Enhanced Polyadenosine Diphosphate-Ribosylation in Gonadotropin-Releasing Hormone Agonist-Treated Uterine Leiomyoma

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Abstract

This study aimed to examine the activation of poly(ADP-ribose) polymerase (PARP) and the accumulation of its end product, poly(ADP-ribose) (PAR), in uterine leiomyoma specimens obtained from 25 patients receiving Leuplin depot [leuprorelin acetate, depot (LA)] treatment and 46 control patients and explore their correlation with tumor shrinkage and degeneration caused by the therapy. Immunoblotting analysis showed that specimens from LA-treated patients had higher PARP expression. The numbers of both PARP- and PAR-immunolabeled cells were higher in leiomyoma with LA treatment. This was correlated with the clinical response of LA therapy that LA induced more leiomyoma degeneration. The analysis of power Doppler sonography indicated a progressive decrease in blood supply to tumor following LA treatment. In vitro experiments using primarily cultured leiomyoma cells exhibited that the deprivation of serum or ovarian hormones or LA directly failed to induce PARP and PAR production. Our results suggested that reduced blood flow and subsequent ischemic damages in leiomyoma could be responsible for PARP over-expression and PAR accumulation, clinical response, and tumor degeneration caused by LA treatment.

Original languageEnglish
Pages (from-to)5009-5016
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume88
Issue number10
DOIs
Publication statusPublished - 2003 Oct 1

Fingerprint

Leuprolide
Diphosphates
Leiomyoma
Gonadotropin-Releasing Hormone
Acetates
Poly(ADP-ribose) Polymerases
Tumors
Blood
Therapeutics
Poly Adenosine Diphosphate Ribose
Ultrasonography
Doppler Ultrasonography
Neoplasms
polyadenosine
Immunoblotting
Cultured Cells
Chemical activation
Hormones

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

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title = "Enhanced Polyadenosine Diphosphate-Ribosylation in Gonadotropin-Releasing Hormone Agonist-Treated Uterine Leiomyoma",
abstract = "This study aimed to examine the activation of poly(ADP-ribose) polymerase (PARP) and the accumulation of its end product, poly(ADP-ribose) (PAR), in uterine leiomyoma specimens obtained from 25 patients receiving Leuplin depot [leuprorelin acetate, depot (LA)] treatment and 46 control patients and explore their correlation with tumor shrinkage and degeneration caused by the therapy. Immunoblotting analysis showed that specimens from LA-treated patients had higher PARP expression. The numbers of both PARP- and PAR-immunolabeled cells were higher in leiomyoma with LA treatment. This was correlated with the clinical response of LA therapy that LA induced more leiomyoma degeneration. The analysis of power Doppler sonography indicated a progressive decrease in blood supply to tumor following LA treatment. In vitro experiments using primarily cultured leiomyoma cells exhibited that the deprivation of serum or ovarian hormones or LA directly failed to induce PARP and PAR production. Our results suggested that reduced blood flow and subsequent ischemic damages in leiomyoma could be responsible for PARP over-expression and PAR accumulation, clinical response, and tumor degeneration caused by LA treatment.",
author = "Huang, {Soon Cen} and Ming-Jer Tang and Ya-Min Cheng and Keng-Fu Hsu and Chung-Liang Ho and Cheng-Yang Chou",
year = "2003",
month = "10",
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doi = "10.1210/jc.2003-030175",
language = "English",
volume = "88",
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journal = "Journal of Clinical Endocrinology and Metabolism",
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T1 - Enhanced Polyadenosine Diphosphate-Ribosylation in Gonadotropin-Releasing Hormone Agonist-Treated Uterine Leiomyoma

AU - Huang, Soon Cen

AU - Tang, Ming-Jer

AU - Cheng, Ya-Min

AU - Hsu, Keng-Fu

AU - Ho, Chung-Liang

AU - Chou, Cheng-Yang

PY - 2003/10/1

Y1 - 2003/10/1

N2 - This study aimed to examine the activation of poly(ADP-ribose) polymerase (PARP) and the accumulation of its end product, poly(ADP-ribose) (PAR), in uterine leiomyoma specimens obtained from 25 patients receiving Leuplin depot [leuprorelin acetate, depot (LA)] treatment and 46 control patients and explore their correlation with tumor shrinkage and degeneration caused by the therapy. Immunoblotting analysis showed that specimens from LA-treated patients had higher PARP expression. The numbers of both PARP- and PAR-immunolabeled cells were higher in leiomyoma with LA treatment. This was correlated with the clinical response of LA therapy that LA induced more leiomyoma degeneration. The analysis of power Doppler sonography indicated a progressive decrease in blood supply to tumor following LA treatment. In vitro experiments using primarily cultured leiomyoma cells exhibited that the deprivation of serum or ovarian hormones or LA directly failed to induce PARP and PAR production. Our results suggested that reduced blood flow and subsequent ischemic damages in leiomyoma could be responsible for PARP over-expression and PAR accumulation, clinical response, and tumor degeneration caused by LA treatment.

AB - This study aimed to examine the activation of poly(ADP-ribose) polymerase (PARP) and the accumulation of its end product, poly(ADP-ribose) (PAR), in uterine leiomyoma specimens obtained from 25 patients receiving Leuplin depot [leuprorelin acetate, depot (LA)] treatment and 46 control patients and explore their correlation with tumor shrinkage and degeneration caused by the therapy. Immunoblotting analysis showed that specimens from LA-treated patients had higher PARP expression. The numbers of both PARP- and PAR-immunolabeled cells were higher in leiomyoma with LA treatment. This was correlated with the clinical response of LA therapy that LA induced more leiomyoma degeneration. The analysis of power Doppler sonography indicated a progressive decrease in blood supply to tumor following LA treatment. In vitro experiments using primarily cultured leiomyoma cells exhibited that the deprivation of serum or ovarian hormones or LA directly failed to induce PARP and PAR production. Our results suggested that reduced blood flow and subsequent ischemic damages in leiomyoma could be responsible for PARP over-expression and PAR accumulation, clinical response, and tumor degeneration caused by LA treatment.

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