The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states.

The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states. Research Abstract Details 

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The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states. Abstract Text:

Charles J Lockwood,Graciela Krikun,Mizanur Rahman,Rebeca Caze,Lynn Buchwalder,Frederick Schatz,

Progesterone-induced decidualized human endometrial stromal cells form a hemostatic envelope that protects against hemorrhage during invasion of endometrial capillaries by implanting blastocyst-derived cytotrophoblasts (CTs). This hemostatic milieu reflects co-upregulated expression of tissue factor (TF), the primary initiator of hemostasis via thrombin generation and plasminogen activator inhibitor type 1, which inactivates tissue-type plasminogen activator, the primary fibrinolytic agent. During deep invasion of the decidua, CTs breach and remodel spiral arteries and arterioles to produce high-conductance vessels. Shallow invasion results in incomplete vascular transformation and an underperfused fetal - placental unit associated with preeclampsia and intrauterine growth restriction. Decidual hemorrhage and severe thrombophilias elicit aberrant thrombin generation from decidual cell-expressed TF. Such thrombin induces decidual cells to synthesize and secrete soluble fms-like tyrosine kinase-1 (sFlt-1), the matrix metalloproteinases MMP-1 and MMP-3, and the neutrophil chemoattractant interleukin-8. Excess sFlt-1 at the implantation site may inhibit CT invasion by altering the angiogenic factor balance. During abruptions, thrombin-enhanced MMP-1, MMP-3 by decidual cells and neutrophil-derived proteases degrade the decidual and fetal membrane extracellular matrix to promote preterm premature rupture of the membranes. In association with long-term progestin-only contraception, overexpression of decidual cell-derived thrombin promotes aberrant angiogenesis and vessel maintenance to contribute to abnormal uterine bleeding.

The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states. Publishing Authors By Initials

CJ Lockwood,G Krikun,M Rahman,R Caze,L Buchwalder,F Schatz,

For similar polycyclic compounds: steroids: pregnanes: pregnenes: pregnenediones: progesterone research abstracts see: polycyclic compounds: steroids: pregnanes: pregnenes: pregnenediones: progesterone research

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The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states. Journal Published:

PUBLICATION TYPE: Review

Journal: Seminars in thrombosis and hemostasis

VOLUME: 33

Page Numbers: 111-7

Journal Abbreviation: Semin. Thromb. Hemost.

ISSN: 0094-6176

DAY: 3

MONTH: Feb

YEAR: 2007

The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states. Information

Number of References: 40

LANGUAGE: eng

NlmUniqueID: 431155

The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states. Keywords Mesh Terms:

KEYWORDS: Progesterone

MESH TERMS: metabolism

Chemical & Substance for Abstract: The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states. Information

Substance Name: Progesterone

Registry Number: 57-83-0

Grant and Affiliation Information for The role of decidualization in regulating endometrial hemostasis during the menstrual cycle, gestation, and in pathological states.

AFFILIATION: Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06511, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL 070004-03

ACRONYM: HL

MEDLINETA: Semin Thromb Hemost

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