interleukin-1 receptor (IL-1R) pool may be beneficial in SCD was pursued. Since potential deleterious effects of IL-1R signaling in SCD could be mediated via downstream production of interleukin-6 (IL-6), the role of the non-hematopoietic IL-6 pool was also addressed. Bone marrow transplantation (BMT) from SCD to wild-type (WT) recipient mice was used to generate SCD mice (Wt,SCDbmt). To generate mice with non-hematopoietic deficiency of IL-1R or IL-6, SCD marrow was transplanted into IL-1R deficient (IL1R-/-,SCDbmt) or IL-6 deficient recipients (IL6-/-,SCDbmt). Blood counts, reticulocytes, soluble E-selectin (Esel), and IL-6 levels were analyzed 14-15 weeks post-BMT. Ischemic stroke was induced by middle cerebral artery (MCA) photothrombosis at 16 weeks post-BMT. A separate group of Wt,SCDbmt mice was given the IL-1R inhibitor, anakinra, following stroke induction. Seventy-two hours after MCA occlusion, stroke volume was assessed by staining brain sections with 2,3,5-triphenyltetrazolium chloride. Formalin-fixed brain sections were also stained for macrophages with MAC3, for endothelial activation with ICAM-1, and for loss of blood brain barrier (BBB) integrity with fibrin(ogen) staining. All SCD mice generated by BMT were anemic and the severity of anemia was not different between Wt,SCDbmt, IL1R-/-,SCDbmt, and IL6-/-,SCDbmt mice. Three days following MCA occlusion, stroke volume was significantly reduced in IL1R-/-,SCDbmt mice compared to Wt,SCDbmt mice and IL6-/-,SCDbmt mice. Plasma levels of sE-sel were lower in IL1R-/-,SCDbmt compared to Wt,SCDbmt and IL-6-/-,SCDbmt mice. Post-stroke treatment of Wt,SCDbmt mice with anakinra decreased stroke size, leukocyte infiltration, ICAM-1 expression, and fibrin(ogen) accumulation compared to vehicle-treated mice. Deficiency of non-hematopoietic IL-1R or treatment with an IL-1R antagonist is sufficient to confer protection against the increased stroke size associated with SCD. These effects of IL1R deficiency are associated with reduced endothelial activation, leukocyte infiltration, and blood brain barrier disruption, and are independent of non-hematopoietic IL-6 signaling.
MeSH term(s)	Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/drug therapy ; Anemia, Sickle Cell/genetics ; Animals ; Disease Models, Animal ; Interleukin 1 Receptor Antagonist Protein ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Interleukin-1
Chemical Substances	Interleukin 1 Receptor Antagonist Protein ; Receptors, Interleukin-1
Language	English
Publishing date	2021-09-01
Publishing country	Italy
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2020.252395
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Article ; Online: Interleukin-1 receptor antagonism leads to improved anaemia in a murine model of sickle cell disease and is associated with reduced ex vivo platelet-mediated erythrocyte sickling.

Venugopal, Jessica / Wang, Jintao / Guo, Chiao / Eitzman, Daniel T

British journal of haematology

2021 Volume 196, Issue 4, Page(s) 1040–1051

Abstract: Sickle cell disease (SCD) is associated with haemolytic anaemia and secondary activation of leucocytes and platelets, which in turn may further exacerbate haemolysis. As cytokine signalling pathways may participate in this cycle, the present study ... ...

Abstract	Sickle cell disease (SCD) is associated with haemolytic anaemia and secondary activation of leucocytes and platelets, which in turn may further exacerbate haemolysis. As cytokine signalling pathways may participate in this cycle, the present study investigated whether pharmacological blockade of the interleukin-1 receptor (IL-1R) would mitigate anaemia in a murine model of SCD. Within 2 weeks of treatment, reduced markers of haemolysis were observed in anakinra-treated mice compared to vehicle-treated mice. After 4 weeks of anakinra treatment, mice showed increased numbers of erythrocytes, haemoglobin, and haematocrit, along with reduced reticulocytes. Blood from anakinra-treated mice was less susceptible to ex vivo erythrocyte sickling and was resistant to exogenous IL-1β-mediated sickling. Supernatant generated from IL-1β-treated platelets was sufficient to promote erythrocyte sickling, an effect not observed with platelet supernatant generated from IL-1R
MeSH term(s)	Anemia/physiopathology ; Anemia, Sickle Cell/genetics ; Animals ; Blood Platelets/metabolism ; Disease Models, Animal ; Erythrocytes, Abnormal ; Humans ; Mice ; Receptors, Interleukin-1/genetics
Chemical Substances	Receptors, Interleukin-1
Language	English
Publishing date	2021-11-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/bjh.17941
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Article ; Online: Beta1-receptor blockade attenuates atherosclerosis progression following traumatic brain injury in apolipoprotein E deficient mice.

