ArticlePloS one2014
The laminin response in inflammatory bowel disease: protection or malignancy?
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
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- Noncanonical functions of adhesion proteins in inflammation.American journal of physiology. Cell physiology · 2024Review
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- Circulating Profile of ECM-Related Proteins as Diagnostic Markers in Inflammatory Bowel Diseases.Journal of clinical medicine · 2022Article
- Tenascin-C is a driver of inflammation in the DSS model of colitis.Matrix biology plus · 2022Article
- FOXO3 Expression in Macrophages Is Lowered by a High-Fat Diet and Regulates Colonic Inflammation and Tumorigenesis.Metabolites · 2022Article
- Cell-Matrix Interactions Contribute to Barrier Function in Human Colon Organoids.Frontiers in medicine · 2022Article
- Involvement of integrin-activating peptides derived from tenascin-C in colon cancer progression.World journal of gastrointestinal oncology · 2021Review
- Developing an advanced gut on chip model enabling the study of epithelial cell/fibroblast interactions.Lab on a chip · 2021Article
- Novel Human Tenascin-C Function-Blocking Camel Single Domain Nanobodies.Frontiers in immunology · 2021Article
- Role of Extracellular Matrix in Gastrointestinal Cancer-Associated Angiogenesis.International journal of molecular sciences · 2020Review
- Tools for probing host-bacteria interactions in the gut microenvironment: From molecular to cellular levels.Bioorganic & medicinal chemistry letters · 2020Review
- The lymph node stromal laminin α5 shapes alloimmunity.The Journal of clinical investigation · 2020Article
- Ulcerative Colitis-Derived Colonoid Culture: A Multi-Mineral-Approach to Improve Barrier Protein Expression.Frontiers in cell and developmental biology · 2020Article
- Role of lymph node stroma and microenvironment in T cell tolerance.Immunological reviews · 2019Review
- Differential Regulation of T-cell Immunity and Tolerance by Stromal Laminin Expressed in the Lymph Node.Transplantation · 2019Article
- Peptide TNIIIA2 Derived from Tenascin-C Contributes to Malignant Progression in Colitis-Associated Colorectal Cancer via β1-Integrin Activation in Fibroblasts.International journal of molecular sciences · 2019Article
- Expression of Laminin in Oral Squamous Cell CarcinomasAsian Pacific journal of cancer prevention : APJCP · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Laminins (LM), basement membrane molecules and mediators of epithelial-stromal communication, are crucial in tissue homeostasis. Inflammatory Bowel Diseases (IBD) are multifactorial pathologies where the microenvironment and in particular LM play an important yet poorly understood role in tissue maintenance, and in cancer progression which represents an inherent risk of IBD. Here we showed first that in human IBD colonic samples and in murine colitis the LMα1 and LMα5 chains are specifically and ectopically overexpressed with a concomitant nuclear p53 accumulation. Linked to this observation, we provided a mechanism showing that p53 induces LMα1 expression at the promoter level by ChIP analysis and this was confirmed by knockdown in cell transfection experiments. To mimic the human disease, we induced colitis and colitis-associated cancer by chemical treatment (DSS) combined or not with a carcinogen (AOM) in transgenic mice overexpressing LMα1 or LMα5 specifically in the intestine. We demonstrated that high LMα1 or LMα5 expression decreased susceptibility towards experimentally DSS-induced colon inflammation as assessed by histological scoring and decrease of pro-inflammatory cytokines. Yet in a pro-oncogenic context, we showed that LM would favor tumorigenesis as revealed by enhanced tumor lesion formation in both LM transgenic mice. Altogether, our results showed that nuclear p53 and associated overexpression of LMα1 and LMα5 protect tissue from inflammation. But in a mutation setting, the same LM molecules favor progression of IBD into colitis-associated cancer. Our transgenic mice represent attractive new models to acquire knowledge about the paradoxical effect of LM that mediate either tissue reparation or cancer according to the microenvironment. In the early phases of IBD, reinforcing basement membrane stability/organization could be a promising therapeutic approach.
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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.