Document Detail

Parathyroid hormone-like hormone (PTHLH) represses decidualization of human uterine fibroblast cells by an autocrine/paracrine mechanism.
MedLine Citation:
PMID:  21068146     Owner:  NLM     Status:  MEDLINE    
CONTEXT: Parathyroid hormone-like hormone (PTHLH) is abundantly expressed by human endometrial stromal cells during decidualization. However, the role for PTHLH in the decidualization process is unknown.
OBJECTIVE: To examine the effects of PTHLH on the induction and maintenance of decidualization of human uterine fibroblast (HUF) cells in vitro.
DESIGN: HUF cells were treated with a PTHLH siRNA or a PTHLH receptor antagonist (bPTH(7-34)) before or after decidualization with medroxyprogesterone acetate (MPA), estradiol (E(2)), and prostaglandin E(2) (PGE(2)). Decidualization was monitored by immunocytochemistry and the induction of decidualization-specific marker genes, including IGFBP-1, prolactin, lefty, and transcription factor FOXO1.
RESULTS: HUF cells decidualized after pretreatment with a PTHLH siRNA showed greater morphologic changes of decidualization, greater IGFBP-1 protein, and two- to threefold more IGFBP-1, prolactin, lefty, and FOXO1 mRNAs than cells pretreated with a nonsilencing RNA. The PTHLH siRNA pretreated cells also had 31% less DNA fragmentation (TUNEL assay) and 30-35% less caspase 3 levels during decidualization than cells pretreated treated with nonsilencing RNA. Treatment of HUF cells with PTHLH siRNA or bPTH(7-34) at 9 d after the induction of decidualization also resulted in 2.1- to 3.2-fold greater IGFBP-1, prolactin, lefty, and FOXO1 mRNA levels than that noted in control cells treated with nonsilencing RNA.
CONCLUSIONS: These finding strongly suggest that PTHLH represses the induction of human decidualization, stimulates stromal cell apoptosis, and limits the extent of uterine stromal cell differentiation. Because PTHLH and its receptor are expressed by HUF cells and placental cells, the inhibitory effect of PTHLH on decidualization appears to be due, at least in part, to an autocrine/paracrine mechanism.
Rosa Sherafat-Kazemzadeh; Jennifer K Schroeder; Cherie A Kessler; Stuart Handwerger
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-11-10
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  96     ISSN:  1945-7197     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-02-07     Completed Date:  2011-03-21     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  509-14     Citation Subset:  AIM; IM    
Department of Pediatrics, University of Cincinnati and Division of Endocrinology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.
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MeSH Terms
Autocrine Communication / drug effects
Caspase 3 / analysis,  biosynthesis
Cells, Cultured
Decidua / drug effects*
Fibroblasts / drug effects*
Forkhead Transcription Factors / biosynthesis
Genetic Markers
In Situ Nick-End Labeling
Insulin-Like Growth Factor Binding Protein 1 / metabolism
Left-Right Determination Factors / biosynthesis
Paracrine Communication / drug effects
Parathyroid Hormone-Related Protein / pharmacology*
Prolactin / biosynthesis
RNA / biosynthesis,  genetics
RNA, Small Interfering / genetics
Reverse Transcriptase Polymerase Chain Reaction
Uterus / cytology,  drug effects*
Grant Support
Reg. No./Substance:
0/FOXO1 protein, human; 0/Forkhead Transcription Factors; 0/Genetic Markers; 0/Insulin-Like Growth Factor Binding Protein 1; 0/Left-Right Determination Factors; 0/PTHLH protein, human; 0/Parathyroid Hormone-Related Protein; 0/RNA, Small Interfering; 63231-63-0/RNA; 9002-62-4/Prolactin; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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