Evidence map›Paper›PMID 20610540›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

Luteinizing hormone receptor-stimulated progesterone production by preovulatory granulosa cells requires protein kinase A-dependent activation/dephosphorylation of the actin dynamizing protein cofilin.

Amelia B Karlsson, Evelyn T Maizels, Maxfield P Flynn, Jonathan C Jones, Eric A Shelden, James R Bamburg, Mary Hunzicker-Dunn

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Actomyosin contraction in the follicular epithelium provides the major mechanical force for follicle rupture duringProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 3 institutions in 1 country.

Amelia B KarlssonSchool of Molecular Biosciences, Washington State University, Pullman, WA 83843, USA.
Evelyn T Maizels
Maxfield P Flynn
Jonathan C Jones
Eric A Shelden
James R Bamburg
Mary Hunzicker-Dunn
Northwestern University · USColorado State University · USWashington State University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008152 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARDEHALI, HOSSEIN · 1987 to 2021
$24.0M
Keratinocyte Migration and Wound HealingR01AR054184 · NIAMS · WASHINGTON STATE UNIVERSITY · PI JONES, JONATHAN C. · 2006 to 2015
$3.3M
TRAINING PROGRAM IN REPRODUCTIVE BIOLOGYT32HD007068 · NICHD · NORTHWESTERN UNIVERSITY · PI LEVINE, JON E · 1985 to 2008
$2.3M
Function of MAP2D in Granulosa CellsR01HD046955 · NICHD · WASHINGTON STATE UNIVERSITY · PI HUNZICKER-DUNN, MARY E · 2005 to 2009
$1.9M
NIAMS NIH HHS R01 AR054184NICHD NIH HHS HD-046955NICHD NIH HHS HD-62503NICHD NIH HHS R01 HD046955NICHD NIH HHS T32 HD007068NICHD NIH HHS T32 HD 07068NIGMS NIH HHS T32 GM008152NIGMS NIH HHS T32-GM08152
6 · The paper itself

Abstract

Activation of the LH receptor (LHR) on preovulatory granulosa cells stimulates the cAMP/protein kinase A (PKA) pathway to regulate expression of genes required for ovulation and luteinization. LHR signaling also initiates rearrangement of the actin cytoskeleton. Because disruption of the actin cytoskeleton has been causally linked to steroidogenesis in various cell models, we sought to identify the cellular mechanisms that may modulate reorganization of the actin cytoskeleton and to determine whether cytoskeletal reorganization is required for steroidogenesis. Herein we report that LHR signaling in preovulatory granulosa cells promotes rapid dephosphorylation of the actin-depolymerizing factor cofilin at Ser3 that is dependent on PKA. The LHR-stimulated dephosphorylation of cofilin(Ser3) switches on cofilin activity to bind actin filaments and enhance their dynamics. Basal phosphorylation of cofilin(Ser3) is mediated by active/GTP-bound Rho and downstream protein kinases; LHR signaling promotes a decrease in active/GTP-bound Rho by a PKA-dependent mechanism. LHR-dependent Rho inactivation and subsequent activation of cofilin does not involve ERK, epidermal growth factor receptor, or phosphatidylinositol 3-kinase pathways downstream of PKA. To understand the biological significance of cofilin activation, preovulatory granulosa cells were transduced with a mutant cofilin adenoviral vector in which Ser3 was mutated to Glu (S-E cofilin). Inactive S-E cofilin abolished LHR-mediated reorganization of the actin cytoskeleton and caused a 70% decrease in LHR-stimulated progesterone that is obligatory for ovulation. Taken together, these results show that LHR signaling via PKA activates a cofilin-regulated rearrangement of the actin cytoskeleton and that active cofilin is required to initiate progesterone secretion by preovulatory granulosa cells.

Indexed as

Actin Depolymerizing FactorsActinsAnimalsChorionic GonadotropinCyclic AMPCyclic AMP-Dependent Protein KinasesCytoskeletonErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFemaleFollicular PhaseGranulosa CellsHumansModels, BiologicalPhosphatidylinositol 3-KinasePhosphorylationActin Depolymerizing FactorsActinsChorionic GonadotropinCyclic AMPCyclic AMP-Dependent Protein KinasesErbB ReceptorsExtracellular Signal-Regulated MAP KinasesPhosphatidylinositol 3-KinaseProgesteroneReceptors, LHrho GTP-Binding Proteins

Identifiers

PMID20610540
PMCPMC2940477
OpenAlexW2137364006

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.