Evidence map›Paper›PMID 11518735›Full record

ArticleThe Journal of clinical investigation2001

A complex role for the progesterone receptor in the response to vascular injury.

R H Karas, M van Eickels, J P Lydon, S Roddy, M Kwoun, M Aronovitz, W E Baur, O Conneely, B W O'Malley, M E Mendelsohn

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 44 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

R H KarasMolecular Cardiology Research Institute, New England Medical Center Hospitals Inc., Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
M van Eickels
J P Lydon
S Roddy
M Kwoun
M Aronovitz
W E Baur
O Conneely
B W O'Malley
M E Mendelsohn
Medical Center Hospital · USBaylor College of Medicine · USTufts University · US

Funding

SEX HORMONE RECEPTOR COMPONENTS AND THE CELL GENOMER01HD007857 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI DAVID M LONARD, JOHN P LYDON · 1985 to 2026
$14.6M
VASCULAR ESTROGEN RECEPTOR SIGNALING PATHWAYSR01HL061298 · NHLBI · TUFTS MEDICAL CENTER · PI KARAS, RICHARD H · 1999 to 2012
$4.4M
VASCULAR SURGERY--ESTROGEN AND THE INJURY RESPONSER01HL056069 · NHLBI · TUFTS MEDICAL CENTER · PI KARAS, RICHARD H · 1997 to 2012
$3.7M
PROGESTERONE RECEPTOR IN BREAST DEVELOPMENT AND CANCERR01CA077530 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LYDON, JOHN P · 2005 to 2008
$1.2M
PROGESTERONE RECEPTOR AND BREAST CANCERR29CA077530 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LYDON, JOHN P · 1998 to 2004
$398k
VASCULAR ESTROGEN RECEPTORS--MOLECULAR MECHANISMSR01HL059953 · NHLBI · TUFTS MEDICAL CENTER · PI MENDELSOHN, MICHAEL E · 1998 to 2001
$394k
SEX HORMONE RECEPTOR COMPONENTS &THE CELL GENOMER37HD007857 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MC KEOWN, MICHAEL B · 1987 to 1996
–
NCI NIH HHS CA-77530-01NCI NIH HHS R01 CA077530NCI NIH HHS R29 CA077530NHLBI NIH HHS HL-56069NHLBI NIH HHS HL-59953NHLBI NIH HHS HL-61298NHLBI NIH HHS R01 HL056069NHLBI NIH HHS R01 HL061298NICHD NIH HHS HD-07857NICHD NIH HHS R01 HD007857
6 · The paper itself

Abstract

Clinical studies of hormone replacement therapy to prevent cardiovascular diseases have heightened interest in the cardiovascular effects of progestins. However, the role of the progesterone receptor (PR) in vascular biology has not been studied in vivo. We studied ovariectomized female PR knockout (PRKO) mice and their wild-type (WT) littermates using the mouse carotid artery injury model. Placebo-treated PRKO mice showed significantly greater vascular medial hypertrophy and vascular smooth muscle cell (VSMC) proliferation in response to vascular injury than did WT mice. Progesterone had no significant effect in the PRKO mice, but worsened the response to injury in WT mice. VSMCs cultured from PRKO mouse aortae were markedly hyperproliferative, and their growth was not affected by progesterone. In contrast to the in vivo findings, progesterone inhibited proliferation of WT-derived VSMCs. Furthermore, reintroduction of PR into PRKO-derived VSMCs using adenoviral methods restored progesterone-mediated inhibition of proliferation to these cells. This effect was reversed by the PR antagonist, RU 486. Thus, the effects of PR and progesterone differ markedly between cultured VSMCs and intact blood vessels. These data demonstrate a direct role for the PR in regulating the response to vascular injury and VSMC proliferation.

Indexed as

Carotid Artery InjuriesAnimalsCarotid Artery, CommonCell DivisionCells, CulturedDNA ReplicationFemaleHormone AntagonistsHyperplasiaMiceMice, KnockoutMifepristoneMuscle, Smooth, VascularOvariectomyProgesteroneReceptors, ProgesteroneHormone AntagonistsMifepristoneProgesteroneReceptors, ProgesteroneRecombinant Fusion Proteins

Identifiers

PMID11518735
PMCPMC209395
OpenAlexW2151451304

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.