-abdominal adiposity and dysfunction of the adipose tissue, resulting in the infiltration of immune cells and development of chronic low-grade inflammation ( Monteiro & Azevedo 2010 ). Macrophage migration inhibitory factor (MIF) is a pleiotropic ubiquitously
Ljupka Gligorovska, Biljana Bursać, Sanja Kovačević, Nataša Veličković, Gordana Matić, and Ana Djordjevic
Timothy J Cole and Morag J Young
No DOC/salt cardiac fibrosis, no macrophage recruitment Rickard et al . (2014) VE-Cad-Cre Obesity-induced dysfunction blunted inflammation Schafer et al . (2013) , Jia et al . (2015) Cardiomyocyte MLC2a-Cre Improved cardiac
Ana Patrícia Mateus, Rita A Costa, João C R Cardoso, Karl B Andree, Alicia Estévez, Enric Gisbert, and Deborah M Power
modifications in the number, size and pigment content of aggregates of macrophages, the melanomacrophage centers (MMCs) of the piscine innate immune system ( Fournie et al. 2001 , Agius & Roberts 2003 , De Vico et al. 2008 ), and this is the predominant
M Sakai, M Kobayashi, and H Kawauchi
The activation of rainbow trout (Oncorhynchus mykiss) phagocytic cells by chum salmon GH, prolactin (PRL) and somatolactin (SL) was investigated in vitro. Rainbow trout kidney leucocytes were cultured in RPMI 1640 medium containing 1, 10, 50 or 100 ng of each hormone/ml and the production of superoxide anion was measured using reduction of nitroblue tetrazolium (NBT) and ferricytochrome C. Macrophages incubated with 10–100 ng GH or PRL/ml showed significantly enhanced production of superoxide anion in both the NBT and ferricytochrome C tests compared with control macrophages (without hormone). SL did not induce enhanced production of superoxide anion in macrophages. The phagocytic cells treated with GH or PRL also showed increased phagocytic activity and phagocytic index. However, the cells treated with SL showed no enhancement of phagocytic activity or index. These results indicate that GH and PRL stimulate macrophages in vitro.
Journal of Endocrinology (1996) 151, 113–118
Wang Xiao, Fei Beibei, Shen Guangsi, Jiang Yu, Zhang Wen, Huang Xi, and Xu Youjia
work, we established a male mouse model to observe the influence of iron on oxidative stress and bone resorption in vivo ( Jia et al . 2012 ). In addition, we treated a murine macrophage cell line, RAW264.7 with ferric ions to test their activity
R. Molenaar, F. F. G. Rommerts, and H. J. van der Molen
The presence of non-specific esterase activity is correlated with different Leydig cell characteristics: 3β-hydroxysteroid dehydrogenase (3β-HSD), human chorionic gonadotrophin binding and LH-stimulated steroid production. This indicates that esterase can be used as a marker enzyme for Leydig cells. Esterase, however, has also been used as a marker enzyme for macrophages. We have compared, using biochemical and histochemical techniques, the esterase activity of Leydig cell preparations from mature and immature rats and of preparations enriched in testicular or peritoneal macrophages. Leydig cells were identified by staining for 3β-HSD, and macrophages by phagocytosis of fluorescent beads. Leydig cell preparations from mature rats showed an approximately 400-fold higher esterase activity than peritoneal macrophage preparations and an approximately 50-fold higher activity than testicular macrophage preparations. Leydig cell preparations from mature rats showed a 60-fold higher esterase activity than Leydig cell preparations from immature rats.
Differences in esterase activity were also demonstrated histochemically. Leydig cells from mature rats showed positive esterase staining after 30 s at room temperature. Testicular macrophages showed esterase activity after staining for 3 min. Only approximately 25% of the 3β-HSD-positive cells from immature rats showed esterase activity after staining for 6 min. Esterase is therefore a useful marker enzyme for Leydig cells from mature rats and can be of help in studies concerning the development of these cells.
J. Endocr. (1986) 108, 329–334
Azusa Sameshima, Tsutomu Wada, Tetsuo Ito, Ayaka Kashimura, Kanae Sawakawa, Rika Yonezawa, Hiroshi Tsuneki, Yoko Ishii, Masakiyo Sasahara, Shigeru Saito, and Toshiyasu Sasaoka
shown to attenuate obesity-induced chronic inflammation in adipose tissue by repressing the inflammatory responses of macrophages ( Ribas et al . 2011 ). Previous studies reported that estrogen acted on the CNS, especially on the hypothalamus
Guillermo García-Eguren, Oriol Giró, María del Mar Romero, Mar Grasa, and Felicia A Hanzu
macrophages in white adipose tissue Sections of 5 µm from the paraffin-embedded epididymal adipose tissue were deparaffinized and rehydrated in water. A pre-treatment using proteinase K was performed, and slides were blocked in 5% donkey serum for 1 h at
Karen Francis, B Mary Lewis, Peter N Monk, and Jack Ham
stimulated the activation of signalling molecules ERK/MAPK and AKT. On the other hand, C5a and C5adR both inhibited the secretion of the inflammatory molecule, macrophage migration inhibitory factor (MIF) yet stimulated the secretion of ACTH. These data
Ronald J van der Sluis, Tim van den Aardweg, Anne Q Reuwer, Marcel T Twickler, Florence Boutillon, Miranda Van Eck, Vincent Goffin, and Menno Hoekstra
aortic root, starting at the appearance of the tricuspid valves. Collagen content of the lesions was determined after Masson's Trichrome staining (Sigma Diagnostics). Sections were stained immunohistochemically for the presence of macrophages using a MOMA