Wang, Jintao / Venugopal, Jessica / Silaghi, Paul / Su, Enming J / Guo, Chiao / Lawrence, Daniel A / Eitzman, Daniel T

PloS one

2023 Volume 18, Issue 5, Page(s) e0285499

Abstract: Traumatic brain injury (TBI) is associated with cardiovascular mortality in humans. Enhanced sympathetic activity following TBI may contribute to accelerated atherosclerosis. The effect of beta1-adrenergic receptor blockade on atherosclerosis progression ...

Abstract	Traumatic brain injury (TBI) is associated with cardiovascular mortality in humans. Enhanced sympathetic activity following TBI may contribute to accelerated atherosclerosis. The effect of beta1-adrenergic receptor blockade on atherosclerosis progression induced by TBI was studied in apolipoprotein E deficient mice. Mice were treated with metoprolol or vehicle following TBI or sham operation. Mice treated with metoprolol experienced a reduced heart rate with no difference in blood pressure. Six weeks following TBI, mice were sacrificed for analysis of atherosclerosis. Total surface area and lesion thickness, analyzed at the level of the aortic valve, was found to be increased in mice receiving TBI with vehicle treatment but this effect was ameliorated in TBI mice receiving metoprolol. No effect of metoprolol on atherosclerosis was observed in mice receiving only sham operation. In conclusion, accelerated atherosclerosis following TBI is reduced with beta-adrenergic receptor antagonism. Beta blockers may be useful to reduce vascular risk associated with TBI.
MeSH term(s)	Animals ; Mice ; Adrenergic beta-Antagonists/pharmacology ; Adrenergic beta-Antagonists/therapeutic use ; Atherosclerosis/pathology ; Blood Pressure ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/drug therapy ; Disease Models, Animal ; Metoprolol/pharmacology ; Metoprolol/therapeutic use ; Mice, Inbred C57BL
Chemical Substances	Adrenergic beta-Antagonists ; Metoprolol (GEB06NHM23)
Language	English
Publishing date	2023-05-26
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0285499
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Article ; Online: Clopidogrel Resistance in a Murine Model of Diet-Induced Obesity Is Mediated by the Interleukin-1 Receptor and Overcome With DT-678.

Sun, Yifang / Venugopal, Jessica / Guo, Chiao / Fan, Yanbo / Li, Jianping / Gong, Yanjun / Chen, Y Eugene / Zhang, Haoming / Eitzman, Daniel T

Arteriosclerosis, thrombosis, and vascular biology

2020 Volume 40, Issue 6, Page(s) 1533–1542

Abstract: Objective: Clopidogrel is a commonly used P2Y: Conclusions: These findings indicate that antiplatelet effects of clopidogrel may be impaired in the setting of diabetes mellitus due to reduced prodrug bioactivation related to IL-1 receptor signaling. ... ...

Abstract	Objective: Clopidogrel is a commonly used P2Y Conclusions: These findings indicate that antiplatelet effects of clopidogrel may be impaired in the setting of diabetes mellitus due to reduced prodrug bioactivation related to IL-1 receptor signaling. Therapeutic targeting of P2Y
MeSH term(s)	Animals ; Carotid Artery Thrombosis/prevention & control ; Clopidogrel/pharmacokinetics ; Clopidogrel/pharmacology ; Clopidogrel/therapeutic use ; Cytochrome P-450 Enzyme System/genetics ; Diabetes Mellitus ; Diet, High-Fat ; Disease Models, Animal ; Drug Resistance ; Fibrinolytic Agents ; Gene Expression ; Male ; Mice ; Mice, Inbred C57BL ; Microsomes, Liver/enzymology ; Obesity/complications ; Obesity/etiology ; Obesity/metabolism ; Platelet Aggregation/drug effects ; Platelet Aggregation Inhibitors ; Prodrugs/pharmacokinetics ; Prodrugs/therapeutic use ; Receptors, Interleukin-1/deficiency ; Receptors, Interleukin-1/physiology
Chemical Substances	Fibrinolytic Agents ; Platelet Aggregation Inhibitors ; Prodrugs ; Receptors, Interleukin-1 ; Cytochrome P-450 Enzyme System (9035-51-2) ; Clopidogrel (A74586SNO7)
Language	English
Publishing date	2020-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.120.314146
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Article ; Online: Traumatic Brain Injury Leads to Accelerated Atherosclerosis in Apolipoprotein E Deficient Mice.

