Rat Sertoli cells in primary culture have been studied for their ability to respond to extracellular matrix macromolecules by increases of [Ca2+](i). We observed that cells seeded oil glass coverslips, loaded with the intracellular Ca2+ indicator fura-2, responded to laminin, but nut to fibronectin, with an immediate [Ca2+](i) raise, with a peak followed by a prolonged plateau. [Ca2+](i) increases were dependent upon Ca2+ influx across the plasma membrane and Ca2+ release from intracellular Ca2+ pools. Ca2+ influx was inhibited by extracellular Ca2+ removal by EGTA, and by treatment with La3+, or with the L-type voltage operated Ca2+ channel blocker, nifedipine. Ca2+ release from intracellular Ca2+ storing organelles, was inhibited by the microsomal Ca2+-ATPase blocker thapsigargin. Responses were mimicked by synthetic peptides carrying the Arg-Gly-Asp adhesion sequence, but not by the control Arg-Gly-Glu-containing peptide, in which aspartic acid was replaced by glutamic acid. Laminin-dependent [Ca2+](i) increases were down-regulated by the follicle-stimulating hormone. However, this occurred only when cells were not subjected to homotypic cell-cell contact, and responded to the hormone with a significant [Ca2+](i) elevation. These results indicate that laminin may regulate Sertoli cells by intracellular signals that perturb Ca2+ homeostasis. This role may be related to an effect exerted by the seminiferous epithelium basement membrane on the regulation of spermatogenesis. (C) 2000 Elsevier Science B.V./International Society of Matrix Biology. All rights reserved.

Immediate cell signal induced by laminin in rat Sertoli cells

TETI, ANNA MARIA;
2000

Abstract

Rat Sertoli cells in primary culture have been studied for their ability to respond to extracellular matrix macromolecules by increases of [Ca2+](i). We observed that cells seeded oil glass coverslips, loaded with the intracellular Ca2+ indicator fura-2, responded to laminin, but nut to fibronectin, with an immediate [Ca2+](i) raise, with a peak followed by a prolonged plateau. [Ca2+](i) increases were dependent upon Ca2+ influx across the plasma membrane and Ca2+ release from intracellular Ca2+ pools. Ca2+ influx was inhibited by extracellular Ca2+ removal by EGTA, and by treatment with La3+, or with the L-type voltage operated Ca2+ channel blocker, nifedipine. Ca2+ release from intracellular Ca2+ storing organelles, was inhibited by the microsomal Ca2+-ATPase blocker thapsigargin. Responses were mimicked by synthetic peptides carrying the Arg-Gly-Asp adhesion sequence, but not by the control Arg-Gly-Glu-containing peptide, in which aspartic acid was replaced by glutamic acid. Laminin-dependent [Ca2+](i) increases were down-regulated by the follicle-stimulating hormone. However, this occurred only when cells were not subjected to homotypic cell-cell contact, and responded to the hormone with a significant [Ca2+](i) elevation. These results indicate that laminin may regulate Sertoli cells by intracellular signals that perturb Ca2+ homeostasis. This role may be related to an effect exerted by the seminiferous epithelium basement membrane on the regulation of spermatogenesis. (C) 2000 Elsevier Science B.V./International Society of Matrix Biology. All rights reserved.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11697/18227
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