Evidence map›Paper›PMID 24023003›Full record

ArticleStem cells (Dayton, Ohio)2014

Smad1 and 5 but not Smad8 establish stem cell quiescence which is critical to transform the premature hair follicle during morphogenesis toward the postnatal state.

Eve Kandyba, Virginia M Hazen, Agnieszka Kobielak, Samantha J Butler, Krzysztof Kobielak

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

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  17. Deciphering principles of morphogenesis from temporal and spatial patterns on the integument.Developmental dynamics : an official publication of the American Association of Anatomists · 2015
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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

5 authors at 3 institutions in 1 country.

Eve KandybaEli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research and Department of Biochemistry and Molecular Biology, USC Norris Cancer Center, University of Southern California, Los Angeles, California, USA; Department of Pathology, Department of Biochemistry and Molecular Biology, USC Norris Cancer Center, University of Southern California, Los Angeles, California, USA.
Virginia M Hazen
Agnieszka Kobielak
Samantha J Butler
Krzysztof Kobielak
University of Southern California · USBroad Center · USUSC Norris Comprehensive Cancer Center · US

Funding

Activator Inhibitor interactions in the cyclic regeneration of hair follicle stemR01AR061552 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KOBIELAK, KRZYSZTOF · 2012 to 2016
$1.8M
Regulation of axonal outgrowth in the developing spinal cordR01NS063999 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BUTLER, SAMANTHA J · 2008 to 2014
$1.8M
Isolation and characterization of new adult stem cells from sweat glands.R03AR061028 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KOBIELAK, KRZYSZTOF · 2011 to 2013
$239k
NIAMS NIH HHS R01 AR061552NIAMS NIH HHS R01-AR061552NIAMS NIH HHS R03 AR061028NIAMS NIH HHS R03-AR061028NINDS NIH HHS NS063999NINDS NIH HHS R01 NS063999PHS HHS R21-5351568360
6 · The paper itself

Abstract

Hair follicles (HFs) are regenerative miniorgans that offer a highly informative model system to study the regulatory mechanisms of hair follicle stem cells (hfSCs) homeostasis and differentiation. Bone morphogenetic protein (BMP) signaling is key in both of these processes, governing hfSCs quiescence in the bulge and differentiation of matrix progenitors. However, whether canonical or noncanonical pathways of BMP signaling are responsible for these processes remains unresolved. Here, we conditionally ablated two canonical effectors of BMP signaling, Smad1 and Smad5 during hair morphogenesis and postnatal cycling in mouse skin. Deletion of Smad1 and Smad5 (dKO) in the epidermis during morphogenesis resulted in neonatal lethality with lack of visible whiskers. Interestingly, distinct patterns of phospho-Smads (pSmads) activation were detected with pSmad8 restricted to epidermis and pSmad1 and pSmad5 exclusively activated in HFs. Engraftment of dKO skin revealed retarded hair morphogenesis and failure to differentiate into visible hair. The formation of the prebulge and bulge reservoir for quiescent hfSCs was precluded in dKO HFs which remained in prolonged anagen. Surprisingly, in postnatal telogen HFs, pSmad8 expression was no longer limited to epidermis and was also present in dKO bulge hfSCs and matrix progenitors. Although pSmad8 activity alone could not prevent dKO hfSCs precocious anagen activation, it sustained efficient postnatal differentiation and regeneration of visible hairs. Together, our data suggest a pivotal role for canonical BMP signaling demonstrating distinguished nonoverlapping function of pSmad8 with pSmad1 and pSmad5 in hfSCs regulation and hair morphogenesis but a redundant role in adult hair progenitors differentiation.

Indexed as

AnimalsCell DifferentiationEpidermisHairHair FollicleMiceMorphogenesisRegenerationSmad1 ProteinSmad5 ProteinSmad8 ProteinStem CellsSmad1 ProteinSmad1 protein, mouseSmad5 ProteinSmad5 protein, mouseSmad8 ProteinSmad9 protein, mouseCanonical bone morphogenetic protein signalingHair follicle stem cellsProgenitor cellsSmad

Identifiers

PMID24023003
PMCPMC4398393
OpenAlexW1523741520

What OpenQuestion holds

Textmetadata
LicenceTDM
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.