Exogenous surfactant changes the phenotype of alveolar macrophages in mice

2001 ◽  
Vol 280 (4) ◽  
pp. L689-L694 ◽  
Author(s):  
Boris W. Kramer ◽  
Alan H. Jobe ◽  
Machiko Ikegami
Keyword(s):  
Alveolar Macrophage ◽  
Alveolar Macrophages ◽  
Scavenger Receptor ◽  
Exogenous Surfactant ◽  
Surface Markers ◽  
Macrophage Phenotype ◽  
Surfactant Treatment ◽  
Class A ◽  
Scavenger Receptor Class

Alveolar macrophages are essential for the maintenance of surfactant homeostasis. We asked whether surfactant treatment would change alveolar macrophage number and whether the alveolar macrophage phenotype would become activated or apoptotic when challenged in vivo with exogenous surfactant. Surfactant pool size in mice was increased by repetitive surfactant treatments containing 120 mg/kg (110 μmol/kg) saturated phosphatidylcholine. The number of alveolar macrophages recovered by alveolar lavage decreased after the first dose by 49% and slightly increased after the second and third doses. Up to 28.5% of the macrophages became large and foamy, and their appearance normalized within 12 h. Surfactant treatment did not increase the percent of apoptotic or necrotic cells. The alveolar macrophages were not activated as indicated by no change in expression of CD14, CD16, CD54, CD95, and scavenger receptor class A types I and II after surfactant treatment. Surfactant treatment in healthy mice transiently changed the phenotype of alveolar macrophages to large and foamy without indications of changes in the surface markers characteristic of activation.

scholarly journals Tumor suppressive effect of scavenger receptor class A member 5 overexpression in colorectal cancer by regulating PI3K/AKT/mTOR pathway

2021 ◽  
Author(s):  
Yi Li ◽  
Feng Peng ◽  
Xiangyun Tan ◽  
Jin Wang ◽  
Yeqing Xu
Keyword(s):  
Colorectal Cancer ◽  
Tumor Volume ◽  
Scavenger Receptor ◽  
Mtor Pathway ◽  
Ki67 Expression ◽  
Class A ◽  
Scavenger Receptor Class ◽  
Sw480 Cells ◽  
And Migration

Abstract Background Colorectal cancer (CRC) exhibits high risks of morbidity and mortality. Objective To investigate the effect of scavenger receptor class A member 5 (SCRAR5) on CRC and its mechanism on modulation of cancer development. Methods The SCRAR5 expression in four kinds of CRC cell lines (SW620, SW480, HT29, and HCT116) was measured by quantitative PCR and western blotting, respectively. The effects of SCRAR5 abnormal expression on cell proliferation, apoptosis, and migration were analyzed by CCK-8 assay, EdU assay, colony-forming assay, flow cytometry assay, Transwell assay and wound healing assay, respectively. Meanwhile, the involvements of PI3K/AKT/mTOR pathway with the role of SCRAR5 were investigated by western blotting. Afterwards, the in vivo effects of SCRAR5 abnormal expression on CRC xenograft mice were finally investigated by evaluating tumor volume, apoptosis and Ki67 expression. Results SCRAR5 was lowly expressed in CRC cell lines, especially SW480 cells. Up-regulation of SCRAR5 significantly promoted cell apoptosis, reduced cell proliferation and migration in SW480 cells. Notably, SCRAR5 overexpression obviously inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Reversely, SCRAR5 silence exhibited promoting effects on HT29 cells. Consistently, in vivo experiments also revealed that SCRAR5 overexpression remarkably suppressed tumor volume and Ki67 expression, as well as promoted cell apoptosis. Conclusions Overall, up-regulating of SCRAR5 obviously inhibited CRC tumor growth in vitro and in vivo, which might be related to PI3K/AKT/mTOR pathway.

scholarly journals Uptake and catabolism of modified LDL in scavenger-receptor class A type I/II knock-out mice

1998 ◽  
Vol 331 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Theo J. C. VAN BERKEL ◽  
Agnes VAN VELZEN ◽  
Johan K. KRUIJT ◽  
Hiroshi SUZUKI ◽  
Tatsushiko KODAMA
Keyword(s):  
Kupffer Cells ◽  
Scavenger Receptor ◽  
Peritoneal Macrophages ◽  
Scavenger Receptors ◽  
Liver Uptake ◽  
Knock Out ◽  
Class A ◽  
Scavenger Receptor Class ◽  
Knock Out Mice