Wang, Jintao / Su, Enming / Wang, Hui / Guo, Chiao / Lawrence, Daniel A / Eitzman, Daniel T

Scientific reports

2018 Volume 8, Issue 1, Page(s) 5639

Abstract: Traumatic brain injury (TBI) has been associated with atherosclerosis and cardiovascular mortality in humans. However the causal relationship between TBI and vascular disease is unclear. This study investigated the direct role of TBI on vascular disease ... ...

Abstract	Traumatic brain injury (TBI) has been associated with atherosclerosis and cardiovascular mortality in humans. However the causal relationship between TBI and vascular disease is unclear. This study investigated the direct role of TBI on vascular disease using a murine model of atherosclerosis. Apolipoprotein E deficient mice were placed on a western diet beginning at 10 weeks of age. Induction of TBI or a sham operation was performed at 14 weeks of age and mice were sacrificed 6 weeks later at 20 weeks of age. MRI revealed evidence of uniform brain injury in all mice subjected to TBI. There were no differences in total cholesterol levels or blood pressure between the groups. Complete blood counts and flow cytometry analysis performed on peripheral blood 6 weeks following TBI revealed a higher percentage of Ly6C-high monocytes in mice subjected to TBI compared to sham-treated mice. Mice with TBI also showed elevated levels of plasma soluble E-selectin and bone marrow tyrosine hydroxylase. Analysis of atherosclerosis at the time of sacrifice revealed increased atherosclerosis with increased Ly6C/G immunostaining in TBI mice compared to sham-treated mice. In conclusion, progression of atherosclerosis is accelerated following TBI. Targeting inflammatory pathways in patients with TBI may reduce subsequent vascular complications.
MeSH term(s)	Animals ; Apolipoproteins E/deficiency ; Atherosclerosis/etiology ; Atherosclerosis/pathology ; Blood Pressure Determination ; Brain Injuries, Traumatic/physiopathology ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
Chemical Substances	Apolipoproteins E
Language	English
Publishing date	2018-04-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-23959-2
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Article ; Online: Hematopoietic Deficiency of miR-223 Attenuates Thrombosis in Response to Photochemical Injury in Mice.

Wang, Hui / Wang, Qian / Kleiman, Kyle / Guo, Chiao / Eitzman, Daniel T

Scientific reports

2017 Volume 7, Issue 1, Page(s) 1606

Abstract: Some studies have shown that levels of MicroRNA (miR)-223 derived from platelets in the plasma are reduced following inhibition of platelet function, while others have shown a correlation between low plasma miR-223 and high on-treatment platelet ... ...

Abstract	Some studies have shown that levels of MicroRNA (miR)-223 derived from platelets in the plasma are reduced following inhibition of platelet function, while others have shown a correlation between low plasma miR-223 and high on-treatment platelet reactivity. The present study seeks to investigate the role of miR-223 in arterial thrombosis. A model of photochemical-induced carotid thrombosis was applied to miR-223 deficient mice and littermate (WT) controls. Mice deficient in miR-223 exhibited significantly prolonged times to occlusive thrombosis compared to WT mice indicating a protective effect of miR-223 deficiency. Bone marrow transplantation experiments confirmed that the hematopoietic pool of miR-223 was responsible for differences in thrombosis times. Transfusion of either WT platelets or extracellular vesicles derived from WT platelets were both sufficient to shorten thrombosis times in miR-223 deficient recipients. The effect of platelet transfusions on IGF-1R was explored. These experiments revealed that vascular IGF-1R was down-regulated by platelet miR-223. Furthermore, inhibition of IGF-1R abolished the protection conferred by miR-223 deficiency on thrombosis. In conclusion, platelet miR-223 is a regulator of arterial thrombosis following endothelial injury through effects on vascular wall IGF-1R. This study indicates that platelet miR-223 is a potential therapeutic target for prevention of arterial thrombosis.
MeSH term(s)	Animals ; Carotid Arteries/pathology ; Endothelial Cells/metabolism ; Female ; Gene Expression Regulation ; Hematopoiesis/genetics ; Male ; Mice, Inbred C57BL ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Photochemical Processes ; Receptor, IGF Type 1/metabolism ; Thrombosis/genetics ; Time Factors
Chemical Substances	MIRN223 microRNA, mouse ; MicroRNAs ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2017-05-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-01887-x
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Article ; Online: Angiotensin II-induced Hypertension is Reduced by Deficiency of P-selectin Glycoprotein Ligand-1.

