ArticleThe Journal of surgical research2009
The effects of increased extracellular deformation, pressure, and integrin phosphorylation on fibroblast migration.
Article in The Journal of surgical research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- Intestinal mucosal atrophy and adaptation.World journal of gastroenterology · 2012Review
- Influence of defunctionalization and mechanical forces on intestinal epithelial wound healing.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Changes in morphology and function in small intestinal mucosa after Roux-en-Y surgery in a rat model.The Journal of surgical research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Wound healing requires fibroblast migration. Increased pressure slows migration and ulcer healing. Pressure also induces beta1 integrin phosphorylation. We hypothesized that beta1 phosphorylation influences cell adhesion and migration. We compared the effects of increased pressure on the adhesion and motility of GD25 beta1-integrin null fibroblasts transfected with wild-type beta1A-integrin, S785A or TT788/9AA (phosphorylation-deficient), or T788D (constitutively phosphomimetic) mutants. GD25 beta1 null cells adhered less than wild type beta1A cells, suggesting adherence by non-integrin mechanisms. Preventing Ser-785 or Thr 788/789 phosphorylation reduced adhesion, suggesting that phosphorylation regulates adhesiveness. Substituting Asp for Thr788 stimulated adhesion on both substrates. Pressure decreased migration in all lines and on all matrixes, the most in wild type beta1A integrin cells and only slightly in beta1A TT788/9AA cells. In comparison, another physical force, repetitive deformation, increased migration in the beta1A integrin T788D, S785A, and wild type cells on fibronectin, and decreased migration on collagen. Deformation did not affect the migration of GD25 beta1-integrin null or TT788/9AA cells. Extracellular signal-regulated kinase (ERK) blockade neither altered basal migration nor prevented pressure inhibition, while the cellular deformation response on fibronectin was altered. beta1-Integrin phosphorylation regulates cellular adhesion and the deformation effects on motility. The pressure-induced motility response is independently regulated.
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Registered trials
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.