The liver is the major organ responsible for the uptake of modified low-density lipoprotein (LDL) from the blood circulation, with endothelial and Kupffer cells as major cellular uptake sites. Scavenger-receptors, which include various classes, are held responsible for this uptake. Mice deficient in scavenger-receptor class A types I and II were created and the fate of acetylated LDL (Ac-LDL) in vivo and its interaction with liver endothelial, Kupffer and peritoneal macrophages was characterized. Surprisingly, the decay in vivo (t½ < 2 min), tissue distribution and liver uptake (at 5 min it was 77.4±4.6% of the injected dose) of Ac-LDL in the knock-out mice were not significantly different from control mice (t½ < 2 min and liver uptake 79.1±4.6% of the injected dose). A separation of mice liver cells into parenchymal, endothelial and Kupffer cells 10 min after injection of Ac-LDL indicated that in both control and knock-out mice the liver endothelial cells were responsible for more than 70% of the liver uptake. Both in control and knock-out mice, preinjection of polyinosinic acid (poly I, 200 µg) completely blocked the liver uptake, indicating that both in control and knock-out mice the scavenger-receptors are sensitive to poly I. Preinjection of suboptimal poly I concentrations (20 and 50 µg) provided evidence that the serum decay and liver uptake of Ac-LDL is more readily inhibited in the knock-out mice as compared with the control mice, indicating less efficient removal of Ac-LDL in vivo in the knock-out mice under these conditions. Studies in vitro with isolated liver endothelial and Kupffer cells from knock-out mice indicate that the cell association of Ac-LDL during 2 h at 37 °C is 50 and 53% of the control, respectively, whereas the degradation reaches values of 58 and 63%. For peritoneal macrophages from knock-out mice the cell association of Ac-LDL was identical to the control mice whereas the Ac-LDL degradation in cells from the knock-out mice was 17% of the control. The low degradation capacity of peritoneal macrophages from knock-out mice for Ac-LDL indicates that scavenger-receptor class A types I and II play a quantitative important role in the degradation of Ac-LDL by macrophages. In liver, the contribution of scavenger-receptor class A types I and II to the maximal uptake and degradation of Ac-LDL by endothelial and Kupffer cells was 40–50%. Binding studies performed at 4 °C indicate that the lower rates of degradation are due to a lower number of surface receptors on the cells from the knock-out mice. From the in vitro and in vivo data it can be concluded that in addition to the classic scavenger-receptors class A types I and II liver does contain additional novel poly I-sensitive scavenger-receptors that facilitate efficient removal of Ac-LDL from the blood circulation. The availability of the scavenger-receptor class A types I and II knock-out mice will stimulate further molecular identification of these receptors.

scholarly journals Apoptotic Thymocyte Clearance in Scavenger Receptor Class A-Deficient Mice Is Apparently Normal

2000 ◽  
Vol 164 (9) ◽  
pp. 4861-4867 ◽  
Author(s):  
Nick Platt ◽  
Hiroshi Suzuki ◽  
Tatsuhiko Kodama ◽  
Siamon Gordon
Keyword(s):  
Scavenger Receptor ◽  
Class A ◽  
Scavenger Receptor Class ◽  
Deficient Mice

scholarly journals Scavenger receptor class-A plays diverse role in innate immunity, cell signaling and different pathologies

2016 ◽  
Vol 6 (7) ◽  
pp. 567-572
Author(s):  
Aamir Rana ◽  
Syed Sajjad Sattar ◽  
Afshann Shahzad ◽  
Ghulam Muhammad Ali ◽  
Yasir Waheed
Keyword(s):  
Innate Immunity ◽  
Cell Signaling ◽  
Scavenger Receptor ◽  
Class A ◽  
Scavenger Receptor Class

scholarly journals Scavenger receptor class a, member 3 is associated with severity of hand, foot, and mouth disease in a case-control study

Medicine ◽  
2019 ◽  
Vol 98 (40) ◽  
pp. e17471
Author(s):  
Ye Tian ◽  
Kai Zhou ◽  
Jing Hu ◽  
Ming-Feng Shan ◽  
Hong-Jian Chen ◽  
...  
Keyword(s):  
Case Control Study ◽  
Scavenger Receptor ◽  
Foot And Mouth Disease ◽  
Case Control ◽  
Mouth Disease ◽  
Class A ◽  
Scavenger Receptor Class ◽  
Foot And Mouth ◽  
Control Study

The structure and function of the scavenger receptor class A

2000 ◽  
pp. 108-114
Author(s):  
Takeshi Murakami ◽  
Yoshihiko Yamada ◽  
Takefumi Doi ◽  
Takao Hamakubo ◽  
Tatsuhiko Kodama
Keyword(s):  
Scavenger Receptor ◽  
Structure And Function ◽  
Class A ◽  
Scavenger Receptor Class ◽  
And Function

scholarly journals Tissue factor and factor VII messenger RNAs in human alveolar macrophages: effects of breathing ozone

Blood ◽  
1990 ◽  
Vol 75 (1) ◽  
pp. 122-127 ◽  
Author(s):  
MP McGee ◽  
R Devlin ◽  
G Saluta ◽  
H Koren
Keyword(s):  
Alveolar Macrophage ◽  
Tissue Factor ◽  
Alveolar Macrophages ◽  
Factor Vii ◽  
Fibrinopeptide A ◽  
Factor Activity ◽  
Tissue Factor Activity ◽  
Mrna Concentration ◽  
Human Alveolar Macrophages

Abstract This study was performed to determine if genes for tissue factor and factor VII proteins are expressed and regulated in vivo in lung macrophages during inflammation. Human alveolar macrophages and alveolar fluids were obtained 18 hours after healthy male adults were exposed, for 2 hours during intermittent exercise, to either air or air with 0.4 ppm ozone, added as a model toxic respiratory agent. Messenger RNA (mRNA) for both tissue factor and factor VII were demonstrated in macrophages isolated after subjects were exposed to unpolluted control air. With the same subjects examined after breathing ozone, the following changes were observed: tissue factor mRNA concentration in macrophages increased 2.6 +/- 0.47-fold. Factor VII mRNA concentration was reduced 0.64 +/- 0.24-fold. Total numbers of macrophages recovered did not change significantly. Ratios of nuclear:cytoplasmic areas of cytocentrifuged macrophages were augmented by 24.8% +/- 3%, giving morphometric evidence that immature cell forms increased in the population. In the lavage, tissue factor activity was increased 2.1 +/- 0.3-fold, while amounts of lipid phosphorous, which estimate total membrane lipids, and estimated volumes of alveolar fluid were not significantly changed. Factor VII activity and fibrinopeptide A levels in lavage were increased approximately twofold. These results using rapidly isolated, noncultured cells indicate that tissue factor and factor VII mRNA are synthesized in the alveolar macrophage population in vivo. In addition, evidence was found that as a result of breathing ozone, a shift in alveolar macrophage maturity occurred in association with tissue factor mRNA, tissue factor activity, and factor VII activity increases, and with formation of fibrinopeptide A in alveolar fluids.

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