ArticleImmunology and cell biology2012
ADAM28 is elevated in humans with the metabolic syndrome and is a novel sheddase of human tumour necrosis factor-α.
Article in Immunology and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Expression ofInternational journal of molecular sciences · 2026Article
- Research progress on ADAM28 in malignant tumors.Discover oncology · 2025Review
- SGLT1/2 inhibition improves glycemic control and multi-organ protection in type 1 diabetes.iScience · 2023Article
- Inflammation and aging: signaling pathways and intervention therapies.Signal transduction and targeted therapy · 2023Review
- ADAM10 and ADAM17 as Biomarkers Linked to Inflammation, Metabolic Disorders and Colorectal Cancer.Current issues in molecular biology · 2022Article
- Role for the metalloproteinase ADAM28 in the control of airway inflammation, remodelling and responsiveness in asthma.Frontiers in immunology · 2022Article
- Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes.Bioscience reports · 2021Review
- Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- The Influence of Hypertensive Therapies on Circulating Factors: Clinical Implications for SCFAs, FGF21, TNFSF14 and TNF-α.Journal of clinical medicine · 2020Article
- Oncogenic ADAM28 induces gemcitabine resistance and predicts a poor prognosis in pancreatic cancer.World journal of gastroenterology · 2019Article
- ADAM28 dramatically regulates the biological features of human gingival fibroblasts.Odontology · 2019Article
- Human CD8Aging cell · 2018Article
- The role of some ADAM-proteins and activation of the insulin growth factor-related pathway in colorectal cancer.Central-European journal of immunology · 2018Review
- ADAMTS and ADAM metalloproteinases in osteoarthritis - looking beyond the 'usual suspects'.Osteoarthritis and cartilage · 2017Review
- The Metalloproteinase ADAM28 Promotes Metabolic Dysfunction in Mice.International journal of molecular sciences · 2017Article
- ADAM19: A Novel Target for Metabolic Syndrome in Humans and Mice.Mediators of inflammation · 2017Article
- MicroRNA-552 enhances metastatic capacity of colorectal cancer cells by targeting a disintegrin and metalloprotease 28.Oncotarget · 2016Article
- Article
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Metalloproteinases are implicated in cleaving numerous proinflammatory mediators from the cell surface. Interestingly, the elevated levels of tumour necrosis factor-α (TNF-α) have been associated with the metabolic syndrome. We aimed to ascertain whether the human metalloproteinase ADAM28 correlates with parameters of the metabolic syndrome and whether ADAM28 is a novel sheddase of human TNF-α. To identify novel metalloproteinases associated with the metabolic syndrome, we conducted microarray studies on peripheral blood mononuclear cells from a well characterised human cohort. Human ADAM28 and TNF-α were overexpressed and ADAM28 expression or activity was reduced with small-interfering RNA (siRNA) or pharmacological inhibition. TNF-α levels were measured in cell supernatant by enzyme-linked immunosorbent assay. We also conducted ADAM28 inhibition studies in human THP-1 macrophages. Human ADAM28 expression levels were positively correlated with parameters of the metabolic syndrome. When human ADAM28 and TNF-α were overexpressed in HEK293 cells, both proteins co-localised, co-immunoprecipitated and promoted TNF-α shedding. The shedding was significantly reduced when ADAM28 activity was inhibited or ADAM28 expression was downregulated. In human THP-1 macrophages, endogenous ADAM28 and TNF-α were co-expressed and TNF-α shedding was significantly reduced when ADAM28 was inhibited by pharmacological inhibition or siRNA knockdown. Our data suggest a novel mechanistic role for the metalloproteinase ADAM28 in inflammation, obesity and type 2 diabetes.
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