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Title: Characterization of perivascular adipose tissue inflammation inpathogenesis of angiotensin II-induced hypertension

Author:

Nosalski, Ryszard

Date:

2017

Type:

Praca doktorska

Abstract:

Recent studies have shown a significant role of immune cells and the perivascular adipose tissue (pvAT) in the pathogenesis of hypertension (HT). The purpose of the studies was to characterize immune cells infiltrating pvAT in the animal models of HT and investigate the mechanism of Chemotaxis of T cells toward pvAT. HT was associated with an increased number of T cells, macrophages, dendritic cells and NK cells in pvAT. NK cells showed the highest induction in spontaneous HT, while T cells in AngII-induced HT. T cells residing in pvAT showed an increased expression of CD25, CD69, CD44, CCR1, CCR3, CCR5 and production of IFNg and IL17. AngII infusion induce mRNA and protein expression of RANTES which escalate chemotaxis of T cells, not B cells. RANTES knockdown protected against the accumulation of macrophages and T cells in pvAT as well as vascular dysfunction after AngII infusion. This effect was associated with diminished an infiltration of IFNg-producing CD8+ and CD4-CD8- T cells in pvAT. Conclusions. HT is associated with an increased number of immune cells in the pvAT. RANTES is important in the regulation of vascular dysfunction through modulation of perivascular inflammation.

Place of publishing:

Kraków

Level of degree:

2 - studia doktoranckie

Degree discipline:

choroby układu krążenia

Degree grantor:

Wydział Lekarski

Promoter:

Guzik, Tomasz

Date issued:

2017

Identifier:

oai:dl.cm-uj.krakow.pl:4239

Call number:

ZB-128097

Language:

pol

Access rights:

nieograniczony

Subject and keywords:

hypertension RANTES T cells perivascular adipose tissue inflammation

Object collections:

Last modified:

Jun 26, 2023

In our library since:

May 9, 2018

Number of object content hits:

238

Number of object content views in PDF format

168

All available object's versions:

http://dl.cm-uj.krakow.pl:8080/publication/4240

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Edition name Date
ZB-128097 Jun 26, 2023

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