Heme oxygenase-1 modulates fetal growth in the rat

Autor: David A. Stevenson, Nader G. Abraham, Phyllis A. Dennery, Xuandai Nguyen, Doron Kreiser, Daniel S. Seidman, Shou Quan, Ronald J. Wong
Rok vydání: 2002
Předmět:
Vascular Endothelial Growth Factor A
medicine.medical_specialty
medicine.medical_treatment
Placenta
Genetic Vectors
Intrauterine growth restriction
Endothelial Growth Factors
Biology
Pathology and Forensic Medicine
Adenoviridae
Receptor
IGF Type 1
chemistry.chemical_compound
Pregnancy
Transduction
Genetic
Internal medicine
medicine
Animals
Humans
Enzyme Inhibitors
Rats
Wistar
Receptor
Molecular Biology
Fetus
Lymphokines
Dose-Response Relationship
Drug
Vascular Endothelial Growth Factors
Growth factor
Membrane Proteins
Cell Biology
medicine.disease
Rats
Vascular endothelial growth factor
Heme oxygenase
Insulin-Like Growth Factor Binding Protein 1
medicine.anatomical_structure
Endocrinology
Cytokine
chemistry
Animals
Newborn
Fetal Weight
Heme Oxygenase (Decyclizing)
Female
Heme Oxygenase-1
Deuteroporphyrins
Zdroj: Laboratory investigation; a journal of technical methods and pathology. 82(6)
ISSN: 0023-6837
Popis: Intrauterine growth restriction is associated with increased perinatal morbidity and mortality as well as with lifelong cardiovascular and metabolic complications. Deficiency of heme oxygenase 1 (HO-1) is associated with growth restriction in mice and in humans, suggesting a role for HO-1 in fetal growth and maintenance of pregnancy. We hypothesized that modulation of HO-1 in the pregnant rat would alter fetal growth. In pregnant dams, placental HO activity was significantly inhibited with zinc deuteroporphyrin IX 2,4 bis glycol, and HO-1 protein was increased by transducing adenoviral human HO-1. Inhibition of HO-1 by zinc deuteroporphyrin IX 2,4 bis glycol resulted in a significant decrease in pup size, whereas transfection with hHO-1 resulted in increased pup size. Furthermore, the expression of IGF binding protein-1 and its receptor paralleled the expression of HO-1 in the placenta and were significantly modulated by modification of HO-1 along with the expression of vascular endothelial growth factor. These observations demonstrate that HO-1 modulates fetal growth by its effects on placental growth factors.
Databáze: OpenAIRE
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