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Geriatric Research, Education and Clinical Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA 94304
1 To whom correspondence should be addressed. e-mail: eve.reaven{at}med.va.gov
This study examined the in vivo relationship between expression of the HDL receptor scavenger receptor class B (SR-BI) and corresponding structural changes in the rat adrenocortical cell microvillar compartment. Using hormonal stimulation and withdrawal protocols, we were able to manipulate adrenal SR-BI levels and carry out qualitative and quantitative measurements correlating SR-BI expression with microvillar mass and microvillar channel formation. Young male rats were used as controls or treated with adrenocorticotropin hormone (ACTH) (24 h), 17
-ethinyl estradiol (17
-E2) (5 days), or dexamethasone (DEX) (24 h). Quantitative Western blot analysis and immunocytochemistry indicated that ACTH and 17
-E2 treatment greatly increased SR-BI expression in the adrenal (especially in the microvillar compartment of adrenocortical cells), whereas DEX treatment led to a decrease of SR-BI by all measurements. At the same time, striking ultrastructural changes occurred in the adrenocortical cell microvillar compartment: e.g., microvillar area and microvillar channel formation and complexity dramatically increased (compared with control values) after ACTH or 17
-E2 treatment, whereas the same values declined after DEX treatment.
These measurements illustrate the exceptional flexibility and responsiveness of the microvillar compartment to hormonal stimuli, and suggest that regulation of SR-BI expression and structural configuration of the surface of steroidogenic cells goes hand in hand.
Abbreviations: ACTH, adrenocorticotropin hormone; CRF, corticotropin-releasing factor; DEX, dexamethasone; SR-BI, scavenger receptor class B type I; 17
-E2, 17
-ethinyl estradiol
Supplementary key words SR-BI HDL steroid hormone ACTH corticosterone cholesterol 17
-ethinyl estradiol steroidogenesis
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