Macrophage Phenotype Is Associated With the Regenerative Response in Experimental Replacement of the Porcine Esophagus

2015 ◽  
Vol 40 (10) ◽  
pp. 950-958 ◽  
Author(s):  
Linus Jönsson ◽  
Michaela Dellenmark Blom ◽  
Lars Friberg ◽  
Vladimir Gatzinsky ◽  
Olof Holmquist ◽  
...  
Keyword(s):  
Macrophage Phenotype ◽  
Regenerative Response ◽  
Experimental Replacement

Reprogrammed M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 extends lifespan of mice with experimental carcinoma

2017 ◽  
pp. 4-9
Author(s):  
С.В. Калиш ◽  
С.В. Лямина ◽  
А.А. Раецкая ◽  
И.Ю. Малышев
Keyword(s):  
Tumor Growth ◽  
Culture Medium ◽  
Ehrlich Carcinoma ◽  
Macrophage Phenotype ◽  
M1 Macrophages ◽  
M1 Macrophage ◽  
Ec Cells ◽  
Experimental Carcinoma

Цель исследования. Репрограммирование М1 фенотипа макрофагов с ингибированными факторами транскрипции М2 фенотипа STAT3, STAТ6 и SMAD и оценка их влияния на развитие карциномы Эрлиха (КЭ) in vitro и in vivo. Методика. Рост опухоли иницировали in vitro путем добавления клеток КЭ в среду культивирования RPMI-1640 и in vivo путем внутрибрюшинной инъекции клеток КЭ мышам. Результаты. Установлено, что M1макрофаги и in vitro, и in vivo оказывают выраженный противоопухолевый эффект, который превосходит антиопухолевые эффекты М1, M1, M1 макрофагов и цисплатина. Заключение. М1 макрофаги с ингибированными STAT3, STAT6 и/или SMAD3 эффективно ограничивают рост опухоли. Полученные данные обосновывают разработку новой технологии противоопухолевой клеточной терапии. Objective. Reprogramming of M1 macrophage phenotype with inhibited M2 phenotype transcription factors, such as STAT3, STAT6 and SMAD and assess their impact on the development of Ehrlich carcinoma (EC) in vitro and in vivo . Methods. Tumor growth in vitro was initiated by addition of EC cells in RPMI-1640 culture medium and in vivo by intraperitoneal of EC cell injection into mice. Results. It was found that M1 macrophages have a pronounced anti-tumor effect in vitro , and in vivo , which was greater than anti-tumor effects of M1, M1, M1 macrophages and cisplatin. Conclusion. M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 effectively restrict tumor growth. The findings justify the development of new anti-tumor cell therapy technology.

scholarly journals Macrophage Phenotype in Mice Deficient in Both Macrophage-Colony–Stimulating Factor (Op) and Apolipoprotein E

1998 ◽  
Vol 18 (4) ◽  
pp. 631-640 ◽  
Author(s):  
Willem J. S. de Villiers ◽  
Jonathan D. Smith ◽  
Masaaki Miyata ◽  
Hayes M. Dansky ◽  
Elizabeth Darley ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Macrophage Phenotype ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

scholarly journals Interactome Analysis of iPSC Secretome and Its Effect on Macrophages In Vitro

2021 ◽  
Vol 22 (2) ◽  
pp. 958
Author(s):  
Luca Tamò ◽  
Kleanthis Fytianos ◽  
Fabienne Caldana ◽  
Cedric Simillion ◽  
Anis Feki ◽  
...  
Keyword(s):  
Tissue Repair ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Critical Role ◽  
Organ Injury ◽  
Macrophage Phenotype ◽  
Gene Interaction Network ◽  
Tissue Repair And Regeneration ◽  
Secretory Pattern

Induced pluripotent stem cell secretome (iPSC-CM) mitigate organ injury and help in repair. Macrophages play a critical role in tissue repair and regeneration and can be directed to promote tissue repair by iPSC-CM, although the exact mechanisms are not known. In the current investigative study, we evaluated the possible mechanism by which iPSC-CM regulates the phenotype and secretory pattern of macrophages in vitro. Macrophages were obtained from human peripheral blood mononuclear cells and differentiated to various subpopulations and treated with either iPSC-CM or control media in vitro. Macrophage phenotype was assessed by flow cytometry, gene expression changes by qRT PCR and secretory pattern by multiplex protein analysis. The protein and gene interaction network revealed the involvement of Amyloid precursor protein (APP) and ELAV-like protein 1 (ELAVL-1) both present in the iPSC-CM to play an important role in regulating the macrophage phenotype and their secretory pattern. This exploratory study reveals, in part, the possible mechanism and identifies two potential targets by which iPSC-CM regulate macrophages and help in repair and regeneration.

scholarly journals Survivin drives tumor-associated macrophage reprogramming: a novel mechanism with potential impact for obesity

