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Molecular Imaging of Breast Cancer
Published in Martin G. Pomper, Juri G. Gelovani, Benjamin Tsui, Kathleen Gabrielson, Richard Wahl, S. Sam Gambhir, Jeff Bulte, Raymond Gibson, William C. Eckelman, Molecular Imaging in Oncology, 2008
Jean H. Lee, Lavanya Sundararajan, William B. Eubank, David A. Mankoff
Imaging approaches that directly target specific components expressed in neovessels [e.g., integrins, vascular endothelial growth factor receptor (VEGF)] have been developed to image angiogenesis directly and to evaluate the efficacy of anti-angiogenic drugs (28). Molecules targeted for imaging are those that play a key role in angiogenesis and metastasis; therefore, in vivo identification of these targets will help facilitate new therapeutic and diagnostic strategies. Recently, Beer and colleagues have successfully demonstrated ability to visualize integrin alpha(v)beta3 expression in human by 18F galacto-RDG PET (34). Cai and colleagues demonstrated the ability to visualize VEGF expression in vivo by VEGFPET (35). This type of imaging may provide specific predictive value for therapy directed at tumor angiogenesis, such as bevacizumab (Avastin) (36).
Association of ITGAV polymorphisms and risk of rheumatoid arthritis: evidence from a meta-analysis
Published in Expert Review of Clinical Immunology, 2020
Jun-Ming Huang, Zhi-Ying Pang, Guo-Bin Qi, Zhe Wang, Zheng-Tao Lv
Integrins are a large group of transmembrane proteins that mediate adherence between cells and extracellular matrix (ECM), and the upregulation of integrins and their ligands has been reported in RA [10]. Among a wide variety of Integrins, Integrin αvβ3, also called as the vitronectin receptor, is commonly detected in macrophages, synovial fibroblasts, endothelial cells, and osteoclasts. Integrin αvβ3 plays a major role in osteoclast-mediated bone resorption, angiogenesis, and macrophage dependent inflammation, which are widely recognized as the key features of RA pathogenesis [11,12]. Integrin alpha V (ITGAV), also known as CD51, is a protein-coding gene located in the 2q31 region [13]. ITGAV encodes the chain αv, which is a subunit of integrin αvβ3. Several genetic association studies have been conducted to assess the possible association between ITGAV polymorphisms and risk of RA, however, achieved inconsistent results [14–19]. Due to the relatively small sample size, each individual association study might be inadequate to determine the genetic effects of ITGAV polymorphism on RA risk. To the best of our knowledge, no meta-analysis has been carried out to evaluate the correlation between ITGAV polymorphisms and RA risk. Therefore, the present systematic review and meta-analysis was conducted to assess the correlation between ITGAV SNPs and risk of RA.
Molecular mechanisms that change synapse number
Published in Journal of Neurogenetics, 2018
Alicia Mansilla, Sheila Jordán-Álvarez, Elena Santana, Patricia Jarabo, Sergio Casas-Tintó, Alberto Ferrús
Early in the last decade, it became evident that glial cells play essential roles in neuron biology. Work in C. elegans showed that glial ablated animals exhibit profound sensory deficits, abnormal neuron morphology and behaviour. One of the glia enriched genes first identified, fig-1, encodes a labile protein with a conserved thrombospondin 1 (TSP1) domain (Bacaj, Tevlin, Lu, & Shaham, 2008). Transcriptomic databases of astrocytes at the times of synapse formation and elimination show that this type of glial cells are particularly enriched in metabolic, lipidogenic and phagocytic pathways such as those mediated by draper/Megf10 and Mertk/integrin alpha(v)beta5. Further, the transcriptional profile of astrocytes reveals it as very different from that of oligodendrocytes consistent with the mounting evidences on glial cell heterogeneity (Cahoy et al., 2008). The repertoire of glial types and their putative homologies across species have been reviewed recently (Losada-Pérez, 2018).
Endothelial dysfunction sustains immune response in atherosclerosis: potential cause for ineffectiveness of prevailing drugs
Published in International Reviews of Immunology, 2022
In vitro treatment with fluvastatin did not affect already elevated release of CD31+ and CD54+ EMPs after TNF-α stimulation, and it further improved the release of CD106+ EMPs. Fluvastatin treatment could only reduce CD51+ (Integrin alpha V) and CD105+ EMPs [60]. Concordantly, simvastatin augmented CD144+ (VE-cadherin) and CD62+ EMP levels in the plasma of diabetes mellitus (DM) and DM-CKD patients and Annexin V+ EMPs in vitro [61,62]. Also, atorvastatin increased CD144+/CD144+CD142+ (tissue factor) EMPs in patients with peripheral occlusive arterial disease and type-1 DM with dyslipidemia and was associated with impaired endothelium-dependent microvascular reactivity [63,64]. Ezetimibe, another lipid-lowering drug, also elevated CD51+ EMPs in coronary heart disease patients [65]. When administered along with simvastatin, ezetimibe also increased CD144+ and CD62+ EMPs in DM and DM-CKD patients [61]. In patients with uncontrolled blood pressure, circulating CD31+ EMPs were elevated compared to healthy controls. On removing the causative agent, i.e. hypertension, one would expect a dip in circulating EMPs. However, in the same study in well-controlled hypertensive patients, circulating EMPs were similar and comparable to patients with uncontrolled blood pressure levels indicating that even after elevated blood pressure was well managed, a sustained ED was evident [66]. Bulut et al. found that short treatment (2 months) with acetylsalicylate diminished circulating CD31+ EMPs in male CAD patients with non-significant stenosis. Nonetheless, the FMD responses and the maximal dilator effects after administration of nitroglycerin were comparable between patients and controls [67] suggesting that even though circulating EMPs were decreased the functionality of ECs was not improved.