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The New Frontiers in Bone Tissue Engineering
Published in Ugo Ripamonti, The Geometric Induction of Bone Formation, 2020
Our systematic studies in calvarial defects of Papio ursinus using the three mammalian hTGF-β isoforms (Ripamonti et al. 1997; Ripamonti et al. 2000; Ripamonti et al. 2008; Ripamonti et al. 2016) have suggested novel regulatory pathways through Id2 and Id3 expression (Ripamonti et al. 2016). The molecular data have also shown that when TGF-β3 expression decreases, Id2 and Id3 expression are upregulated (Ripamonti et al. 2016). This has suggested that TGF-β signalling to regulate Id2 and Id3 gene expression promotes or inhibits the induction of calvarial bone formation. Interplays of Id genes, TGF-βs, Notch and BMPs control endothelial cell migration and differentiation (Itoh et al. 2004). Upregulation of Id gene expression promotes endothelial cell migration, with molecular interplay between Notch and BMP receptor signalling pathways. This regulates endothelial cell migration via upregulation of Id1 (Itoh et al. 2004). Segregated calvarial defects showed the induction of bone formation with capillary sprouting and invasion, directly correlating to Id2 and Id3 upregulation (Ripamonti et al. 2016). The application of exogenous hTGF-β3 to defects segregated from the dura mater creates a microenvironment that is permissive for bone formation (Ripamonti et al. 2016).
Chronic Otitis Media
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
George G. Browning, Justin Weir, Gerard Kelly, Iain R.C. Swan
Recently, Yamamoto-Fukuda et al. 62 performed an elegant study using a hybrid gerbil model to demonstrate that the epithelial cells in cholesteatoma are derived from the tympanic membrane and not from the epithelial cells within the middle ear or epithelium from the external auditory canal. Indeed, the molecular pathology of cholesteatoma has been investigated by a number of authors. Using DNA chip analysis, 282 genes were found to be differentially expressed in comparison to the control samples63 and Klenke et al. 64 identified 3558 new cholesteatoma-related transcripts. Of those, 811 were upregulated and 334 downregulated more than twofold. The genes involved are found in a number of different biological processes including signal transduction, cell growth, cell communication, metabolism, transport and the immune response. Hamajima et al. 65 determined the role of inhibitor of DNA-binding (Id1) in the proliferation of cholesteatoma keratinocytes. They found that Id1, a protein that leads to cell immortalization, induces up regulation of NF-ºB/cyclin D1/keratin 10 in the keratinocytes. The authors concluded that Id1 contributed to the thickening of the middle ear mucosa, cell cycle progression and removal of cell cycle inhibition.
Bladder Cancer
Published in Dongyou Liu, Tumors and Cancers, 2017
In non-muscle-invasive bladder cancers (NMIBCs), class 1 tumors (which have a lower risk of progression and a better prognosis than classes 2 and 3 tumors) show upregulation of early-cell-cycle genes (CCND1, ID1, and RBL2), class 2 tumors display upregulation of late-cell-cycle genes (CDC20, CDC25A, CDKs, and PLK1) and overexpression of cancer stem cell markers (ALDH1A1, ALDH1A2, PROM1, NES, and THY1), and class 2 and/or class 3 tumors show increased expression of the keratin (KRT) gene family. Additionally, NMIBCs show a high frequency (~80%) of activating mutations in the fibroblast growth factor receptor 3 (FGFR3) signaling pathway. The FGFR3 and RAS gene mutations are mutually exclusive in bladder cancer [3–5].
Identification of immune-associated prognostic biomarkers in lung adenocarcinoma on the basis of gene co-expression network
Published in Immunopharmacology and Immunotoxicology, 2023
Jianhai Zhang, Ange Chen, Zhang Xue, Chengzhi Liang
High expression of risk factors such as CUB Domain Containing Protein 1 (CDCP1), Inhibitor Of DNA Binding 1 (ID1), and Phospholipid Scramblase 1 (PLSCRI) in the prognostic model led to poor prognosis of LUAD patients. Lately, CDCP1 has been proved to be linked with poor prognoses of patients with breast cancer, colorectal cancer and lung cancer. It is at high level in human colon cancer and lung cancer tissues, and plays a crucial role in cell adhesion or extracellular matrix interaction [28–30]. ID1 is closely associated with tumorigenesis, cell proliferation and survival. It has been proved to be overexpressed in lung cancer, glioblastoma and breast cancer and plays an important role in vital processes [31]. One study found that ID1 may also be an important immunosuppressive target in lung cancer. Iosune Baraibar et al. [32] found that when ID1 expression is inhibited by lung cancer tumor cells, the proportion of CD + T cells in the tumor increases. Enhancing the tumor infiltration degree of CD8 + T cells shows better anti-tumor effect. Abnormally increased expression of PLSCR1 acitivates the Signal Transducer And Activator Of Transcription 1 (STAT1) signaling pathway in breast cancer, ultimately resulting in tumor volume enlargement, tumor deterioration and metastasis [33]. These risk factor genes also play a carcinogenic role in other cancers, which is similar to our results, indicating that the abnormal expression of these genes may promote development of LUAD and might be a potential marker in LUAD progression.
Prolactin activates IRF1 and leads to altered balance of histone acetylation: Implications for systemic lupus erythematosus
Published in Modern Rheumatology, 2020
Yiu Tak Leung, Kelly Maurer, Li Song, Jake Convissar, Kathleen E. Sullivan
We performed chromatin immunoprecipitation (ChIP) assays to directly quantitate IRF1 recruitment to chromatin with PRL treatment as a proof of principle for PRL effects. ChIP assays were performed with in THP-1 cells stimulated with PRL for 24 h. Known PRL-responsive genes (JUN, NR3C1, TGFB, ID1 and PIM1) were selected for study. Known IRF1 binding sites were extracted from UCSC Genome Browser and primers were generated to capture IRF1, p300, and H4ac at the recognized sites of IRF1 binding in K562 cells. Figure 7 depicts the ChIP assay results from PRL-stimulated cells. Increased IRF1 binding and increased H4ac at the ID1 promoter was seen in the cells stimulated by PRL for 24 h. None of the other PRL target genes exhibited increased ChIP signal (not shown). This is consistent with ID1 being the sole PRL target where we observed mRNA induction with PRL in this cell type.
Altered Immunity in Endometriosis: What Came First?
Published in Immunological Investigations, 2018
Milena Králíčková, Ludek Fiala, Petr Losan, Pavel Tomes, Vaclav Vetvicka
Transforming growth factor-beta 1 (TGF-β1), an essential growth factor, is responsible for regulating cell proliferation, differentiation, angiogenesis, and immune responses. TGF-β is abundantly and differentially expressed in the endometrium, most likely under hormonal control. The increasing evidences indicate that TGF-β1 expression is high in endometriotic lesions. Many mechanisms must contribute to the development of endometriosis and TGF-β1 was hypothesized to play a key role in endometriotic lesion formation (Omwandho et al., 2010) (Hull et al., 2012). Levels of all three TGF-βs are increased around menstruation, with particular high levels of TGF-β3 in postmenstrual period; it is hypothesized that they might participate in postmenstrual regeneration of endometrium (Omwandho et al., 2010). In addition, TGF-β1 increased the concentration of ID1 mRNA and the VEGF-A-ID1 axis was confirmed by the use of siRNA (Young et al., 2015). The study suggested that ID inhibitors might be beneficial in endometriosis treatment (Fong et al., 2004).