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Your search keyword '"Alfazema, Neza"' showing total 14 results
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14 results on '"Alfazema, Neza"'

4. Glioblastomas acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion

Author

Gangoso, Ester, Southgate, Benjamin, Bradley, Leanne, Rus, Stefanie, Galvez-Cancino, Felipe, McGivern, Niamh, Güç, Esra, Kapourani, Chantriolnt-Andreas, Byron, Adam, Ferguson, Kirsty M., Alfazema, Neza, Morrison, Gillian, Grant, Vivien, Blin, Carla, Sou, IengFong, Marques-Torrejon, Maria Angeles, Conde, Lucia, Parrinello, Simona, Herrero, Javier, Beck, Stephan, Brandner, Sebastian, Brennan, Paul M., Bertone, Paul, Pollard, Jeffrey W., Quezada, Sergio A., Sproul, Duncan, Frame, Margaret C., Serrels, Alan, and Pollard, Steven M.

Published
2021
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11. Complement Factor B Is a Determinant of Both Metabolic and Cardiovascular Features of Metabolic Syndrome

Author

Coan, Philip M, Barrier, Marjorie, Alfazema, Neza, Carter, Roderick N, Marion de Procé, Sophie, Dopico, Xaquin C, Garcia Diaz, Ana, Thomson, Adrian, Jackson-Jones, Lucy H, Moyon, Ben, Webster, Zoe, Ross, David, Moss, Julie, Arends, Mark J, Morton, Nicholas M, Aitman, Timothy J, Coan, Philip M, Barrier, Marjorie, Alfazema, Neza, Carter, Roderick N, Marion de Procé, Sophie, Dopico, Xaquin C, Garcia Diaz, Ana, Thomson, Adrian, Jackson-Jones, Lucy H, Moyon, Ben, Webster, Zoe, Ross, David, Moss, Julie, Arends, Mark J, Morton, Nicholas M, and Aitman, Timothy J

Abstract

CFB (complement factor B) is elevated in adipose tissue and serum from patients with type 2 diabetes mellitus and cardiovascular disease, but the causal relationship to disease pathogenesis is unclear. Cfb is also elevated in adipose tissue and serum of the spontaneously hypertensive rat, a well-characterized model of metabolic syndrome. To establish the role of CFB in metabolic syndrome, we knocked out the Cfb gene in the spontaneously hypertensive rat. Cfb -/- rats showed improved glucose tolerance and insulin sensitivity, redistribution of visceral to subcutaneous fat, increased adipocyte mitochondrial respiration, and marked changes in gene expression. Cfb -/- rats also had lower blood pressure, increased ejection fraction and fractional shortening, and reduced left ventricular mass. These changes in metabolism and gene expression, in adipose tissue and left ventricle, suggest new adipose tissue-intrinsic and blood pressure-independent mechanisms for insulin resistance and cardiac hypertrophy in the spontaneously hypertensive rat. In silico analysis of the human CFB locus revealed 2 cis-regulated expression quantitative trait loci for CFB expression significantly associated with visceral fat, circulating triglycerides and hypertension in genome-wide association studies. Together, these data demonstrate a key role for CFB in the development of spontaneously hypertensive rat metabolic syndrome phenotypes and of related traits in humans and indicate the potential for CFB as a novel target for treatment of cardiometabolic disease.

Published
2017

14. New Wistar Kyoto and spontaneously hypertensive rat transgenic models with ubiquitous expression of green fluorescent protein

Author

Garcia Diaz, Ana Isabel, Moyon, Ben, Coan, Philip M., Alfazema, Neza, Venda, Lara, Woollard, Kevin, and Aitman, Tim

Abstract

The Wistar Kyoto (WKY) rat and the spontaneously hypertensive (SHR) rat inbred strains are well-established models for human crescentic glomerulonephritis (CRGN) and metabolic syndrome, respectively. Novel transgenic (Tg) strains add research opportunities and increase scientific value to well-established rat models. We have created two novel Tg strains using Sleeping Beauty transposon germline transgenesis, ubiquitously expressing green fluorescent protein (GFP) under the rat elongation factor 1 alpha (EF1a) promoter on the WKY and SHR genetic backgrounds. The Sleeping Beauty system functioned with high transgenesis efficiency; 75% of new rats born after embryo microinjections were transgene positive. By ligation-mediated PCR, we located the genome integration sites, confirming no exonic disruption and defining a single or low copy number of the transgenes in the new WKY-GFP and SHR-GFP Tg lines. We report GFP-bright expression in embryos, tissues and organs in both lines and show preliminary in vitro and in vivo imaging data that demonstrate the utility of the new GFP-expressing lines for adoptive transfer, transplantation and fate mapping studies of CRGN, metabolic syndrome and other traits for which these strains have been extensively studied over the past four decades.

Published
2016
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