Thrombin and Interleukin-1β Regulate HOXA10 Expression in Human Term Decidual Cells: Implications for Preterm Labor
Author(s) -
Jennifer Sarno,
Frederick Schatz,
Charles J. Lockwood,
S.T. Joseph Huang,
Hugh S. Taylor
Publication year - 2006
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2005-1807
Subject(s) - decidua , thrombin , decidual cells , context (archaeology) , decidualization , proinflammatory cytokine , medicine , andrology , interleukin 8 , stromal cell , endocrinology , chemistry , biology , placenta , inflammation , pregnancy , fetus , platelet , paleontology , genetics
Preterm delivery is commonly caused by intraamniotic infection with expression of proinflammatory cytokines (IL-1beta) or by abruption resulting in generation of decidual thrombin. Although human parturition is not preceded by overt progesterone withdrawal, progesterone resistance likely leads to labor. The uteri of Hoxa10(-/-) mice demonstrate progesterone resistance; several genes, including prostaglandin receptors, are inappropriately regulated in response to progesterone.
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