TRANSGLUTAMINASE AND ORNITHINE DECARBOXYLASE AS MARKERS OF PROLIFERATION AND DIFFERENTIATION.

Persistent Link:
http://hdl.handle.net/10150/186027
Title:
TRANSGLUTAMINASE AND ORNITHINE DECARBOXYLASE AS MARKERS OF PROLIFERATION AND DIFFERENTIATION.
Author:
FRASIER-SCOTT, KAREN FRANCES.
Issue Date:
1983
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:
This study elucidates the temporal expression and regulation of transglutaminase (TGase) and ornithine decarboxylase (ODCase) during cell proliferation and differentiation. In synchronized CHO cells, there were two peaks of TGase activity expressed in G₁ and a smaller peak of activity in mid S phase. ODCase exhibited a single peak of expression in mid G₁ which was inhibited by the administration of both cycloheximide and actinomycin D. In contrast, the increase in TGase activity was not inhibited at any time measured by administration of either cycloheximide or actinomycin D to these cells. TGase activity in CHO cells was not affected by the addition of analogs of cyclic AMP, whereas ODCase activity was increased at all times measured. Retinol administration increased TGase activity 1 hr after release in CHO cells and the activity remained elevated for 4 hr. Retinol administration resulted in the inhibition of ODCase expression in these cells. The administration of α-melanocyte-stimulating hormone (MSH) to mouse melanoma cells resulted in a biphasic increase of TGase activity and a single peak of ODCase activity within 7 hr. In melanoma cells, addition of cycloheximide abolished the first peak of TGase activity but not the second peak. Actinomycin D did not inhibit either peak of TGase expression. The administration of both cycloheximide and actinomycin D inhibited ODCase activity after MSH stimulation. Analogs of cyclic AMP, when added to log phase mouse melanoma cells, increased ODCase but not TGase activity at all points measured. In these cells, retinoic acid plus MSH markedly enhanced the activity of the initial TGase peak compared to MSH alone. ODCase expression was attenuated with retinoic acid plus MSH. Dexamethasone (DEX) induced the first peak of TGase activity but not the second peak seen with MSH administration alone. Administration of DEX resulted in a peak expression of ODCase activity approximately 30% of that seen with MSH alone. In general, chelation of extracellular calcium with EGTA totally blocked ODCase expression with MSH, retinoic acid or DEX. Partial or total ablation of TGase expression was seen with addition of MSH or retinoic acid, but very little inhibition of this enzyme was evident when EGTA was added with DEX or DEX plus MSH. Addition of calcium after all CA⁺⁺-blocks restored the expression of both enzymes.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Cell differentiation.; Cell proliferation.; Enzyme inhibitors.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Molecular and Medical Microbiology; Graduate College
Degree Grantor:
University of Arizona

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleTRANSGLUTAMINASE AND ORNITHINE DECARBOXYLASE AS MARKERS OF PROLIFERATION AND DIFFERENTIATION.en_US
dc.creatorFRASIER-SCOTT, KAREN FRANCES.en_US
dc.contributor.authorFRASIER-SCOTT, KAREN FRANCES.en_US
dc.date.issued1983en_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.abstractThis study elucidates the temporal expression and regulation of transglutaminase (TGase) and ornithine decarboxylase (ODCase) during cell proliferation and differentiation. In synchronized CHO cells, there were two peaks of TGase activity expressed in G₁ and a smaller peak of activity in mid S phase. ODCase exhibited a single peak of expression in mid G₁ which was inhibited by the administration of both cycloheximide and actinomycin D. In contrast, the increase in TGase activity was not inhibited at any time measured by administration of either cycloheximide or actinomycin D to these cells. TGase activity in CHO cells was not affected by the addition of analogs of cyclic AMP, whereas ODCase activity was increased at all times measured. Retinol administration increased TGase activity 1 hr after release in CHO cells and the activity remained elevated for 4 hr. Retinol administration resulted in the inhibition of ODCase expression in these cells. The administration of α-melanocyte-stimulating hormone (MSH) to mouse melanoma cells resulted in a biphasic increase of TGase activity and a single peak of ODCase activity within 7 hr. In melanoma cells, addition of cycloheximide abolished the first peak of TGase activity but not the second peak. Actinomycin D did not inhibit either peak of TGase expression. The administration of both cycloheximide and actinomycin D inhibited ODCase activity after MSH stimulation. Analogs of cyclic AMP, when added to log phase mouse melanoma cells, increased ODCase but not TGase activity at all points measured. In these cells, retinoic acid plus MSH markedly enhanced the activity of the initial TGase peak compared to MSH alone. ODCase expression was attenuated with retinoic acid plus MSH. Dexamethasone (DEX) induced the first peak of TGase activity but not the second peak seen with MSH administration alone. Administration of DEX resulted in a peak expression of ODCase activity approximately 30% of that seen with MSH alone. In general, chelation of extracellular calcium with EGTA totally blocked ODCase expression with MSH, retinoic acid or DEX. Partial or total ablation of TGase expression was seen with addition of MSH or retinoic acid, but very little inhibition of this enzyme was evident when EGTA was added with DEX or DEX plus MSH. Addition of calcium after all CA⁺⁺-blocks restored the expression of both enzymes.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectCell differentiation.en_US
dc.subjectCell proliferation.en_US
dc.subjectEnzyme inhibitors.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineMolecular and Medical Microbiologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.identifier.proquest8315283en_US
dc.identifier.oclc688637493en_US
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