| http://purl.uniprot.org/citations/22906243 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22906243 | http://www.w3.org/2000/01/rdf-schema#comment | "Substance P (SP), also considered a proinflammatory cytokine, as well as others such as transforming growth factor-β1 (TGF-β1) and interleukin-1 (IL-1), and the extracellular matrix protein fibronectin (FN) have been associated with the pathophysiology of myelofibrosis. SP is encoded by the TAC1 gene. The relationships among SP, TGF-β1, IL-1 and FN are poorly understood. This study determined the mechanisms for concomitant production of IL-1, TGF-β1 and SP and also determined the synergistic role of FN in SP release. Enzyme-linked immunosorbent assay (ELISA) indicated increased levels of SP and TGF-β1 in the blood of patients with myelofibrosis. Monocytes, shown to be activated in patients with bone marrow (BM) fibrosis, expressed the TAC1 gene for SP release, in a nuclear factor-κB (NFκB)-dependent manner. Reporter gene assay with the 5' regulatory region of TAC1 indicated its expression by high levels of FN and TGF-β1. Immunohistochemical studies of paraffin-embedded BM biopsies from patients with myelofibrosis, and age-matched controls without fibrosis, indicated co-localization of SP and its receptor neurokinin-1 (NK1). In summary, myelofibrotic monocytes have autocrine loops that stimulate the release of SP and TGF-β1, and that are potentiated by fibronectin. The FN-mediated induction of SP in turn stimulates monocytes through autostimulation by NK1 receptors. These findings, combined with those of previous studies, demonstrate an adhesion-mediated NFκB/IL-1/TGF-β1 axis that can be initiated by increased FN in patients with myelofibrosis for the production of SP. These findings show how TGF-β1 and SP production are coupled, and suggest new therapeutic targets to reverse immune-mediated fibrosis."xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://purl.org/dc/terms/identifier | "doi:10.3109/10428194.2012.722218"xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://purl.uniprot.org/core/author | "Chang V.T."xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://purl.uniprot.org/core/author | "Rameshwar P."xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://purl.uniprot.org/core/author | "Yook C."xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/22906243 | http://purl.uniprot.org/core/name | "Leuk Lymphoma"xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://purl.uniprot.org/core/pages | "631-638"xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://purl.uniprot.org/core/title | "Synergism between fibronectin and transforming growth factor-beta1 in the production of substance P in monocytes of patients with myelofibrosis."xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://purl.uniprot.org/core/volume | "54"xsd:string |
| http://purl.uniprot.org/citations/22906243 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22906243 |
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