Chromogranin A: a novel regulator of parathyroid gland secretion.

Chromogranin A (CgA) is a major protein of the parathyroid gland that is costored and cosecreted with parathyroid hormone (PTH). CgA, widely distributed in endocrine and neuroendocrine cells in addition to parathyroid cells, appears to be a precursor of biologically active autocrine or paracrine peptides that include pancreastatin (CgA240-288) and parastatatin (CgA347-419), compounds that strongly inhibit stimulated secretion of PTH and costored CgA. The biosynthesis of CgA and PTH via gene expression and mRNA translation are noncoordinately altered by agents that affect parathyroid cell secretion including 1,25 dihydroxycholecalciferol, dexamethasone and Ca2+. These data have been interpreted to support an important physiological role for CgA-derived peptides as autocrine, paracrine and endocrine agents in the regulation of parathyroid cell function and secretion.

Cytoskeletal changes accompanying ACTH-induced steroidogenesis in cultured embryonic adrenal gland cells from the Pekin duck.

Cells derived from the adrenal glands of duck embryos immediately prior to hatching were grown in culture and used to study the morphological and cytoskeletal changes and steroidogenic responses induced by 1-24 ACTH. Changes in the cytoskeletal components were observed by rhodamine-phalloidin staining for actin and by staining the tubulin immunoreactive components with FITC. The cultures were comprised of a small population of chromaffin cells and a larger population of steroidogenic cells. The chromaffin cells were distinguished by their tyrosine hydroxylase immunoreactivity. The steroidogenic cells were characterized by the presence of sudanophilic lipid droplets, numerous mitochondria, abundant smooth endoplasmic reticulum, microtubules distributed as a fairly even network throughout the cytoplasm, and microfilaments that formed an extensive and elaborate system of stress fibers with many parallel arrays. The cells readily responded to stimulation with ACTH by releasing corticosterone, aldosterone and deoxycorticosterone. Stimulation with ACTH also induced changes in both the cell morphology and the cytoskeleton. Exposure of the cells to Krebs-Henseleit buffer containing 1-24 ACTH caused them to form numerous fine filopodia, to lose their stress fibers, and to form a thick ring of actin at the periphery of the cell. In addition, many cells became extremely arborized with many long branched dendritic processes. The morphological changes appeared to be related to a redistribution of the actin components, and may be explained only in part by the rounding up or retraction of the cytoplasm. The results strongly suggest an involvement of the actin components of the cytoskeleton in the steroidogenic response to corticotropic stimulation.