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Am J Pathol. 1990 May;136(5):1187-99.

Dehydroepiandrosterone and related steroids induce multilamellar lipid structures in cultured human endothelial cells.

The American journal of pathology

M M Sholley, S A Gudas, C C Schwartz, M Y Kalimi

Affiliations

  1. Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0709.

PMID: 2140927 PMCID: PMC1877427
Free PMC Article

Abstract

Pharmacologic doses of dehydroepiandrosterone (DHEA), a steroid hormone produced naturally by the adrenal cortex, may lower plasma lipoprotein levels in humans and reduce the severity of experimental atherosclerosis in rabbits. Effects of DHEA on cells of the vascular wall, particularly endothelial cells (EC), which are in direct contact with the plasma, have not been documented. The authors have found that micromolar doses of DHEA induce a consistent and reversible morphologic change in cultured EC derived from the human umbilical vein. During 24 hours of exposure to DHEA, cultured EC became loaded with phase-dense, perinuclear cytoplasmic granules, which persisted while DHEA remained in the culture medium. Certain steroids related to DHEA, particularly 17-ketosteroids, also induced perinuclear cytoplasmic granules. The granules lost their phase-density after fixed monolayers were extracted using ethanol or methanol. The granules did not form in media made with lipoprotein-deficient serum, suggesting that serum lipoproteins were involved in formation of the granules. Ultrastructurally, the granules were identical to multilamellar lipid structures, a type of pleomorphic lipid-containing lysosome found in foam cells. The granules were identified as lysosomes by positive reaction for acid phosphatase. The mechanism by which DHEA induces formation of lysosomal lipid structures remains to be determined.

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References

  1. J Atheroscler Res. 1966 Mar-Apr;6(2):184-9 - PubMed
  2. Arteriosclerosis. 1989 Mar-Apr;9(2):159-66 - PubMed
  3. J Cell Biol. 1974 Mar;60(3):673-84 - PubMed
  4. Clin Chim Acta. 1975 Nov 15;65(1):5-13 - PubMed
  5. Acta Univ Carol Med Monogr. 1976;71:1-137, 146-71 - PubMed
  6. Atherosclerosis. 1977 Apr;26(4):465-82 - PubMed
  7. N Engl J Med. 1978 Nov 30;299(22):1232-6 - PubMed
  8. Lab Invest. 1979 Aug;41(2):160-7 - PubMed
  9. J Cell Biol. 1979 Sep;82(3):597-613 - PubMed
  10. Science. 1980 May 2;208(4443):512-4 - PubMed
  11. J Biol Chem. 1980 Oct 10;255(19):9344-52 - PubMed
  12. J Cell Biol. 1981 Nov;91(2 Pt 1):420-6 - PubMed
  13. J Clin Endocrinol Metab. 1983 May;56(5):930-5 - PubMed
  14. J Clin Endocrinol Metab. 1983 Jul;57(1):8-14 - PubMed
  15. J Cell Biol. 1983 Oct;97(4):1156-68 - PubMed
  16. Science. 1983 Nov 11;222(4624):623-5 - PubMed
  17. Eur J Cell Biol. 1984 Jan;33(1):127-33 - PubMed
  18. Acta Pathol Jpn. 1985 Mar;35(2):385-408 - PubMed
  19. Am J Pathol. 1986 Jun;123(3):413-24 - PubMed
  20. N Engl J Med. 1986 Dec 11;315(24):1519-24 - PubMed
  21. J Steroid Biochem. 1987 May;26(5):561-7 - PubMed
  22. Atherosclerosis. 1987 Oct;67(2-3):127-42 - PubMed
  23. J Clin Endocrinol Metab. 1988 Jan;66(1):57-61 - PubMed
  24. Ann N Y Acad Sci. 1988;521:260-73 - PubMed
  25. J Clin Invest. 1988 Aug;82(2):712-20 - PubMed
  26. J Clin Invest. 1973 Nov;52(11):2745-56 - PubMed

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