Potential mechanism for recruitment and migration of CD133 positive cells to areas of vascular inflammation

Rastogi, Prerna; White, Maureen C.; Rickard, Alice; McHowat, Jane

doi:10.1016/j.thromres.2008.03.020

Cited by 17 publications

(17 citation statements)

References 30 publications

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“…CD68 is expressed on monocytes, and consequently tissue macrophages, and is therefore a reliable marker of atherosclerotic disease. Treatments for atherosclerosis define its benefits by, among other things, reducing the number of CD68 + cells derived from monocytes in the atherosclerotic plaque (Rastogi et al 2008). Our studies demonstrated marking to CD68 in the AT 21 days group on endothelial cells as well as a characteristic monocyte migration to a possible internal region of the arterial wall.…”

Section: Discussionmentioning

confidence: 53%

“…In addition, CD133 is a marker of tumor cells that initiate a number of human neoplastic tumors, and therefore it may be possible to develop a marker in future therapies for cancer cells (Mizrak et al 2008). Following transmigration of these hematopoietic stem cells, a subset of progenitor cells can mature in the subendothelial space, and mast cells play a role in propagating the inflammation in atherosclerosis (Rastogi et al 2008). Our studies demonstrate marking CD133 on endothelial region of the aorta in AT 14 days group.…”

Section: Discussionmentioning

confidence: 99%

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Structural and ultrastructural evaluation of the aortic wall after transplantation of bone marrow-derived cells (BMCs) in a model for atherosclerosis

Felix

Monteiro

Rocha

et al. 2015

Biochem. Cell Biol.

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Stem cells are characterized by their ability to differentiate into multiple cell lineages and display the paracrine effect. The aim of this work was to evaluate the effect of therapy with bone marrow-derived cells (BMCs) on glucose, lipid metabolism, and aortic wall remodeling in mice through the administration of a high-fat diet and subsequent BMCs transplantation. C57BL/6 mice were fed a control diet (CO group) or an atherogenic diet (AT group). After 16 weeks, the AT group was divided into 4 subgroups: an AT 14 days group and AT 21 days group that were given an injection of vehicle and sacrificed after 14 and 21 days, respectively, and an AT-BMC 14 days group and AT-BMC 21 days group that were given an injection of BMCs and sacrificed after 14 and 21 days, respectively. The BMCs transplant had reduced blood glucose, triglycerides, and total cholesterol. There was no significant difference in relation to body mass between the transplanted groups and non-transplanted groups, and all were different than CO. There was no significant difference in the glycemic curve among AT 14 days, AT-BMC 14 days, and AT 21 days, and these were different than the CO and the AT-BMC 21 days groups. The increased thickness of the aortic wall was observed in all atherogenic groups, but was significantly smaller in group AT-BMC 21 days compared to AT 14 days and AT 21 days. Vacuoles in the media tunic, delamination and the thinning of the elastic lamellae were observed in AT 14 days and AT 21 days. The smallest number of these was displayed on the AT-BMC 14 days and AT-BMC 21 days. Marking to CD105, CD133, and CD68 were observed in AT 14 days and AT 21 days. These markings were not observed in AT-BMC 14 days or in AT-BMC 21 days. Electron micrographs show the beneficial remodeling in AT-BMC 14 days and AT-BMC 21 days, and the structural organization was similar to the CO group. Vesicles of pinocytosis, projection of smooth muscle cells, and delamination of the internal elastic lamina are seen in groups AT 14 days and AT 21 days. Endothelial cells were preserved, and regular and continuous contour in internal elastic lamelae were observed in the CO, the AT-BMC 14 days, and AT-BMC 21 days groups. In conclusion, in an atherosclerotic model using mice and atherogenic diet, the injection of BMCs improves glucose, lipid metabolism, and causes a beneficial remodeling of the aortic wall.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Structural and ultrastructural evaluation of the aortic wall after transplantation of bone marrow-derived cells (BMCs) in a model for atherosclerosis

Felix

Monteiro

Rocha

et al. 2015

Biochem. Cell Biol.

