Evidence map›Paper›PMID 22556141›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012

Hyaluronic acid regulates normal intestinal and colonic growth in mice.

Terrence E Riehl, Xueping Ee, William F Stenson

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
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  13. Article
  14. Hyaluronidases in Human Diseases.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Article
  17. Hyaluronic acid promotes Lgr5American journal of physiology. Gastrointestinal and liver physiology · 2020
    Article
  18. Review
  19. Review
  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

3 authors at 1 institution in 1 country.

Terrence E RiehlDivision of Gastroenterology, Washington University, St. Louis, Missouri, USA.
Xueping Ee
William F Stenson
Washington University in St. Louis · US

Funding

Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
PROSTAGLANDINS IN EPITHELIAL INJURYR01DK055753 · NIDDK · WASHINGTON UNIVERSITY · PI STENSON, WILLIAM F. · 1999 to 2013
$3.8M
Mediators of Inflammation in Intestinal InjuryR37DK033165 · NIDDK · WASHINGTON UNIVERSITY · PI STENSON, WILLIAM F. · 2007 to 2016
$3.5M
NIDDK NIH HHS P30-DK-52574NIDDK NIH HHS R01-DK-55753NIDDK NIH HHS R37 DK-33165
6 · The paper itself

Abstract

Hyaluronic acid (HA), a component of the extracellular matrix, affects gastrointestinal epithelial proliferation in injury models, but its role in normal growth is unknown. We sought to determine the effects of exogenous HA on intestinal and colonic growth by intraperitoneal injection of HA twice a week into C57BL/6 mice from 3 to 8 wk of age. Similarly, to determine the effects of endogenous HA on intestinal and colonic growth, we administered PEP-1, a peptide that blocks the binding of HA to its receptors, on the same schedule. In mice treated with exogenous HA, villus height and crypt depth in the intestine, crypt depth in the colon, and epithelial proliferation in the intestine and colon were increased. In mice treated with PEP-1, intestinal and colonic length were markedly decreased and crypt depth and villus height in the intestine, crypt depth in the colon, and epithelial proliferation in the intestine and colon were decreased. Administration of HA was associated with increased levels of EGF (intestine) and IGF-I (colon), whereas administration of PEP-1 was associated with decreased levels of IGF-I (intestine) and epiregulin (colon). Exogenous HA increases intestinal and colonic epithelial proliferation, resulting in hyperplasia. Blocking the binding of endogenous HA to its receptors results in decreased intestinal and colonic length and a mucosal picture of hypoplasia, suggesting that endogenous HA contributes to the regulation of normal intestinal and colonic growth.

Indexed as

AnimalsCell ProliferationColonEpidermal Growth FactorEpiregulinEpithelial CellsGlucuronosyltransferaseHyaluronan ReceptorsHyaluronan SynthasesHyaluronic AcidHyaluronoglucosaminidaseInsulin-Like Growth Factor IIntestinesMiceMice, Inbred C57BLPeptidesEpidermal Growth FactorEpiregulinEreg protein, mouseGlucuronosyltransferaseglycyl-alanyl-histidyl-tryptophyl-glutaminyl-phenylalanyl-asparagyl-alanyl-leucyl-threonyl-valyl-arginineHyaluronan ReceptorsHyaluronan SynthasesHyaluronic AcidHyaluronoglucosaminidaseInsulin-Like Growth Factor IPeptidesRNA, Messenger

Identifiers

PMID22556141
PMCPMC3423109
OpenAlexW2118831064

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.