Evidence map›Paper›PMID 9176411›Full record

ArticleThe American journal of pathology1997

Evidence for the genetic control of estradiol-regulated responses. Implications for variation in normal and pathological hormone-dependent phenotypes.

J S Griffith, S M Jensen, J K Lunceford, M W Kahn, Y Zheng, E A Falase, C R Lyttle, C Teuscher

Abstract read
In one paragraph

Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Genetic variation in sensitivity to estrogens and breast cancer risk.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  5. Article
  6. The role of genetics in estrogen responses: a critical piece of an intricate puzzle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Review
  7. Article
  8. Article
  9. Role of nuclear receptors in blastocyst implantation.Seminars in cell & developmental biology · 2013
    Review
  10. Article
  11. Genetic control of estrogen-regulated transcriptional and cellular responses in mouse uterus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  12. Obesity and asthma.Lung India : official organ of Indian Chest Society · 2013
    Article
  13. Article
  14. Article
  15. Genetic mapping of Eutr1, a locus controlling E2-induced pyometritis in the Brown Norway rat, to RNO5.Mammalian genome : official journal of the International Mammalian Genome Society · 2005
    Article
  16. Article
  17. Article
  18. Review
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

J S GriffithDepartment of Microbiology, Brigham Young University, Provo, Utab, USA.
S M Jensen
J K Lunceford
M W Kahn
Y Zheng
E A Falase
C R Lyttle
C Teuscher
Brigham Young University · US

Funding

INFERTILITY AND TESTICULAR AUTOIMMUNITYR01HD021926 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI TEUSCHER, CORY · 1987 to 1995
–
INFERTILITY AND OVARIAN AUTOIMMUNITYR01HD027275 · NICHD · BRIGHAM YOUNG UNIVERSITY · PI TEUSCHER, CORY · 1991 to 1993
–
NIAID NIH HHS AI40712NICHD NIH HHS HD21926NICHD NIH HHS HD27275
6 · The paper itself

Abstract

The ovarian steroid hormone estrogen (E2) elicits a multiplicity of both systemic and uterotropic responses in vivo. For example, the administration of E2 to ovariectomized (Ovx) and sexually immature rodents leads to uterine-specific inflammatory infiltrates. In this study, we quantitated the number of eosinophils and BM8+, Ia+, and CD4+ cells in uteri obtained from adult Ovx control and E2-treated C57BL/6J, C3H/HeJ, and (C57BL/6J x C3H/HeJ) (B6C3) F1 hybrid mice. All three strains exhibited a significant increase in the number of uterine eosinophils and BM8+ macrophages after E2 treatment. However, C57BL/6J and B6C3 F1 hybrid mice responded with a greater number of infiltrating eosinophils and macrophages as compared with C3H/HeJ. A similar analysis of Ia+ and CD4+ cells showed that E2 treatment either down-regulates or does not affect the number of such cells in all three strains. Genome exclusion mapping using a (C57BL/6J x C3H/HeJ) x C3H/HeJ backcross population localized Est1, the major locus controlling the number of eosinophils infiltrating the uterus after E2 treatment, to chromosome 4. In addition, suggestive linkage to marker loci on chromosomes 10 and 16 was detected and evidence for locus interaction is presented. Our results conclusively demonstrate that E2-regulated/ dependent responses can be genetically controlled, indicating that the phenotypic variation observed in both the normal and pathological effects of E2 may, in part, be due to a genetic component.

Indexed as

Chromosome MappingAnimalsCD4-Positive T-LymphocytesEosinophilsEstradiolFemaleGenetic LinkageInflammationMacrophagesMiceMice, Inbred StrainsOvariectomySpecies SpecificityUterusEstradiol

Identifiers

PMID9176411
PMCPMC1858318
OpenAlexW26072114

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.