Genetic programs expressed in resting and IL-4 alternatively activated mouse and human macrophages: similarities and differences

Blood ◽  
2013 ◽  
Vol 121 (9) ◽  
pp. e57-e69 ◽  
Author(s):  
Fernando O. Martinez ◽  
Laura Helming ◽  
Ronny Milde ◽  
Audrey Varin ◽  
Barbro N. Melgert ◽  
...  

Key Points Human and mouse macrophages share partially conserved gene and protein expression programs in the resting or M2 activated state. TGM2 is a novel M2 marker consistently induced in human and mouse M2 macrophages.

Life Sciences ◽  
2019 ◽  
Vol 224 ◽  
pp. 222-231 ◽  
Author(s):  
Richa Shrivastava ◽  
Nidhi Shukla

2017 ◽  
Vol 37 (10) ◽  
pp. 1913-1922 ◽  
Author(s):  
Philipp J. Hohensinner ◽  
Johanna Baumgartner ◽  
Julia B. Kral-Pointner ◽  
Pavel Uhrin ◽  
Benjamin Ebenbauer ◽  
...  

1996 ◽  
Vol 121 (1) ◽  
pp. 151-163 ◽  
Author(s):  
Thomas Grewal ◽  
Anna Bartlett ◽  
James W. Burgess ◽  
Nicolle H. Packer ◽  
Keith K. Stanley

Blood ◽  
2017 ◽  
Vol 130 (18) ◽  
pp. 1995-2005 ◽  
Author(s):  
Yue Zhao ◽  
Min Liu ◽  
Xue Ying Chan ◽  
Sue Yee Tan ◽  
Sharrada Subramaniam ◽  
...  

Key Points Human circulating leukocytes in humanized mice reproduce similar circadian oscillations as seen in humans. A novel molecular clock network exhibiting opposite effects on regulating human and mouse leukocyte circadian rhythm is discovered.


2011 ◽  
pp. OR31-6-OR31-6 ◽  
Author(s):  
Pamela Fischer-Posovszky ◽  
Qiong Wang ◽  
Ingrid W Asterholm ◽  
Joseph M Rutkowski ◽  
Martin Wabitsch ◽  
...  

2020 ◽  
Vol 11 (1) ◽  
pp. 31-51
Author(s):  
Dmitry A. Shcheglov

Abstract. This article aims to explain how Ptolemy could have constructed a map of the Pontus Euxinus (Black Sea), as described in his Geography, under the assumption that his sources were similar to those that have come down to us. The method employed is based on the comparison of Ptolemy's data with corresponding information from other ancient sources, revealing the most conspicuous similarities and differences between them. Three types of information are considered as possible “constituent elements” of Ptolemy's map: latitudes, coastline lengths, and straight-line distances. It is argued that the latitudes Ptolemy used for the key points determining the overall shape of the Pontus (Byzantium, Trapezus, the mouth of the Borysthenes and the Cimmerian Bosporus, the mouth of the Tanais, etc.) were most likely inherited from earlier geographers (Eratosthenes, Hipparchus, and Marinus). In exactly the same way, Ptolemy's data on the circumference of the Pontus and the length of the coastal stretches between the key points (from the Thracian Bosporus to Cape Karambis, Sinope, Trapezus, and the mouth of the Phasis, etc.) closely correlate with the corresponding estimates reported by other geographers (Eratosthenes, Artemidorus, Strabo, Pliny, Arrian, and Pseudo-Arrian), which implies that Ptolemy drew on similar coastline length information. The shortening of Ptolemy's west coast of the Pontus (from the Thracian Bosporus to the mouth of the Borysthenes) relative to the corresponding distances reported by other sources is explained by his underestimation of the circumference of the Earth. The lengthening of Ptolemy's north-east Pontus coast (from the Cimmerian Bosporus to the mouth of the Phasis) can, in part, be accounted for by his attempt to incorporate the straight-line distances across the open sea reported by Pliny. Overall, Ptolemy's configuration of the Black Sea can be satisfactorily explained as a result of fitting contradictory pieces of information together that were inherited from earlier geographical traditions.


2021 ◽  
Vol 5 (7) ◽  
pp. 2012-2016
Author(s):  
Reine El Omar ◽  
Emmanuelle Julien ◽  
Katia Biasch ◽  
Blandine Guffroy ◽  
Bruno Lioure ◽  
...  

Key Points Expression of caudal-related homeobox gene 2 (CDX2) and angiotensin-converting enzyme (ACE) correlates during hematopoietic emergence. This emergence occurs in human and mouse embryos and in human acute myeloid leukemia; CDX2 homeoprotein also binds to the ACE promoter.


2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Mihaela-Loredana Vlad ◽  
Simona-Adriana Manea ◽  
Alexandra-Gela Lazar ◽  
Monica Raicu ◽  
Horia Muresian ◽  
...  

Histone acetylation plays a major role in epigenetic regulation of gene expression. Monocyte-derived macrophages express functional NADPH oxidase 5 (Nox5) that contributes to oxidative stress in atherogenesis. The mechanisms of Nox5 regulation are not entirely elucidated. The aim of this study was to investigate the expression pattern of key histone acetyltransferase subtypes (p300, HAT1) in human atherosclerosis and to determine their role in mediating the upregulation of Nox5 in macrophages under inflammatory conditions. Human nonatherosclerotic and atherosclerotic tissue samples were collected in order to determine the expression of p300 and HAT1 isoforms, H3K27ac, and Nox5. In vitro determinations were done on human macrophages exposed to lipopolysaccharide in the absence or presence of histone acetyltransferase inhibitors. Western blot, immunohistochemistry, immunofluorescence, real-time PCR, transfection, and chromatin immunoprecipitation assay were employed. The protein levels of p300 and HAT1 isoforms, H3K27ac, and Nox5 were found significantly elevated in human atherosclerotic specimens. Immunohistochemistry/immunofluorescence staining revealed that p300, HAT1, H3K27ac, H3K9ac, and Nox5 proteins were colocalized in the area of CD45+/CD68+ immune cells and lipid-rich deposits within human atherosclerotic plaques. Lipopolysaccharide induced the levels of HAT1, H3K27ac, H3K9ac, and Nox5 and the recruitment of p300 and HAT1 at the sites of active transcription within Nox5 gene promoter in cultured human macrophages. Pharmacological inhibition of histone acetyltransferase significantly reduced the Nox5 gene and protein expression in lipopolysaccharide-challenged macrophages. The overexpression of p300 or HAT1 enhanced the Nox5 gene promoter activity. The histone acetyltransferase system is altered in human atherosclerosis. Under inflammatory conditions, HAT subtypes control Nox5 overexpression in cultured human macrophages. The data suggest the existence of a new epigenetic mechanism underlying oxidative stress in atherosclerosis.


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