A Timing Effect of 17-β Estradiol on Atherosclerotic Lesion Development in Female ApoE−/− Mice

Autor: Alison K. Heather, Obialunanma V Ebenebe, Zoe Ashley, Jeffrey R. Erickson
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Pathology
Time Factors
Apolipoprotein B
menopause
030204 cardiovascular system & hematology
calcification
lcsh:Chemistry
Mice
chemistry.chemical_compound
0302 clinical medicine
estrogen therapy
Fibrosis
Medicine
lcsh:QH301-705.5
Aorta
Spectroscopy
Mice
Knockout
Estradiol
biology
General Medicine
Lipids
Computer Science Applications
Menopause
Cholesterol
Female
medicine.symptom
medicine.medical_specialty
medicine.drug_class
Article
Catalysis
Inorganic Chemistry
Lesion
03 medical and health sciences
Apolipoproteins E
intimal thickening
medicine.artery
Brachiocephalic artery
Animals
Physical and Theoretical Chemistry
Vascular Calcification
Molecular Biology
business.industry
Organic Chemistry
fibrosis
Estrogens
medicine.disease
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
chemistry
lcsh:Biology (General)
lcsh:QD1-999
Estrogen
biology.protein
atherosclerosis
business
Calcification
Zdroj: International Journal of Molecular Sciences, Vol 21, Iss 4710, p 4710 (2020)
International Journal of Molecular Sciences
Volume 21
Issue 13
ISSN: 1661-6596
1422-0067
Popis: Differences in size or composition of existing plaques at the initiation of estrogen (E2) therapy may underpin evidence of increased risk of atherosclerosis-associated clinical sequelae. We investigated whether E2 had divergent effects on actively-growing versus established-advanced atherosclerotic lesions. Eight weeks of subcutaneous bi-weekly injections of 3 µ
g/g 17&beta
estradiol (n = 18) or vehicle control (n = 22) were administered to female Apolipoprotein null-mice aged 25- or 45 weeks old. Histological assessment of lesion size within the brachiocephalic artery was conducted. Lesion composition was also assessed with acellular, calcification and fibrosis areas measured and other cellular features (intimal thickening, foam cells, lipid pools and cholesterol) scored (0&ndash
3) for severity. The comparison showed increased lesion size and calcified area with advancing age but no effect of E2. However, subtle changes in composition were observed following E2. Within the younger group, E2 increased intima thickening and acceleration of calcification. In the older group, E2 increased the thickness of the lesion cap. Therefore, this study shows different effects of E2 depending on the underlying stage of lesion development at the time of initiation of treatment. These divergent changes help explain the controversy of the adverse effects of E2 treatment in cardiovascular disease.
Databáze: OpenAIRE
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