Document Detail


Expressions of vitamin D metabolic components VDBP, CYP2R1, CYP27B1, CYP24A1, and VDR in placentas from normal and preeclamptic pregnancies.
MedLine Citation:
PMID:  22871339     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Vitamin D insufficiency/deficiency during pregnancy has been linked to increased risk of preeclampsia. Placenta dysfunction plays an important role in the pathogenesis of this pregnancy disorder. In this study, we tested the hypothesis that disturbed vitamin D metabolism takes place in preeclamptic placentas. Protein expressions of vitamin D binding protein (VDBP), 25-hydroxylase (CYP2R1), 1α-hydroxylase (CYP27B1), 24-hydroxylase (CYP24A1), and vitamin D receptor (VDR) were examined in placentas from normotensive and preeclamptic pregnancies. By immunostaining we found that in normal placenta VDBP, CYP24A1, and VDR expressions are localized mainly in trophoblasts, whereas CYP2R1 and CYP27B1 expressions are localized mainly in villous core fetal vessel endothelium. Protein expressions of CYP2R1 and VDR are reduced, but CYP27B1 and CYP24A1 expressions are elevated, in preeclamptic compared with normotensive placentas. Because increased oxidative stress is an underlying pathophysiology in placental trophoblasts in preeclampsia, we further determined whether oxidative stress contributes to altered vitamin D metabolic system in placental trophoblasts. Trophoblasts isolated from normal-term placentas were treated with hypoxic-inducing agent CoCl(2), and protein expressions of VDBP, CYP2R1, CYP27B1, CYP24A1, and VDR were determined. We found that hypoxia-induced downregulation of VDBP, CYP2R1, and VDR and upregulation of CYP27B1 and CYP24A1 expressions were consistent with that seen in preeclamptic placentas. CuZnSOD expression was also downregulated in trophoblasts treated with CoCl(2). These results provide direct evidence of disrupted vitamin D metabolic homeostasis in the preeclamptic placenta and suggest that increased oxidative stress could be a causative factor of altered vitamin D metabolism in preeclamptic placentas.
Authors:
Rong Ma; Yang Gu; Shuang Zhao; Jingxia Sun; Lynn J Groome; Yuping Wang
Related Documents :
11536139 - Microbial growth by a net heat up-take: a calorimetric and thermodynamic study on aceto...
16330369 - Late pregnancy exposures to disinfection by-products and growth-related birth outcomes.
3675449 - Antepartum cardiotocography--an audit.
10986429 - Origins of fetal growth restriction.
3834949 - Growth-promoting activity of serum throughout pregnancy and at delivery: evaluation by ...
12953179 - Timing is everything: a reconsideration of fetal growth velocity patterns identifies th...
18671769 - Trypanosoma cruzi in non-human primates with a history of stillbirths: a retrospective ...
10625209 - Detection of decreased response to activated protein c during pregnancy by an endogenou...
12507969 - Prevalence of fatty acid ethyl esters in meconium specimens.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-08-07
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  303     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-02     Completed Date:  2013-01-07     Revised Date:  2014-01-13    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E928-35     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
25-Hydroxyvitamin D3 1-alpha-Hydroxylase / biosynthesis*
Adolescent
Adult
Cholestanetriol 26-Monooxygenase / biosynthesis*
Cobalt / toxicity
Female
Humans
Oxidative Stress / drug effects,  physiology
Placenta / chemistry,  metabolism*,  pathology
Pre-Eclampsia / metabolism*,  pathology
Pregnancy
Pregnancy Trimester, Third
Receptors, Calcitriol / biosynthesis*
Steroid Hydroxylases / biosynthesis*
Superoxide Dismutase / metabolism
Vitamin D / metabolism*
Vitamin D-Binding Protein / biosynthesis*
Young Adult
Grant Support
ID/Acronym/Agency:
HD-36822/HD/NICHD NIH HHS; HL-65997/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Calcitriol; 0/Vitamin D-Binding Protein; 1406-16-2/Vitamin D; 3G0H8C9362/Cobalt; 7646-79-9/cobaltous chloride; EC 1.14.-/25-Hydroxyvitamin D3 1-alpha-Hydroxylase; EC 1.14.-/Steroid Hydroxylases; EC 1.14.13.126/vitamin D 24-hydroxylase; EC 1.14.13.15/CYP2R1 protein, human; EC 1.14.13.15/Cholestanetriol 26-Monooxygenase; EC 1.15.1.1/Superoxide Dismutase
Comments/Corrections

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


Previous Document:  Method of removal of volatile organic compounds by using wet scrubber coupled with photo-Fenton reac...
Next Document:  Role of fatty acid transport protein 4 in oleic acid-induced glucagon-like peptide-1 secretion from ...