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Induction of Placental Heme Oxygenase-1 Is Protective Against TNFα-induced Cytotoxicity and Promotes Vessel Relaxation

Overview of attention for article published in Molecular Medicine, May 2000
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (86th percentile)
  • High Attention Score compared to outputs of the same age and source (81st percentile)

Mentioned by

policy
1 policy source
patent
2 patents
wikipedia
1 Wikipedia page

Citations

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133 Dimensions

Readers on

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84 Mendeley
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Title
Induction of Placental Heme Oxygenase-1 Is Protective Against TNFα-induced Cytotoxicity and Promotes Vessel Relaxation
Published in
Molecular Medicine, May 2000
DOI 10.1007/bf03401783
Pubmed ID
Authors

Asif Ahmed, Mahbubur Rahman, Xian Zhang, Carmen H. Acevedo, Sarbjit Nijjar, Ian Rushton, Benedetta Bussolati, Justin St. John

Abstract

Pregnancy is characterized by an inflammatory-like process and this may be exacerbated in preeclampsia. The heme oxygenase (HO) enzymes generate carbon monoxide (CO) that induces blood vessel relaxation and biliverdin that acts as an endogenous antioxidant. We examined the expression and localization of HO-1 and HO-2 in normal and preeclamptic placenta using reverse transcription polymerase chain reaction (RT-PCR), RNase protection assay, immunoblotting and immunohistochemistry. In addition, the effect of HO activation on tumor necrosis factor-alpha (TNFalpha) induced placental damage and on feto-placental circulation was studied. We provide the first evidence for the role of HO as an endogenous placental factor involved with cytoprotection and placental blood vessel relaxation. HO-1 was significantly higher at term, compared with first trimester placentae indicating its role in placental vascular development and regulation. HO-1 predominantly localized in the extravascular connective tissue that forms the perivascular contractile sheath around the developing blood vessels. HO-2 was localized in the capillaries, as well as the villous stroma, with weak staining of trophoblast. Induction of HO-1 caused a significant attenuation of TNFalpha-mediated cellular damage in placental villous explants, as assessed by lactate dehydrogenase leakage (p < 0.01). HO-1 protein was significantly reduced in placentae from pregnancies complicated with preeclampsia, compared with gestationally matched normal pregnancies. This suggests that the impairment of HO-1 activation may compromise the compensatory mechanism and predispose the placenta to cellular injury and subsequent maternal endothelial cell activation. Isometric contractility studies showed that hemin reduced vascular tension by 61% in U46619-preconstricted placental arteries. Hemin-induced vessel relaxation and CO production was inhibited by HO inhibitor, tin protoporphyrin IX. Our findings establish HO-1 as an endogenous system that offers protection against cytotoxic damage in the placenta, identifies the HO-CO pathway to regulate feto-placental circulation and provides a new approach to study the disease of preeclampsia.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 84 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Brazil 1 1%
Unknown 83 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 14 17%
Student > Bachelor 14 17%
Researcher 9 11%
Student > Master 9 11%
Student > Doctoral Student 8 10%
Other 11 13%
Unknown 19 23%
Readers by discipline Count As %
Medicine and Dentistry 28 33%
Agricultural and Biological Sciences 16 19%
Biochemistry, Genetics and Molecular Biology 7 8%
Psychology 4 5%
Nursing and Health Professions 3 4%
Other 7 8%
Unknown 19 23%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 9. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 08 August 2023.
All research outputs
#3,799,858
of 25,377,790 outputs
Outputs from Molecular Medicine
#138
of 1,206 outputs
Outputs of similar age
#3,673
of 40,865 outputs
Outputs of similar age from Molecular Medicine
#2
of 11 outputs
Altmetric has tracked 25,377,790 research outputs across all sources so far. Compared to these this one has done well and is in the 83rd percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,206 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.6. This one has done well, scoring higher than 85% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 40,865 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 86% of its contemporaries.
We're also able to compare this research output to 11 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 81% of its contemporaries.