Wang, Qian / Wang, Hui / Wang, Jintao / Venugopal, Jessica / Kleiman, Kyle / Guo, Chiao / Sun, Yingxian / Eitzman, Daniel T

Scientific reports

2018 Volume 8, Issue 1, Page(s) 3223

Abstract: Identification of inflammatory mediators that regulate the vascular response to vasopressor molecules may aid in the development of novel therapeutic agents to treat or prevent hypertensive vascular diseases. Leukocytes have recently been shown to be ... ...

Abstract	Identification of inflammatory mediators that regulate the vascular response to vasopressor molecules may aid in the development of novel therapeutic agents to treat or prevent hypertensive vascular diseases. Leukocytes have recently been shown to be capable of modifying blood pressure responses to vasopressor molecules. The purpose of this study was to test the hypothesis that deficiency of the leukocyte ligand, Psgl-1, would reduce the pressor response to angiotensin II (Ang II). Mice deficient in Psgl-1 (Psgl-1
MeSH term(s)	Angiotensin II/administration & dosage ; Angiotensin II/metabolism ; Animals ; Blood Pressure/drug effects ; Disease Models, Animal ; Hypertension/physiopathology ; Interleukin-17/metabolism ; Membrane Glycoproteins/deficiency ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Knockout ; Vasoconstrictor Agents/metabolism
Chemical Substances	Il17a protein, mouse ; Interleukin-17 ; Membrane Glycoproteins ; P-selectin ligand protein ; Vasoconstrictor Agents ; Angiotensin II (11128-99-7)
Language	English
Publishing date	2018-02-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-21588-3
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Article ; Online: Obesity-induced Endothelial Dysfunction is Prevented by Neutrophil Extracellular Trap Inhibition.

Wang, Hui / Wang, Qian / Venugopal, Jessica / Wang, Jintao / Kleiman, Kyle / Guo, Chiao / Eitzman, Daniel T

Scientific reports

2018 Volume 8, Issue 1, Page(s) 4881

Abstract: Endothelial dysfunction precedes atherosclerosis and may constitute a critical link between obesity-related inflammation and cardiovascular disease. Neutrophil extracellular traps (NETs) have been shown to promote vascular damage in murine models of ... ...

Abstract	Endothelial dysfunction precedes atherosclerosis and may constitute a critical link between obesity-related inflammation and cardiovascular disease. Neutrophil extracellular traps (NETs) have been shown to promote vascular damage in murine models of autoimmune disease and atherosclerosis. The impact of NETs towards endothelial dysfunction associated with obesity is unknown. Using a diet-induced obesity (DIO) mouse model, this study investigated whether the inhibition or degradation of NETs could reduce the endothelial dysfunction observed in DIO mice. Following induction of DIO, there were elevated plasma concentrations of monocyte chemoattractant protein-1 (MCP-1) and impairment of mesenteric arteriolar vasorelaxation in response to acetylcholine as measured by pressure myography. A marker of NET formation, cathelicidin-related antimicrobial peptide (CRAMP), was markedly increased in mesenteric arterial walls of DIO mice compared to mice on standard chow. Prevention of NET formation with Cl-amidine or dissolution of NETs with DNase restored endothelium-dependent vasodilation to the mesenteric arteries of DIO mice. These findings suggest an instrumental role for NETs in obesity-induced endothelial dysfunction.
MeSH term(s)	Animals ; Antimicrobial Cationic Peptides/analysis ; Antimicrobial Cationic Peptides/blood ; Cardiovascular Diseases/physiopathology ; Chemokine CCL2/analysis ; Chemokine CCL2/blood ; Diet, High-Fat ; Disease Models, Animal ; Endothelium, Vascular/metabolism ; Extracellular Traps/metabolism ; Extracellular Traps/physiology ; Inflammation/metabolism ; Male ; Mesenteric Arteries/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Obesity/physiopathology ; Vascular Diseases/physiopathology ; Vasodilation
Chemical Substances	Antimicrobial Cationic Peptides ; Ccl2 protein, mouse ; Chemokine CCL2 ; ropocamptide (3DD771JO2H)
Language	English
Publishing date	2018-03-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-23256-y
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Article ; Online: Renal denervation attenuates progression of atherosclerosis in apolipoprotein E-deficient mice independent of blood pressure lowering.

