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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

T-cell subsets in isolated pVAT are regulated by RANTES in hypertension; links to vascular dysfunction. A, B) Flow cytometric analyses were used to determine number of CCR5+ T cells (A) and CCR6+ T cells (B) in pVAT of sham- and Ang II–infused mice (n = 5). C) Ang II–dependent changes in IL-17-producing CD4+ T cells in pVAT from WT and RANTES−/− mice (n = 5). D) Ang II–dependent changes in IFN-γ-producing CD8+ T cells in pVAT from WT and RANTES−/− mice (n = 5). E) Effect of Ang II on mRNA expression (real-time PCR) of IFN-γ in pVAT from WT and RANTES−/− mice (n = 5). F) Effects of IFN-γ (50 ng/ml) on endothelium-dependent and -independent relaxations in mouse aorta. Role of reactive oxygen species was examined using PEG-SOD (500 IU/ml) preincubation (n = 6; P, repeated measures ANOVA).
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Figure 5: T-cell subsets in isolated pVAT are regulated by RANTES in hypertension; links to vascular dysfunction. A, B) Flow cytometric analyses were used to determine number of CCR5+ T cells (A) and CCR6+ T cells (B) in pVAT of sham- and Ang II–infused mice (n = 5). C) Ang II–dependent changes in IL-17-producing CD4+ T cells in pVAT from WT and RANTES−/− mice (n = 5). D) Ang II–dependent changes in IFN-γ-producing CD8+ T cells in pVAT from WT and RANTES−/− mice (n = 5). E) Effect of Ang II on mRNA expression (real-time PCR) of IFN-γ in pVAT from WT and RANTES−/− mice (n = 5). F) Effects of IFN-γ (50 ng/ml) on endothelium-dependent and -independent relaxations in mouse aorta. Role of reactive oxygen species was examined using PEG-SOD (500 IU/ml) preincubation (n = 6; P, repeated measures ANOVA).

Mentions: RANTES’ effect on relative content of T cells was, however, more pronounced than on other leukocyte subsets (Fig. 4D). Thus, in Ang II–dependent hypertension, RANTES plays an important role in homing of T cells, and particularly CCR5+ cells, to pVAT (Fig. 5A). CCR5+ cells exhibited particularly high production of IFN-γ. Accumulation of cells bearing CCR6 remained unaffected (Fig. 5B). In line with this, recruitment of T-helper (Th)17 cells (CD4 cells producing IL-17) upon Ang II infusion, predominantly modulated by CCR6, was not affected by RANTES−/− (Fig. 5C). CD8+ T-cell production of IL-17 was negligible (data not shown).


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)

T-cell subsets in isolated pVAT are regulated by RANTES in hypertension; links to vascular dysfunction. A, B) Flow cytometric analyses were used to determine number of CCR5+ T cells (A) and CCR6+ T cells (B) in pVAT of sham- and Ang II–infused mice (n = 5). C) Ang II–dependent changes in IL-17-producing CD4+ T cells in pVAT from WT and RANTES−/− mice (n = 5). D) Ang II–dependent changes in IFN-γ-producing CD8+ T cells in pVAT from WT and RANTES−/− mice (n = 5). E) Effect of Ang II on mRNA expression (real-time PCR) of IFN-γ in pVAT from WT and RANTES−/− mice (n = 5). F) Effects of IFN-γ (50 ng/ml) on endothelium-dependent and -independent relaxations in mouse aorta. Role of reactive oxygen species was examined using PEG-SOD (500 IU/ml) preincubation (n = 6; P, repeated measures ANOVA).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: T-cell subsets in isolated pVAT are regulated by RANTES in hypertension; links to vascular dysfunction. A, B) Flow cytometric analyses were used to determine number of CCR5+ T cells (A) and CCR6+ T cells (B) in pVAT of sham- and Ang II–infused mice (n = 5). C) Ang II–dependent changes in IL-17-producing CD4+ T cells in pVAT from WT and RANTES−/− mice (n = 5). D) Ang II–dependent changes in IFN-γ-producing CD8+ T cells in pVAT from WT and RANTES−/− mice (n = 5). E) Effect of Ang II on mRNA expression (real-time PCR) of IFN-γ in pVAT from WT and RANTES−/− mice (n = 5). F) Effects of IFN-γ (50 ng/ml) on endothelium-dependent and -independent relaxations in mouse aorta. Role of reactive oxygen species was examined using PEG-SOD (500 IU/ml) preincubation (n = 6; P, repeated measures ANOVA).
Mentions: RANTES’ effect on relative content of T cells was, however, more pronounced than on other leukocyte subsets (Fig. 4D). Thus, in Ang II–dependent hypertension, RANTES plays an important role in homing of T cells, and particularly CCR5+ cells, to pVAT (Fig. 5A). CCR5+ cells exhibited particularly high production of IFN-γ. Accumulation of cells bearing CCR6 remained unaffected (Fig. 5B). In line with this, recruitment of T-helper (Th)17 cells (CD4 cells producing IL-17) upon Ang II infusion, predominantly modulated by CCR6, was not affected by RANTES−/− (Fig. 5C). CD8+ T-cell production of IL-17 was negligible (data not shown).

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