ArticleGut2009
FGF9-induced proliferative response to eosinophilic inflammation in oesophagitis.
Article in Gut, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 78 citations in OpenAlex.
- Review
- Circular RNA circ-SLC7A5 Functions as a Competing Endogenous RNA to Impact Cell Biological Behaviors in Esophageal Squamous Cell Carcinoma (ESCC).Cell biochemistry and biophysics · 2024Article
- Steroid-induced fibroblast growth factors drive an epithelial-mesenchymal inflammatory axis in severe asthma.Science translational medicine · 2022Article
- Type 2 Inflammation in Eosinophilic Esophagitis: From Pathophysiology to Therapeutic Targets.Frontiers in physiology · 2021Review
- Eosinophils in Eosinophilic Esophagitis: The Road to Fibrostenosis is Paved With Good Intentions.Frontiers in immunology · 2020Review
- Pathophysiology of Eosinophilic Esophagitis.Clinical reviews in allergy & immunology · 2018Review
- Noncanonical NF-κB signaling and the essential kinase NIK modulate crucial features associated with eosinophilic esophagitis pathogenesis.Disease models & mechanisms · 2017Article
- Tissue Remodeling in Chronic Eosinophilic Esophageal Inflammation: Parallels in Asthma and Therapeutic Perspectives.Frontiers in medicine · 2017Review
- Mechanisms of Disease of Eosinophilic Esophagitis.Annual review of pathology · 2016Review
- Eosinophilic esophagitis: From pathophysiology to treatment.World journal of gastrointestinal pathophysiology · 2015Review
- Cytoskeletal changes induced by allosteric modulators of calcium-sensing receptor in esophageal epithelial cells.Physiological reports · 2015Article
- Article
- Clinical implications and pathogenesis of esophageal remodeling in eosinophilic esophagitis.Gastroenterology clinics of North America · 2014Review
- Remodeling and fibrosis in chronic eosinophil inflammation.Digestive diseases (Basel, Switzerland) · 2014Review
- The pathophysiology of eosinophilic esophagitis.Frontiers in pediatrics · 2014Review
- The pathogenesis of eosinophilic esophagitis: beyond the eosinophil.Digestive diseases and sciences · 2013Article
- Epithelial calcium-sensing receptor activation by eosinophil granule protein analog stimulates collagen matrix contraction.Pediatric research · 2013Article
- Current hurdles in the management of eosinophilic oesophagitis: the next steps.World journal of gastroenterology · 2013Article
- Impact of gastro-oesophageal reflux on microRNA expression, location and function.BMC gastroenterology · 2013Article
- Tissue remodeling in eosinophilic esophagitis.American journal of physiology. Gastrointestinal and liver physiology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOesophagitis is characterised by basal cell hyperplasia and activated eosinophils, which release mediators including major basic protein (MBP). MBP and its mimetic polyarginine activate the calcium sensing receptor (CaSR) on oesophageal epithelium. Fibroblast growth factor 9 (FGF9) is implicated in epithelial homeostasis and proliferative response to injury, but has not been characterised in the oesophagus.
objectiveTo characterise FGF9 in oesophageal epithelium and oesophagitis, as the result of MBP activation of the CaSR.
methodsHuman oesophageal epithelial cells (HET-1A) were used to compare affects of calcium, polyarginine and MBP-peptide on FGF9. HET-1A were transfected with interfering RNA (siRNA(CaSR)). FGF9, FGF receptors 2 and 3, bone morphogenetic protein (BMP)-2, BMP-4 and noggin mRNA expression were detected by reverse transcriptase polymerase chain reaction. FGF9 was measured from HET-1A and from normal, gastro-oesophageal reflux and eosinophilic oesophagitis (EoE) patient biopsies using ELISA and immunohistochemistry. HET-1A proliferation was studied using bromodeoxyuridine and MTT.
resultsFGF9 was secreted by HET-1A cells treated with polyarginine and MBP-peptide, but not calcium. This effect was abrogated by siRNA(CaSR). FGF9 receptor mRNA was present. HET-1A cells proliferated following rhFGF9, but not MBP-peptide treatment, and rhFGF9 altered transcription of downstream proliferation-related genes (noggin, BMP-2 and BMP-4). FGF9 was increased in biopsies from patients with eosinophilic oesophagitis, which correlated with basal hyperplasia.
conclusionEosinophil-released MBP acts on the CaSR to increase FGF9 in oesophageal epithelial cells, leading to proliferation. Increased FGF9 is found in biopsies of EoE patients and may play a role in the pathogenesis of oesophagitis.
Indexed as
Identifiers
What OpenQuestion holds
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.