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VEGF mRNA levels are upregulated by lipopolyssacharide in the cervix of pregnant mice
Author(s) -
Newell Allison,
Thompson Morgan,
Mowa Chishimba Nathan
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1003.10
Subject(s) - inflammation , cervix , vascular endothelial growth factor , downregulation and upregulation , infiltration (hvac) , vegf receptors , messenger rna , endocrinology , medicine , saline , andrology , immunology , biology , cancer , gene , biochemistry , physics , thermodynamics
Cervical remodeling (CR) is one of the few biological processes that entails physiological inflammation, and can be significantly enhanced by inflammation‐inducing agents, such as lipopolyssacharide (LPS), a component of bacteria cell wall. Infection is one of the leading causes of preterm labor, and CR and inflammation are both closely associated with microvascular alterations. Of note, we recently identified and characterized expression of a potent regulator of the vasculature, vascular endothelial growth factor (VEGF) and VEGF signaling molecules in the cervix of pregnant and parturient rats. Our long term goal is to investigate whether the mechanism(s) underlying LPS‐enhanced CR involve VEGF and alters microvasculature. Here, we sought to characterize the pattern of VEGF mRNA expression in LPS‐treated pregnant mice using PCR. LPS dissolved in normal saline was administered intra‐cervically in a dose‐dependent manner to three groups of mice at day 12 of pregnancy (n=3 per group), namely vehicle only, 250ng and 300ng. The cervix was harvested 6 hrs later and levels of VEGF mRNA were analyzed by PCR. Our preliminary data revealed that LPS up regulated levels of VEGF mRNA in a dose‐dependent manner. These studies show that LPS‐induced preterm labor involves enhanced VEGF synthesis, which may lead to abnormal microvascular remodeling and mobilization and infiltration of vascular‐derived CR mediators.