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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

Leukocyte infiltration, chemokine receptors, and RANTES expression in pVAT during Ang II–dependent hypertension. Hypertension was induced by chronic 14 d Ang II infusion by osmotic minipump (490 ng/min/kg), and AT was obtained from periaortic fat pad (pVAT) and epididymal AT (visceral AT). A) Representative flow cytometric analysis of major leukocyte subpopulations in vascular stromal fraction isolated from periaortic AT of sham- and Ang II–infused mice. B) Effect of Ang II infusion on absolute numbers of CD45+ total leukocyte content in pVAT compartment expressed per mg of tissue (n = 14). C) Effect of Ang II infusion on content CD3+ T cells, CD19+ B cells, I-Ab+CD11b+ macrophages, and I-Ab+CD11c+ DCs in pVAT (n = 12–14 for each). D) Effect of Ang II–dependent hypertension on content of CCR1, CCR3, and CCR5+ T lymphocyte (CD3+) in isolated pVAT (n = 6). E) Effect of 7 d Ang II–induced hypertension on mRNA expression of RANTES in pVAT and visceral AT (n = 5), and immunostaining of aortas from sham-treated and Ang II–infused C57BL/6J mice using anti-RANTES antibody (representative of 5 experiments). F) Effect of 14 d Ang II–induced hypertension on mRNA expression of RANTES in pVAT, visceral AT, and BAT (n = 5) and immunostaining of aortas from sham-treated and Ang II–infused C57BL/6J mice using anti-RANTES antibody (representative of 5 experiments).
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Figure 1: Leukocyte infiltration, chemokine receptors, and RANTES expression in pVAT during Ang II–dependent hypertension. Hypertension was induced by chronic 14 d Ang II infusion by osmotic minipump (490 ng/min/kg), and AT was obtained from periaortic fat pad (pVAT) and epididymal AT (visceral AT). A) Representative flow cytometric analysis of major leukocyte subpopulations in vascular stromal fraction isolated from periaortic AT of sham- and Ang II–infused mice. B) Effect of Ang II infusion on absolute numbers of CD45+ total leukocyte content in pVAT compartment expressed per mg of tissue (n = 14). C) Effect of Ang II infusion on content CD3+ T cells, CD19+ B cells, I-Ab+CD11b+ macrophages, and I-Ab+CD11c+ DCs in pVAT (n = 12–14 for each). D) Effect of Ang II–dependent hypertension on content of CCR1, CCR3, and CCR5+ T lymphocyte (CD3+) in isolated pVAT (n = 6). E) Effect of 7 d Ang II–induced hypertension on mRNA expression of RANTES in pVAT and visceral AT (n = 5), and immunostaining of aortas from sham-treated and Ang II–infused C57BL/6J mice using anti-RANTES antibody (representative of 5 experiments). F) Effect of 14 d Ang II–induced hypertension on mRNA expression of RANTES in pVAT, visceral AT, and BAT (n = 5) and immunostaining of aortas from sham-treated and Ang II–infused C57BL/6J mice using anti-RANTES antibody (representative of 5 experiments).

Mentions: Leukocytes represented 2% of the vascular stromal fraction of pVAT in sham-treated mice. Ang II infusion significantly increased both the percentage and absolute quantity of leukocytes in pVAT (Fig. 1A, B). Using antibodies against specific markers for T cells (CD3), B cells (CD19), macrophages (I-Ab/CD11b), and dendritic cells (DCs; CD11c/I-Ab), we found that pVAT contained all of these cell types (Fig. 1C). Ang II infusion markedly increased the number of T cells, macrophages, and DCs in pVAT (Fig. 1C) while not affecting the content of these in visceral or subcutaneous fat. Although there was a modest increase in B cells in the pVAT in response to Ang II, this was not statistically significant (Fig. 1C). Thus, macrophages, DCs, and T cells are the most prevalent leukocytes in the pVAT of Ang II hypertensive mice. Ang II caused greatest increase of T cells in pVAT percentage-wise (15 ± 2 to 24 ± 5%; P < 0.05).