Wang, Hui / Wang, Jintao / Guo, Chiao / Luo, Wei / Kleiman, Kyle / Eitzman, Daniel T

Hypertension (Dallas, Tex. : 1979)

2015 Volume 65, Issue 4, Page(s) 758–765

Abstract: The renal autonomic nervous system may contribute to hypertension and vascular disease. Although the effects of renal artery denervation on blood pressure lowering are controversial, there may be other beneficial vascular effects independent of blood ... ...

Abstract	The renal autonomic nervous system may contribute to hypertension and vascular disease. Although the effects of renal artery denervation on blood pressure lowering are controversial, there may be other beneficial vascular effects independent of blood pressure lowering. Bilateral renal denervation (RDN) or sham operation (SO) was performed in 14-week-old male apolipoprotein E-deficient mice on a Western diet starting at 10 weeks of age. Efficacy of RDN was confirmed by reduction of renal norepinephrine levels (SO: 3.8±0.1 versus RDN: 1.7±0.3 ng/mL; P<0.01) at 6 weeks after procedure. Compared with SO, RDN had no effect on blood pressure (SO: 101.0±2.4 versus RDN: 97.5±1.6 mm Hg; P=0.25), total cholesterol (SO: 536.7±28.5 versus RDN: 535.7±62.9 mg/dL; P=0.99), or triglycerides (SO: 83.7±3.5 versus RDN: 86.9±10.2 mg/dL; P=0.78). Quantification of atherosclerosis at 20 weeks of age demonstrated reduced atherosclerosis in mice receiving RDN compared with SO (arterial tree oil-red-O surface staining RDN: 4.2±0.5% versus SO: 6.3±0.7%; P<0.05). Reduced atherosclerosis was associated with increased smooth muscle cell content in atherosclerotic plaques (RDN: 13.3±2.1 versus SO: 8.1±0.6%; P<0.05). Serum levels of aldosterone, monocyte chemoattractant protein-1, and 8-isoprostane were lower in mice that received RDN compared with sham-operated mice (aldosterone; RDN: 206.8±33.2 versus SO: 405.5±59.4 pg/mL, P<0.05; monocyte chemoattractant protein-1; RDN: 51.7±7.9 versus SO: 91.71±4.6 pg/mL, P<0.05; 8-isoprostane; RDN: 331.9±38.2 versus SO: 468.5±42.0 pg/mL, P<0.05). RDN reduces progression of atherosclerosis in apolipoprotein E-deficient mice. These changes are associated with reduced aldosterone levels, monocyte chemoattractant protein-1, and markers of oxidative stress.
MeSH term(s)	Animals ; Apolipoproteins E/blood ; Apolipoproteins E/deficiency ; Atherosclerosis/blood ; Atherosclerosis/physiopathology ; Atherosclerosis/surgery ; Blood Pressure Determination ; Chemokine CCL2/blood ; Dinoprost/analogs & derivatives ; Dinoprost/blood ; Disease Models, Animal ; Disease Progression ; Hypertension/blood ; Hypertension/physiopathology ; Hypertension/surgery ; Kidney ; Male ; Mice ; Oxidative Stress ; Sympathectomy/methods
Chemical Substances	Apolipoproteins E ; Chemokine CCL2 ; 8-epi-prostaglandin F2alpha (27415-26-5) ; Dinoprost (B7IN85G1HY)
Language	English
Publishing date	2015-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.114.04648
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