ArticleJournal of cellular and molecular medicine2015
High glucose-induced intestinal epithelial barrier damage is aggravated by syndecan-1 destruction and heparanase overexpression.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 35 citations in OpenAlex.
- Low-molecular-weight heparin ameliorates intestinal barrier dysfunction in aged male rats via protection of tight junction proteins.Biogerontology · 2024Article
- Enteric neuropathy in diabetes: Implications for gastrointestinal function.World journal of gastroenterology · 2024Article
- Endothelial glycocalyx in retina, hyperglycemia, and diabetic retinopathy.American journal of physiology. Cell physiology · 2023Review
- Integrative biology of extracellular vesicles in diabetes mellitus and diabetic complications.Theranostics · 2022Review
- Hyperglycemia-induced effects on glycocalyx components in the retina.Experimental eye research · 2021Article
- Dichotomic role of heparanase in a murine model of metabolic syndrome.Cellular and molecular life sciences : CMLS · 2021Article
- Effect of High Glucose-Induced Oxidative Stress on Paraoxonase 2 Expression and Activity in Caco-2 Cells.Cells · 2019Article
- Anti-inflammatory and renal protective effect of gingerol in high-fat diet/streptozotocin-induced diabetic rats via inflammatory mechanism.Inflammopharmacology · 2019Article
- Regulation of Heparanase in Diabetes-Associated Pancreatic Carcinoma.Frontiers in oncology · 2019Article
- Epithelial Heparan Sulfate Contributes to Alveolar Barrier Function and Is Shed during Lung Injury.American journal of respiratory cell and molecular biology · 2018Article
- The Protective Effects of a Synthetic Geranyl Acetophenone in a Cellular Model of TNF-α-Induced Pulmonary Epithelial Barrier Dysfunction.Molecules (Basel, Switzerland) · 2018Article
- Diabetes and the Small Intestine.Current treatment options in gastroenterology · 2017Review
- Heparanase Mediates Intestinal Inflammation and Injury in a Mouse Model of Sepsis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2017Article
- Heparanase augments insulin receptor signaling in breast carcinoma.Oncotarget · 2017Article
- Soluble Syndecan-1: A Novel Biomarker of Small Bowel Mucosal Damage in Children with Celiac Disease.Digestive diseases and sciences · 2017Article
- BLT2 expression improves skin integrity and protects from alterations caused by hyperglycemia in type 2 diabetes.Dermato-endocrinology · 2017Article
- Cell surface-anchored syndecan-1 ameliorates intestinal inflammation and neutrophil transmigration in ulcerative colitis.Journal of cellular and molecular medicine · 2017Article
- Kuwanon G Preserves LPS-Induced Disruption of Gut Epithelial Barrier In Vitro.Molecules (Basel, Switzerland) · 2016Article
- Immunohistochemical expression of heparanase isoforms and syndecan-1 proteins in colorectal adenomas.European journal of histochemistry : EJH · 2016Observational
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Syndecan-1 (Sdc1) and its endo-beta-D-glucuronidase heparanase (HPSE) are implicated in maintenance of intestinal epithelial barrier (IEB), but their alterations and roles in high-glucose/hyperglycaemia (HG) conditions have not been fully investigated. This study aimed to determine the expression pattern, the possible regulation mechanism of Sdc1 and HPSE in HG conditions, and their potential effects on IEB. Therefore, diabetic mice/cell models were developed, and tissue/serum samples, cell lysate and culture supernatants were harvested. The expression of Sdc1 and HPSE in control, HG and designated interventions groups were detected. Phosphorylations of mitogen-activated protein kinase signalling pathway (MAPK), the expressions of Occludin and ZO-1, and the levels of transepithelial electrical resistance (TEER) were measured and monitored. The results showed that in HG conditions, intestinal tissue and cellular Sdc1 were significantly decreased, but the expression of HPSE, and soluble Sdc1 in serum and culture supernatants were remarkably increased. Such alterations of Sdc1 and HPSE were associated with solely p38 MAPK activation, and were correlated with the reductions of Occludin, ZO-1 and TEER. Heparin (Sdc1 analogue) and SB203580 (a p38 MAPK inhibitor), instead of insulin, alleviated Sdc1 destruction and HPSE overexpression, and effectively prevented against the reductions of tight junctions and the abnormality of intestinal permeability in HG conditions. In conclusion, we confirm the unique alterations of Sdc1 and HPSE in HG conditions, and found their interactions with p38 MAPK activation and IEB. These indicate that Sdc1/HPSE modulation can be viewed as an important complementary treatment for relieving HG-induced gastrointestinal damage.
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.