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)

Leukocyte infiltration, chemokine receptors, and RANTES expression in pVAT during Ang II–dependent hypertension. Hypertension was induced by chronic 14 d Ang II infusion by osmotic minipump (490 ng/min/kg), and AT was obtained from periaortic fat pad (pVAT) and epididymal AT (visceral AT). A) Representative flow cytometric analysis of major leukocyte subpopulations in vascular stromal fraction isolated from periaortic AT of sham- and Ang II–infused mice. B) Effect of Ang II infusion on absolute numbers of CD45+ total leukocyte content in pVAT compartment expressed per mg of tissue (n = 14). C) Effect of Ang II infusion on content CD3+ T cells, CD19+ B cells, I-Ab+CD11b+ macrophages, and I-Ab+CD11c+ DCs in pVAT (n = 12–14 for each). D) Effect of Ang II–dependent hypertension on content of CCR1, CCR3, and CCR5+ T lymphocyte (CD3+) in isolated pVAT (n = 6). E) Effect of 7 d Ang II–induced hypertension on mRNA expression of RANTES in pVAT and visceral AT (n = 5), and immunostaining of aortas from sham-treated and Ang II–infused C57BL/6J mice using anti-RANTES antibody (representative of 5 experiments). F) Effect of 14 d Ang II–induced hypertension on mRNA expression of RANTES in pVAT, visceral AT, and BAT (n = 5) and immunostaining of aortas from sham-treated and Ang II–infused C57BL/6J mice using anti-RANTES antibody (representative of 5 experiments).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Leukocyte infiltration, chemokine receptors, and RANTES expression in pVAT during Ang II–dependent hypertension. Hypertension was induced by chronic 14 d Ang II infusion by osmotic minipump (490 ng/min/kg), and AT was obtained from periaortic fat pad (pVAT) and epididymal AT (visceral AT). A) Representative flow cytometric analysis of major leukocyte subpopulations in vascular stromal fraction isolated from periaortic AT of sham- and Ang II–infused mice. B) Effect of Ang II infusion on absolute numbers of CD45+ total leukocyte content in pVAT compartment expressed per mg of tissue (n = 14). C) Effect of Ang II infusion on content CD3+ T cells, CD19+ B cells, I-Ab+CD11b+ macrophages, and I-Ab+CD11c+ DCs in pVAT (n = 12–14 for each). D) Effect of Ang II–dependent hypertension on content of CCR1, CCR3, and CCR5+ T lymphocyte (CD3+) in isolated pVAT (n = 6). E) Effect of 7 d Ang II–induced hypertension on mRNA expression of RANTES in pVAT and visceral AT (n = 5), and immunostaining of aortas from sham-treated and Ang II–infused C57BL/6J mice using anti-RANTES antibody (representative of 5 experiments). F) Effect of 14 d Ang II–induced hypertension on mRNA expression of RANTES in pVAT, visceral AT, and BAT (n = 5) and immunostaining of aortas from sham-treated and Ang II–infused C57BL/6J mice using anti-RANTES antibody (representative of 5 experiments).
Mentions: Leukocytes represented 2% of the vascular stromal fraction of pVAT in sham-treated mice. Ang II infusion significantly increased both the percentage and absolute quantity of leukocytes in pVAT (Fig. 1A, B). Using antibodies against specific markers for T cells (CD3), B cells (CD19), macrophages (I-Ab/CD11b), and dendritic cells (DCs; CD11c/I-Ab), we found that pVAT contained all of these cell types (Fig. 1C). Ang II infusion markedly increased the number of T cells, macrophages, and DCs in pVAT (Fig. 1C) while not affecting the content of these in visceral or subcutaneous fat. Although there was a modest increase in B cells in the pVAT in response to Ang II, this was not statistically significant (Fig. 1C). Thus, macrophages, DCs, and T cells are the most prevalent leukocytes in the pVAT of Ang II hypertensive mice. Ang II caused greatest increase of T cells in pVAT percentage-wise (15 ± 2 to 24 ± 5%; P < 0.05).

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