Recruitment of CD34+ progenitor cells into peripheral blood and asthma severity

Makowska, Joanna; Grzegorczyk, Janina; Cieślak, M; Bieńkiewicz, Barbara; Kowalski, Marek L.

doi:10.1016/s1081-1206(10)60317-1

Cited by 14 publications

(17 citation statements)

References 24 publications

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“…Similar to the mature eosinophil, the lineage-committed eosinophil progenitor (EoP) is mobilized during allergic disease [5]. EoP frequency is increased in the peripheral blood of adult patients with asthma in response to allergen challenge [6, 7]. Also, EoP levels are increased in the lung tissue and sputum of allergen-challenged patients with asthma, suggesting a direct contribution to tissue eosinophilia via in situ differentiation after migration from the peripheral blood [6, 8].…”

Section: To the Editormentioning

confidence: 99%

“…EoP frequency is increased in the peripheral blood of adult patients with asthma in response to allergen challenge [6, 7]. Also, EoP levels are increased in the lung tissue and sputum of allergen-challenged patients with asthma, suggesting a direct contribution to tissue eosinophilia via in situ differentiation after migration from the peripheral blood [6, 8]. Notably, peripheral blood EoP levels correlate with the severity of asthma in adults, advancing the concept of the EoP as a clinically useful biomarker [6].…”

Section: To the Editormentioning

confidence: 99%

See 1 more Smart Citation

Eosinophil progenitor levels are increased in patients with active pediatric eosinophilic esophagitis

Morris

Stucke

Martin

et al. 2016

Journal of Allergy and Clinical Immunology

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Section: To the Editormentioning

confidence: 99%

Section: To the Editormentioning

confidence: 99%

Eosinophil progenitor levels are increased in patients with active pediatric eosinophilic esophagitis

Morris

Stucke

Martin

et al. 2016

Journal of Allergy and Clinical Immunology

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“…Previous studies have already found a response of BMMS cells in the lung to injury perpetrated by inflammation observed in asthma (6), and circulating CD34 + progenitor cells migrating to lung tissue were indeed involved in the airway remodeling (5,38). Recently, Wu et al (39) showed that CD34 + smooth muscle progenitor cells were increased in peripheral blood of asthmatic patients and involved in airway remodeling.…”

Section: Discussionmentioning

confidence: 95%

“…Significant research evidence supported that ASM cells do not only migrate in the muscle bundle to induce ASM mass thickening, but also migrate through the potentially antiproliferative extracellular matrix to appear in subepithelial tissues. Furthermore, in addition to the local ASM cells migration, recent studies led us to consider the possibility of circulating CD34 + progenitor cells from bone marrow (also known as progenitor for smooth muscle cells) to be another source of excess ASM mass (3), because these cells were observed to be involved in the pathogenesis of smooth muscle layer thickening in vascular remodeling disease such as atherosclerosis and neointimal lesions (4) and a response of circulating progenitor cells migrating to injured lung exists in asthma cases (5,6). Although these structural changes are known to cause substantial airflow limitation in asthma, they cannot be reversed by currently available asthma therapies.…”

mentioning

confidence: 99%

HB-EGF–Promoted Airway Smooth Muscle Cells and Their Progenitor Migration Contribute to Airway Smooth Muscle Remodeling in Asthmatic Mouse

Wang

Yao

et al. 2016

The Journal of Immunology

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The airway smooth muscle (ASM) cells’ proliferation, migration, and their progenitor’s migration are currently regarded as causative factors for ASM remodeling in asthma. Heparin-binding epidermal growth factor (HB-EGF), a potent mitogen and chemotactic factor, could promote ASM cell proliferation through MAPK pathways. In this study, we obtained primary ASM cells and their progenitors from C57BL/6 mice and went on to explore the role of HB-EGF in these cells migration and the underlying mechanisms. We found that recombinant HB-EGF (rHB-EGF) intratracheal instillation accelerated ASM layer thickening in an OVA-induced asthmatic mouse. Modified Boyden chamber assay revealed that rHB-EGF facilitate ASM cell migration in a dose-dependent manner and ASM cells from asthmatic mice had a greater migration ability than that from normal counterparts. rHB-EGF could stimulate the phosphorylation of ERK1/2 and p38 in ASM cells but further migration assay showed that only epidermal growth factor receptor inhibitor (AG1478) or p38 inhibitor (SB203580), but not ERK1/2 inhibitor (PD98059), could inhibit rHB-EGF–mediated ASM cells migration. Actin cytoskeleton experiments exhibited that rHB-EGF could cause actin stress fibers disassembly and focal adhesions formation of ASM cells through the activation of p38. Finally, airway instillation of rHB-EGF promoted the recruitment of bone marrow–derived smooth muscle progenitor cells, which were transferred via caudal vein, migrating into the airway from the circulation. These observations demonstrated that ASM remodeling in asthma might have resulted from HB-EGF–mediated ASM cells and their progenitor cells migration, via p38 MAPK-dependent actin cytoskeleton remodeling.

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“…L-selectin (SELL) is classically reported as a surface protein on leukocytes that aids in their extravasation from blood into nearby tissues by binding ligands (e.g., CD34) found on the surface of endothelial cells. In some cases, SELL is also found on the surface of endothelial cells while CD34 is present on leukocytes (Makowska et al, 2008). Although this method of leukocyte tethering is not the most common via SELL, it is possible that the increased expression of SELL on the endothelial cell surface increases binding to antigens on the leukocytes cell surface, including CD34.…”

Section: Discussionmentioning

confidence: 99%

Molecular responses of choroidal endothelial cells to elastin derived peptides through the elastin-binding protein (GLB1)

et al. 2012

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Purpose Neovascular AMD involves the activation of choroidal endothelial cells to increase their inflammatory and angiogenic behaviors. Elastin derived peptides (EDPs) can elicit some of these phenotypic changes in endothelial cells. This investigation was performed to follow up on those findings by determining a receptor for these peptides in the human eye as well as evaluating the effects of elevated EDPs on choroidal cells in vitro and in vivo. Methods The expression of elastin receptor genes including GLB1 was analyzed using reverse transcription PCR. Migration of choroidal endothelial cells was quantified in the presence of inhibitors to different EDP binding proteins. C57BL6 mice were injected with EDPs and studied by electroretinography, transmission electron microscopy, and microarray analysis. Results An alternatively spliced form of beta-galactosidase (GLB1) is present on human choroidal endothelial cells and acts as a receptor for EDPs. Elevated levels of circulating EDPs do not affect retinal function in the mouse, but do increase the expression and deposition of collagen IV in the RPE/choroid complex. Conclusions EDPs may play a role in neovascular AMD by binding to and inducing neovascular phenotypes in choroidal endothelial cells through their receptor, GLB1. These peptides also cause an increased mRNA expression and deposition of collagen IV in the RPE/choroid, which may alter diffusion properties between the retina and choriocapillaris.

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Recruitment of CD34+ progenitor cells into peripheral blood and asthma severity

Cited by 14 publications

References 24 publications

Eosinophil progenitor levels are increased in patients with active pediatric eosinophilic esophagitis

Eosinophil progenitor levels are increased in patients with active pediatric eosinophilic esophagitis

HB-EGF–Promoted Airway Smooth Muscle Cells and Their Progenitor Migration Contribute to Airway Smooth Muscle Remodeling in Asthmatic Mouse

Molecular responses of choroidal endothelial cells to elastin derived peptides through the elastin-binding protein (GLB1)

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