2021 ◽  
Author(s):  
E. Benaiges ◽  
V. Ceperuelo-Mallafré ◽  
A. Madeira ◽  
R. Bosch ◽  
C. Núñez-Roa ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Expression Patterns ◽  
Intracellular Localization ◽  
Immunohistochemical Analysis ◽  
Subcellular Fractionation ◽  
Migration And Invasion ◽  
Macrophage Phenotype ◽  
Tumor Associated Macrophages ◽  
Obesity And Cancer ◽  
The Impact

Abstract Purpose Recent studies point to adipose-derived stem cells (ASCs) as a link between obesity and cancer. We aimed to determine whether survivin, which is highly secreted by ASCs from subjects with obesity, might drive a pro-tumoral phenotype in macrophages. Methods The effect of ASC conditioned medium on the macrophage phenotype was assessed by expression studies. Survivin intracellular localization and internalization were examined by subcellular fractionation and immunofluorescence, respectively. Loss- and gain-of-function studies were performed using adenoviral vectors, and gene expression patterns, migration and invasion capacities of cancer cells were examined. Heterotypic cultures of ASCs, macrophages and cancer cells were established to mimic the tumor microenvironment. Survivin-blocking experiments were used to determine the impact of survivin on both macrophages and cancer cells. Immunohistochemical analysis of survivin was performed in macrophages from ascitic fluids of cancer patients and healthy controls. Results We found that obese-derived ASCs induced a phenotypic switch in macrophages characterized by the expression of both pro- and anti-inflammatory markers. Macrophages were found to internalize extracellular survivin, generating hybrid macrophages with a tumor-associated phenotype that included secretion of survivin. Exogenous expression of survivin in macrophages generated a similar phenotype and enhanced the malignant characteristics of cancer cells by a mechanism dependent on survivin phosphorylation at threonine 34. Survivin secreted by both ASCs from subjects with obesity and tumor-associated macrophages synergistically boosted the malignancy of cancer cells. Importantly, survivin was mainly detected in ascites-associated macrophages from patients with a malignant diagnosis. Conclusion Our data indicate that survivin may serve as a molecular link between obesity and cancer and as a novel marker for tumor-associated macrophages.

scholarly journals Lipodystrophy and obesity are associated with decreased number of T cells with regulatory function and pro-inflammatory macrophage phenotype

2017 ◽  
Vol 41 (11) ◽  
pp. 1676-1684 ◽  
Author(s):  
S Berger ◽  
G Ceccarini ◽  
G Scabia ◽  
I Barone ◽  
C Pelosini ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory Function ◽  
Macrophage Phenotype ◽  
Inflammatory Macrophage

scholarly journals Glia maturation factor-γ regulates murine macrophage iron metabolism and M2 polarization through mitochondrial ROS

2019 ◽  
Vol 3 (8) ◽  
pp. 1211-1225 ◽  
Author(s):  
Wulin Aerbajinai ◽  
Manik C. Ghosh ◽  
Jie Liu ◽  
Chutima Kumkhaek ◽  
Jianqing Zhu ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Mitochondrial Function ◽  
Regulatory Protein ◽  
M2 Macrophage ◽  
Macrophage Phenotype ◽  
Glia Maturation Factor ◽  
Altered Expression ◽  
Murine Macrophages ◽  
Cellular Iron ◽  
Maturation Factor

Abstract In macrophages, cellular iron metabolism status is tightly integrated with macrophage phenotype and associated with mitochondrial function. However, how molecular events regulate mitochondrial activity to integrate regulation of iron metabolism and macrophage phenotype remains unclear. Here, we explored the important role of the actin-regulatory protein glia maturation factor-γ (GMFG) in the regulation of cellular iron metabolism and macrophage phenotype. We found that GMFG was downregulated in murine macrophages by exposure to iron and hydrogen peroxide. GMFG knockdown altered the expression of iron metabolism proteins and increased iron levels in murine macrophages and concomitantly promoted their polarization toward an anti-inflammatory M2 phenotype. GMFG-knockdown macrophages exhibited moderately increased levels of mitochondrial reactive oxygen species (mtROS), which were accompanied by decreased expression of some mitochondrial respiration chain components, including the iron-sulfur cluster assembly scaffold protein ISCU as well as the antioxidant enzymes SOD1 and SOD2. Importantly, treatment of GMFG-knockdown macrophages with the antioxidant N-acetylcysteine reversed the altered expression of iron metabolism proteins and significantly inhibited the enhanced gene expression of M2 macrophage markers, suggesting that mtROS is mechanistically linked to cellular iron metabolism and macrophage phenotype. Finally, GMFG interacted with the mitochondrial membrane ATPase ATAD3A, suggesting that GMFG knockdown–induced mtROS production might be attributed to alteration of mitochondrial function in macrophages. Our findings suggest that GMFG is an important regulator in cellular iron metabolism and macrophage phenotype and could be a novel therapeutic target for modulating macrophage function in immune and metabolic disorders.

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