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Reduced expression of angiotensin II and angiotensin receptor type 1 and type 2 in resistance arteries from nasal lesions in granulomatosis with polyangiitis (Wegener's granulomatosis).

Dimitrijevic, Ivan LU ; Rissler, Pehr; Luts, Lena LU and Edvinsson, Lars LU (2011) In Scandinavian Journal of Rheumatology 40. p.448-452
Abstract
Objectives: Angiotensin II (ANGII) is involved in vessel inflammation and is important in the development of cardiovascular disorders such as atherosclerosis. During active disease, patients with granulomatosis with polyangiitis (GPA; Wegener's granulomatosis) have accelerated atherosclerosis and ANGII inhibitors are recommended to these patients to reduce atherosclerosis. We assessed the hypothesis that the expression of ANGII and its receptors in arteries in granulomatous lesions change in GPA. Methods: ANGII and angiotensin receptors were quantified in vessels from granulomatous lesions from patients with GPA using immunohistochemistry. Anti- ANGI type 1 (AT1) and type 2 (AT2) antibodies were applied on formalin-fixed and... (More)
Objectives: Angiotensin II (ANGII) is involved in vessel inflammation and is important in the development of cardiovascular disorders such as atherosclerosis. During active disease, patients with granulomatosis with polyangiitis (GPA; Wegener's granulomatosis) have accelerated atherosclerosis and ANGII inhibitors are recommended to these patients to reduce atherosclerosis. We assessed the hypothesis that the expression of ANGII and its receptors in arteries in granulomatous lesions change in GPA. Methods: ANGII and angiotensin receptors were quantified in vessels from granulomatous lesions from patients with GPA using immunohistochemistry. Anti- ANGI type 1 (AT1) and type 2 (AT2) antibodies were applied on formalin-fixed and paraffin-embedded biopsies from nasal mucous membranes from eight patients with GPA and eight controls. Results: ANGII expression was localized to the endothelial cells (ECs) in arteries and sparsely to vascular smooth muscle cells (VSMCs) in nasal biopsies. AT1 receptor (AT1R) staining was intense and located in the VSMCs in the medial layer of the control arteries. AT2 receptor (AT2R) immunostaining was faint and was located only in the ECs. Patients with GPA showed marked down-regulation of positively immunostained ECs for ANGII or AT2R, and a reduced number of AT1R in VSMCs. ANGII, AT1R, and AT2R staining was persistent on infiltrating leucocytes. Conclusions: These results suggest down-regulation of the angiotensin system in arteries in granulomatous nasal lesions in GPA. Inhibition of the angiotensin system may prove less efficient in inhibiting the vascular inflammation process in GPA. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Scandinavian Journal of Rheumatology
volume
40
pages
448 - 452
publisher
Taylor & Francis
external identifiers
  • wos:000297852500007
  • pmid:21936613
  • scopus:83455219943
ISSN
1502-7732
DOI
10.3109/03009742.2011.593545
language
English
LU publication?
yes
id
18dd6568-3fee-446b-863f-f100c675b973 (old id 2168698)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21936613?dopt=Abstract
date added to LUP
2011-10-03 11:45:06
date last changed
2017-01-01 04:15:44
@article{18dd6568-3fee-446b-863f-f100c675b973,
  abstract     = {Objectives: Angiotensin II (ANGII) is involved in vessel inflammation and is important in the development of cardiovascular disorders such as atherosclerosis. During active disease, patients with granulomatosis with polyangiitis (GPA; Wegener's granulomatosis) have accelerated atherosclerosis and ANGII inhibitors are recommended to these patients to reduce atherosclerosis. We assessed the hypothesis that the expression of ANGII and its receptors in arteries in granulomatous lesions change in GPA. Methods: ANGII and angiotensin receptors were quantified in vessels from granulomatous lesions from patients with GPA using immunohistochemistry. Anti- ANGI type 1 (AT1) and type 2 (AT2) antibodies were applied on formalin-fixed and paraffin-embedded biopsies from nasal mucous membranes from eight patients with GPA and eight controls. Results: ANGII expression was localized to the endothelial cells (ECs) in arteries and sparsely to vascular smooth muscle cells (VSMCs) in nasal biopsies. AT1 receptor (AT1R) staining was intense and located in the VSMCs in the medial layer of the control arteries. AT2 receptor (AT2R) immunostaining was faint and was located only in the ECs. Patients with GPA showed marked down-regulation of positively immunostained ECs for ANGII or AT2R, and a reduced number of AT1R in VSMCs. ANGII, AT1R, and AT2R staining was persistent on infiltrating leucocytes. Conclusions: These results suggest down-regulation of the angiotensin system in arteries in granulomatous nasal lesions in GPA. Inhibition of the angiotensin system may prove less efficient in inhibiting the vascular inflammation process in GPA.},
  author       = {Dimitrijevic, Ivan and Rissler, Pehr and Luts, Lena and Edvinsson, Lars},
  issn         = {1502-7732},
  language     = {eng},
  pages        = {448--452},
  publisher    = {Taylor & Francis},
  series       = {Scandinavian Journal of Rheumatology},
  title        = {Reduced expression of angiotensin II and angiotensin receptor type 1 and type 2 in resistance arteries from nasal lesions in granulomatosis with polyangiitis (Wegener's granulomatosis).},
  url          = {http://dx.doi.org/10.3109/03009742.2011.593545},
  volume       = {40},
  year         = {2011},
}