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Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension.

Mikolajczyk TP, Nosalski R, Szczepaniak P, Budzyn K, Osmenda G, Skiba D, Sagan A, Wu J, Vinh A, Marvar PJ, Guzik B, Podolec J, Drummond G, Lob HE, Harrison DG, Guzik TJ - FASEB J. (2016)

Bottom Line: IFN-γ ex vivo caused significant endothelial dysfunction, which was reduced by superoxide anion scavenging.E., Harrison, D.G., Guzik, T.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Jagiellonian University, Cracow, Poland British Heart Foundation Centre for Excellence, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.

No MeSH data available.


Related in: MedlinePlus

Effects of met-RANTES on vascular function and perivascular T-cell infiltration in Ang II–dependent hypertension. A) Effect of Ang II–induced hypertension on endothelium-dependent vasodilatation to ACh in aortas of saline (saline) and met-RANTES-treated (50 mg/kg i.p.) mice (left; n = 5 for each). Relaxations to sodium nitroprusside as measure of non-endothelium-dependent vasodilatation (right;n = 5 for each). B) Aortic superoxide levels measured by monitoring oxidation of dihydroethidium to 2-hydroxyethidium using HPLC in control and met-RANTES-treated mice infused for 14 d with buffer (sham) or Ang II (n = 5). C) Effects of met-RANTES on mean T-cell (CD45+CD3+) infiltration in isolated pVAT (minus aorta) during Ang II–dependent hypertension (n = 5).
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Figure 7: Effects of met-RANTES on vascular function and perivascular T-cell infiltration in Ang II–dependent hypertension. A) Effect of Ang II–induced hypertension on endothelium-dependent vasodilatation to ACh in aortas of saline (saline) and met-RANTES-treated (50 mg/kg i.p.) mice (left; n = 5 for each). Relaxations to sodium nitroprusside as measure of non-endothelium-dependent vasodilatation (right;n = 5 for each). B) Aortic superoxide levels measured by monitoring oxidation of dihydroethidium to 2-hydroxyethidium using HPLC in control and met-RANTES-treated mice infused for 14 d with buffer (sham) or Ang II (n = 5). C) Effects of met-RANTES on mean T-cell (CD45+CD3+) infiltration in isolated pVAT (minus aorta) during Ang II–dependent hypertension (n = 5).

Mentions: To determine whether met-RANTES, a pharmacologic inhibitor of RANTES-dependent inflammation, exerts vasoprotective effects in Ang II–induced hypertension, we treated C57Bl/6 mice intraperitoneally with met-RANTES (50 mg/kg) every 3 d, beginning 3 d before initiation of Ang II infusion. Intraperitoneal injection of saline was used as a control. Met-RANTES treatment prevented the development of endothelial dysfunction in response to Ang II (Fig. 7A) while not significantly affecting blood pressure increase (tail cuff blood pressure 152 ± 8 mmHg in vehicle-treated mice vs. 150 ± 9 mmHg in met-RANTES-treated mice). Similarly, the increase in vascular superoxide production caused by Ang II was inhibited by met-RANTES (Fig. 7B). These changes of vascular phenotypes were accompanied by significant reductions of leukocyte and T-cell recruitment into pVAT (Fig. 7C).


Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension.

Mikolajczyk TP, Nosalski R, Szczepaniak P, Budzyn K, Osmenda G, Skiba D, Sagan A, Wu J, Vinh A, Marvar PJ, Guzik B, Podolec J, Drummond G, Lob HE, Harrison DG, Guzik TJ - FASEB J. (2016)

Effects of met-RANTES on vascular function and perivascular T-cell infiltration in Ang II–dependent hypertension. A) Effect of Ang II–induced hypertension on endothelium-dependent vasodilatation to ACh in aortas of saline (saline) and met-RANTES-treated (50 mg/kg i.p.) mice (left; n = 5 for each). Relaxations to sodium nitroprusside as measure of non-endothelium-dependent vasodilatation (right;n = 5 for each). B) Aortic superoxide levels measured by monitoring oxidation of dihydroethidium to 2-hydroxyethidium using HPLC in control and met-RANTES-treated mice infused for 14 d with buffer (sham) or Ang II (n = 5). C) Effects of met-RANTES on mean T-cell (CD45+CD3+) infiltration in isolated pVAT (minus aorta) during Ang II–dependent hypertension (n = 5).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4836375&req=5

Figure 7: Effects of met-RANTES on vascular function and perivascular T-cell infiltration in Ang II–dependent hypertension. A) Effect of Ang II–induced hypertension on endothelium-dependent vasodilatation to ACh in aortas of saline (saline) and met-RANTES-treated (50 mg/kg i.p.) mice (left; n = 5 for each). Relaxations to sodium nitroprusside as measure of non-endothelium-dependent vasodilatation (right;n = 5 for each). B) Aortic superoxide levels measured by monitoring oxidation of dihydroethidium to 2-hydroxyethidium using HPLC in control and met-RANTES-treated mice infused for 14 d with buffer (sham) or Ang II (n = 5). C) Effects of met-RANTES on mean T-cell (CD45+CD3+) infiltration in isolated pVAT (minus aorta) during Ang II–dependent hypertension (n = 5).
Mentions: To determine whether met-RANTES, a pharmacologic inhibitor of RANTES-dependent inflammation, exerts vasoprotective effects in Ang II–induced hypertension, we treated C57Bl/6 mice intraperitoneally with met-RANTES (50 mg/kg) every 3 d, beginning 3 d before initiation of Ang II infusion. Intraperitoneal injection of saline was used as a control. Met-RANTES treatment prevented the development of endothelial dysfunction in response to Ang II (Fig. 7A) while not significantly affecting blood pressure increase (tail cuff blood pressure 152 ± 8 mmHg in vehicle-treated mice vs. 150 ± 9 mmHg in met-RANTES-treated mice). Similarly, the increase in vascular superoxide production caused by Ang II was inhibited by met-RANTES (Fig. 7B). These changes of vascular phenotypes were accompanied by significant reductions of leukocyte and T-cell recruitment into pVAT (Fig. 7C).

Bottom Line: IFN-γ ex vivo caused significant endothelial dysfunction, which was reduced by superoxide anion scavenging.E., Harrison, D.G., Guzik, T.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Jagiellonian University, Cracow, Poland British Heart Foundation Centre for Excellence, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.

No MeSH data available.


Related in: MedlinePlus