The interaction of cytosolic-free calcium in PGF(2alpha)-induced luteal regression in ovine corpus luteum.

Persistent Link:
http://hdl.handle.net/10150/185210
Title:
The interaction of cytosolic-free calcium in PGF(2alpha)-induced luteal regression in ovine corpus luteum.
Author:
Wegner, Julie Anne
Issue Date:
1990
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
The corpus luteum is an endocrine gland which forms in the ovary each reproductive cycle, secretes progesterone, and regresses if pregnancy does not occur. An understanding of the factors and mechanisms that determine the function and lifespan of the corpus luteum is fundamental to the understanding of the mechanisms that cause luteal dysfunction. Prostaglandin F₂(α)(PGF₂(α)) is the primary lutelytic agent in ewes and appears to initiate luteal regression by altering cytosolic-free calcium ([Ca²⁺]ᵢ) and stimulating calcium-dependent intracellular pathways. The primary focus of this dissertation was to investigate the roles of PGF₂(α) and calcium in the regulation of progesterone secretion in the ovine corpus luteum. In fura-2 loaded large cells, PGF₂(α) (0.5 μM) induced a rapid transient increase in [Ca²⁺]ᵢ followed by a sustained elevation of [Ca²⁺]ᵢ. The transient nature of the [Ca²⁺]ᵢ increase was due, at least in part, to the ability of PGF₂(α) to stimulate (p < 0.05)⁴⁵Ca²⁺ efflux. PGF₂(α) did not alter [Ca²⁺]ᵢ in small cells. The PGF₂(α)-induced calcium transient was modified by incubation of large cells in conditions known to alter calcium homeostasis. The transient was attenuated by incubation of large cells in Ca²⁺-free medium (±EGTA). These results suggest that PGF₂(α) induces release of calcium from intracellular calcium pools. However, pre-incubation (2 min) of large cells with 1mM LaCl₃ eliminated the PGF₂(α)-induced calcium transient, suggesting a role of extracellular calcium. Two different results were observed in this study regarding the role of calcium in the regulation of progesterone secretion. First, the inhibitory effect of PGF₂(α) on secretion of progesterone was reduced under conditions that reduced the magnitude of the PGF₂(α)-induced calcium transient. Second, a sustained elevation or reduction in [Ca²⁺]ᵢ level also reduced basal progesterone secretion in large cells. Thus, both phases of the PGF₂(α)-induced [Ca²⁺]ᵢ response, transient increase and sustained elevation, appear to be linked to the inhibitory action of PGF₂(α) on progesterone secretion. Finally, this study provides evidence to suggest that large and small cells differ in their ability to regulate calcium homeostasis.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Biology
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Physiology; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Hoyer, Patricia B.

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleThe interaction of cytosolic-free calcium in PGF(2alpha)-induced luteal regression in ovine corpus luteum.en_US
dc.creatorWegner, Julie Anneen_US
dc.contributor.authorWegner, Julie Anneen_US
dc.date.issued1990en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractThe corpus luteum is an endocrine gland which forms in the ovary each reproductive cycle, secretes progesterone, and regresses if pregnancy does not occur. An understanding of the factors and mechanisms that determine the function and lifespan of the corpus luteum is fundamental to the understanding of the mechanisms that cause luteal dysfunction. Prostaglandin F₂(α)(PGF₂(α)) is the primary lutelytic agent in ewes and appears to initiate luteal regression by altering cytosolic-free calcium ([Ca²⁺]ᵢ) and stimulating calcium-dependent intracellular pathways. The primary focus of this dissertation was to investigate the roles of PGF₂(α) and calcium in the regulation of progesterone secretion in the ovine corpus luteum. In fura-2 loaded large cells, PGF₂(α) (0.5 μM) induced a rapid transient increase in [Ca²⁺]ᵢ followed by a sustained elevation of [Ca²⁺]ᵢ. The transient nature of the [Ca²⁺]ᵢ increase was due, at least in part, to the ability of PGF₂(α) to stimulate (p < 0.05)⁴⁵Ca²⁺ efflux. PGF₂(α) did not alter [Ca²⁺]ᵢ in small cells. The PGF₂(α)-induced calcium transient was modified by incubation of large cells in conditions known to alter calcium homeostasis. The transient was attenuated by incubation of large cells in Ca²⁺-free medium (±EGTA). These results suggest that PGF₂(α) induces release of calcium from intracellular calcium pools. However, pre-incubation (2 min) of large cells with 1mM LaCl₃ eliminated the PGF₂(α)-induced calcium transient, suggesting a role of extracellular calcium. Two different results were observed in this study regarding the role of calcium in the regulation of progesterone secretion. First, the inhibitory effect of PGF₂(α) on secretion of progesterone was reduced under conditions that reduced the magnitude of the PGF₂(α)-induced calcium transient. Second, a sustained elevation or reduction in [Ca²⁺]ᵢ level also reduced basal progesterone secretion in large cells. Thus, both phases of the PGF₂(α)-induced [Ca²⁺]ᵢ response, transient increase and sustained elevation, appear to be linked to the inhibitory action of PGF₂(α) on progesterone secretion. Finally, this study provides evidence to suggest that large and small cells differ in their ability to regulate calcium homeostasis.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectBiologyen_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorHoyer, Patricia B.en_US
dc.contributor.committeememberGillies, Roberten_US
dc.contributor.committeememberAllen, Ronald E.en_US
dc.contributor.committeememberKomm, Barryen_US
dc.contributor.committeememberBenson, Bryanten_US
dc.identifier.proquest9105915en_US
dc.identifier.oclc709782671en_US
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