V. Petursdottir et al., Estrogen receptors in giant cell arteritis. An immunocytochemical, Westernblot and RT-PCR study, CLIN EXP RH, 17(6), 1999, pp. 671-677
Objective
Giant cell arteritis (GCA) is a chronic form of vasculitis which predominan
tly affects women over 50 years of age. The aim of this study was to analys
e the presence of estrogen receptor a (ER) in the temporal arteries of pati
ents with GCA.
Methods
Inflamed temporal artery biopsies from 43 GCA patients were stained with mo
noclonal antibodies to two different segments of the ER and compared with n
on-inflamed arteries from age- and sex-matched controls who had not receive
d a clinical diagnosis of GCA. The protein that was extracted from 4 GCA-po
sitive biopsies and 4 non-GCA controls was analysed using the Western blot
method with a monoclonal antibody to ER. Reverse transcriptase-polymerase c
hain reaction (RT-PCR) analysis using primer pairs specific to ER-cDNA was
performed on the total RNA from 4 GCA-positive biopsies and 4 non-GCA contr
ols.
Results
The inflamed arteries expressed distinct cytoplasmic immunoreactivity to ER
in activated mononuclear inflammatory cells and in giant cells. Biopsies f
rom GCA patients and controls displayed cytoplasmic ER positivity in smooth
muscle cells. Western blot analysis revealed two bands corresponding to ap
proximately 64 and 54 kDa, respectively, in the inflamed arteries and contr
ols. In the inflamed biopsies and non-GCA controls, RT-PCR analysis reveale
d a strong band corresponding to approximately 670 bp, as expected, and a w
eaker band corresponding to approximately 440 bp.
Conclusion
In inflamed arteries from GCA patients, smooth muscle cells, activated mono
nuclear inflammatory cells and giant cells express cytoplasmic ER. Non-infl
amed control arteries also express cytoplasmic ER in smooth muscle cells. T
he accumulation of cytoplasmic ER may suggest the involvement of estrogen n
ot only in GCA but also in normal vascular aging The results justify furthe
r investigations into the pathogenetic roles of estrogen metabolism in GCA.