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“…We have demonstrated previously that CD133+ cells, a mast cell precursor population, utilizes the PAF–PAFR interaction in a manner similar to that involved in PMN transendothelial migration (Rastogi et al. ). Therefore, we propose that increased endothelial cell PAF production in smokers may result in increased recruitment and accumulation of mast cells in the bladder wall.…”

Section: Discussionmentioning

confidence: 96%

“…; Rastogi et al. ). Generation of endothelial cell PAF is initiated by calcium‐independent phospholipase A 2 β (iPLA 2 β ) activation, which hydrolyzes the sn ‐2 fatty acid from membrane phospholipids, yielding a free fatty acid and lysophospholipid.…”

Section: Introductionmentioning

confidence: 97%

Increased susceptibility to bladder inflammation in smokers: targeting the PAF-PAF receptor interaction to manage inflammatory cell recruitment

2015

Self Cite

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Chronic bladder inflammation can result in a significant reduction in quality of life. Smoking remains a leading preventable risk factor in many diseases. Despite the large amount of evidence supporting the risks of smoking, roughly 45 million people in the United States remain smokers. The impact of cigarette smoking on inflammation is well established, but how smoking promotes bladder inflammation is currently unknown. The aim of this study was to determine if cigarette smoke exposure impacts inflammatory cell adherence to bladder endothelial cells and if targeting the platelet‐activating factor (PAF)–PAF receptor (PAFR) interaction could be beneficial in managing bladder inflammation. In response to cigarette smoke extract (CSE) incubation, bladder endothelial cells from human or mouse displayed increased PAF accumulation, decreased PAF‐AH activity, and increased inflammatory cell adherence. Inhibition of endothelial cell calcium‐independent phospholipase A2 β (iPLA 2 β) with (S)‐BEL, to block PAF production, prevented adherence of inflammatory cells. Pretreatment of inflammatory cells with PAFR antagonists, ginkgolide B or WEB2086 significantly reduced the number of adhered cells to bladder endothelium. Wild‐type mice exposed to cigarette smoke displayed increased presence of inflammatory infiltration which was absent in iPLA 2 β −/− mice and those exposed to room air. In conclusion, cigarette smoke exposure increases endothelial cell PAF accumulation and increased inflammatory cell adherence. Inhibition of PAF accumulation or PAFR antagonism markedly attenuated inflammatory cell adherence to bladder endothelial cells. The results detailed in this study highlight to potential therapeutic targets for managing bladder inflammation.

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“…Second, when PAF-receptor knockout mice were exposed to UV radiation, no suppression of DTH or CHS was observed [137, 138]. Third, PAF is known to regulate the migration of many cell types, including tumor cells, neutrophils and leukocytes as well as mast cells [139–144], and mast cells are known to express the PAF receptor and are able to respond to PAF [145]. Chacón-Salinas and colleagues confirmed that mast cell-deficient mice were resistant to the suppressive effect of UV-irradiation, and suppression of the CHS reaction was restored by reconstituting mast cell-deficient mice with normal bone marrow-derived mast cells.…”

Section: Paf and Uv-induced Immune Suppressionmentioning

confidence: 99%

Understanding the connection between platelet-activating factor, a UV-induced lipid mediator of inflammation, immune suppression and skin cancer

Damiani

Ullrich

2016

Progress in Lipid Research

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Lipid mediators of inflammation play important roles in several diseases including skin cancer, the most prevalent type of cancer found in the industrialized world. Ultraviolet (UV) radiation is a complete carcinogen and is the primary cause of skin cancer. UV radiation is also a potent immunosuppressive agent, and UV-induced immunosuppression is a well-known risk factor for skin cancer induction. An essential mediator in this process is the glyercophosphocholine 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine commonly referred to as platelet-activating factor (PAF). PAF is produced by keratinocytes in response to diverse stimuli and exerts its biological effects by binding to a single specific G-protein-coupled receptor (PAF-R) expressed on a variety of cells. This review will attempt to describe how this lipid mediator is involved in transmitting the immunosuppressive signal from the skin to the immune system, starting from its production by keratinocytes, to its role in activating mast cell migration in vivo, and to the mechanisms involved that ultimately lead to immune suppression. Recent findings related to its role in regulating DNA repair and activating epigenetic mechanisms, further pinpoint the importance of this bioactive lipid, which may serve as a critical molecular mediator that links the environment (UVB radiation) to the immune system and the epigenome.

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Potential mechanism for recruitment and migration of CD133 positive cells to areas of vascular inflammation

Cited by 17 publications

References 30 publications

Structural and ultrastructural evaluation of the aortic wall after transplantation of bone marrow-derived cells (BMCs) in a model for atherosclerosis

Structural and ultrastructural evaluation of the aortic wall after transplantation of bone marrow-derived cells (BMCs) in a model for atherosclerosis

Increased susceptibility to bladder inflammation in smokers: targeting the PAF-PAF receptor interaction to manage inflammatory cell recruitment

Understanding the connection between platelet-activating factor, a UV-induced lipid mediator of inflammation, immune suppression and skin cancer

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