The Role of Tubulin in Steroidogenesis of Mouse Adrenal Y-1 Cells and Rat Leydig CCL 43 Cells

Mike A. Clark and Jerry W. Shay
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Mike A. Clark: The University of Texas Health Science Center at Dallas, Department of Cell Biology
Jerry W. Shay: The University of Texas Health Science Center at Dallas, Department of Cell Biology

Chapter 4 in Cell and Muscle Motility, 1982, pp 53-61 from Springer

Abstract: Abstract The mechanisms of adrenocorticotropic hormone (ACTH)-induced steroid secretion in the adrenal cortex have not been clearly elucidated. However, it has been demonstrated that ACTH acts in the regulation of the steroidogenic pathway by controlling the conversion of cholesterol into pregnenolone. Cellular-fractionation studies have demonstrated that the enzymes necessary for this conversion are located in the mitochondria, whereas the cholesterol is stored in the cytoplasm. Kowal (1970) demonstrated that all the enzymes necessary to synthesize steroids are present prior to ACTH stimulation, and he concluded that steroidogenesis was regulated by controlling the transport of cholesterol to the mitochondria. Temple and Wolff (1973) showed that colchicine, and other drugs that depolymerize microtubules, could induce steroidogenesis independent of ACTH, and from these data they hypothesized that microtubules prevented the transport of cholesterol to the mitochondria and that the mechanism of ACTH-induced steroidogenesis involved the removal of this restriction.

Keywords: Cholesterol Crystal; Granular Form; Organize Microtubule; ACTH Treatment; Steroidogenic Pathway (search for similar items in EconPapers)
Date: 1982
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DOI: 10.1007/978-1-4684-4037-9_4

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