Increased angiotensin II type 1 receptor expression in temporal arteries from patients with giant cell arteritis.
(2009) In Ophthalmology 116(5). p.990-996- Abstract
- PURPOSE: Currently, giant cell arteritis (GCA) is primarily treated with corticosteroids or immunomodulating agents, but there is interest in identifying other noncorticosteroid alternatives. Similarities exist in the injury pathways between GCA and atherosclerosis. Angiotensin II is a vasoactive peptide involved in vessel inflammation during atherosclerosis, and angiotensin II receptor inhibitors are effective in preventing atherosclerosis. The present study was performed to elucidate the role of angiotensin type 1 (AT(1)) and type 2 (AT(2)) receptors in GCA. DESIGN: Experimental retrospective immunohistochemical study of temporal arteries using archival formalin-fixed, paraffin-embedded tissue. PARTICIPANTS: Ten patients with GCA and 10... (More)
- PURPOSE: Currently, giant cell arteritis (GCA) is primarily treated with corticosteroids or immunomodulating agents, but there is interest in identifying other noncorticosteroid alternatives. Similarities exist in the injury pathways between GCA and atherosclerosis. Angiotensin II is a vasoactive peptide involved in vessel inflammation during atherosclerosis, and angiotensin II receptor inhibitors are effective in preventing atherosclerosis. The present study was performed to elucidate the role of angiotensin type 1 (AT(1)) and type 2 (AT(2)) receptors in GCA. DESIGN: Experimental retrospective immunohistochemical study of temporal arteries using archival formalin-fixed, paraffin-embedded tissue. PARTICIPANTS: Ten patients with GCA and 10 control patients, who were clinically suspected of having GCA but were diagnosed as not having GCA, were included. METHODS: Immunohistochemistry, using anti-AT(1) and anti-AT(2) antibodies, was performed on formalin-fixed and paraffin-embedded temporal arteries. MAIN OUTCOME MEASURES: AT(1) and AT(2) receptor immunostaining intensity was quantified. RESULTS: Hematoxylin-eosin-stained sections of temporal arteries from patients with GCA showed intimal hyperplasia, internal elastic lamina degeneration, and band-shaped infiltrates of inflammatory cells, including lymphocytes, histocytes, and multinucleated giant cells. AT(1) receptor staining was primarily observed in the medial layer of the temporal arteries and was higher in the patients with GCA than in the control patients. This was a result of increased AT(1) receptor immunostaining of both vascular smooth muscle cells and infiltrating inflammatory cells. Only faint immunostaining was seen for AT(2) receptors, primarily in the endothelial cells, and to a lesser extent on the smooth muscle cells. Immunostaining with antibodies for the AT(2) receptor was similar in the patients with GCA and in controls. CONCLUSIONS: These results suggest that AT(1) receptors play a role in the development of GCA. Inhibition of the angiotensin system may thus provide a noncorticosteroid alternative for the treatment of GCA. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1412765
- author
- Dimitrijevic, Ivan LU ; Malmsjö, Malin LU ; Andersson, Christina LU ; Rissler, Pehr LU and Edvinsson, Lars LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Temporal Arteries: metabolism, Type 2: metabolism, Angiotensin, Receptor, Type 1: metabolism, Vascular: metabolism, Smooth, Muscle, Endothelium, Giant Cell Arteritis: metabolism
- in
- Ophthalmology
- volume
- 116
- issue
- 5
- pages
- 990 - 996
- publisher
- Elsevier
- external identifiers
-
- wos:000270907500025
- pmid:19410957
- scopus:65349092825
- pmid:19410957
- ISSN
- 1549-4713
- DOI
- 10.1016/j.ophtha.2008.12.021
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Pathology, (Lund) (013030000), Medicine (Lund) (013230025)
- id
- f19e4d2d-9a36-4969-9782-a79451d744a6 (old id 1412765)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/19410957?dopt=Abstract
- date added to LUP
- 2016-04-04 08:53:58
- date last changed
- 2024-01-12 06:45:16
@article{f19e4d2d-9a36-4969-9782-a79451d744a6,
abstract = {{PURPOSE: Currently, giant cell arteritis (GCA) is primarily treated with corticosteroids or immunomodulating agents, but there is interest in identifying other noncorticosteroid alternatives. Similarities exist in the injury pathways between GCA and atherosclerosis. Angiotensin II is a vasoactive peptide involved in vessel inflammation during atherosclerosis, and angiotensin II receptor inhibitors are effective in preventing atherosclerosis. The present study was performed to elucidate the role of angiotensin type 1 (AT(1)) and type 2 (AT(2)) receptors in GCA. DESIGN: Experimental retrospective immunohistochemical study of temporal arteries using archival formalin-fixed, paraffin-embedded tissue. PARTICIPANTS: Ten patients with GCA and 10 control patients, who were clinically suspected of having GCA but were diagnosed as not having GCA, were included. METHODS: Immunohistochemistry, using anti-AT(1) and anti-AT(2) antibodies, was performed on formalin-fixed and paraffin-embedded temporal arteries. MAIN OUTCOME MEASURES: AT(1) and AT(2) receptor immunostaining intensity was quantified. RESULTS: Hematoxylin-eosin-stained sections of temporal arteries from patients with GCA showed intimal hyperplasia, internal elastic lamina degeneration, and band-shaped infiltrates of inflammatory cells, including lymphocytes, histocytes, and multinucleated giant cells. AT(1) receptor staining was primarily observed in the medial layer of the temporal arteries and was higher in the patients with GCA than in the control patients. This was a result of increased AT(1) receptor immunostaining of both vascular smooth muscle cells and infiltrating inflammatory cells. Only faint immunostaining was seen for AT(2) receptors, primarily in the endothelial cells, and to a lesser extent on the smooth muscle cells. Immunostaining with antibodies for the AT(2) receptor was similar in the patients with GCA and in controls. CONCLUSIONS: These results suggest that AT(1) receptors play a role in the development of GCA. Inhibition of the angiotensin system may thus provide a noncorticosteroid alternative for the treatment of GCA. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.}},
author = {{Dimitrijevic, Ivan and Malmsjö, Malin and Andersson, Christina and Rissler, Pehr and Edvinsson, Lars}},
issn = {{1549-4713}},
keywords = {{Temporal Arteries: metabolism; Type 2: metabolism; Angiotensin; Receptor; Type 1: metabolism; Vascular: metabolism; Smooth; Muscle; Endothelium; Giant Cell Arteritis: metabolism}},
language = {{eng}},
number = {{5}},
pages = {{990--996}},
publisher = {{Elsevier}},
series = {{Ophthalmology}},
title = {{Increased angiotensin II type 1 receptor expression in temporal arteries from patients with giant cell arteritis.}},
url = {{https://lup.lub.lu.se/search/files/5202395/1439161.pdf}},
doi = {{10.1016/j.ophtha.2008.12.021}},
volume = {{116}},
year = {{2009}},
}