Isolation and characterization of peripheral blood-derived endothelial progenitor cells from broiler chickens

Bi, Shicheng; Tan, Xiaohong; Ali, Shah Qurban; Wei, Liang-Jun

doi:10.1016/j.tvjl.2014.08.017

Cited by 10 publications

(4 citation statements)

References 10 publications

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“…In addition, pchAEC actively incorporated acetylated low density lipoproteins (AcLDL), as a typical functional feature of EC (McGuire & Orkin, 1987). Thus, pchAEC exhibit the same phenotypic characteristics of cells that were previously described to be precursors of chicken EC isolated from whole blood (Bi et al, 2014) and bone-marrow (Bai et al, 2012;Davis et al, 2018). However, the pchAEC preparation protocol provides the advantage of allowing the production of a large quantity of primary chicken EC in an easy tissue/cell culture procedure, thus permitting their widespread use in studies addressing avian host-pathogen interactions and/or the role of chicken EC in immune homeostasis and pathogenesis.…”

Section: Discussionmentioning

confidence: 70%

Chicken endothelial cells are highly responsive to viral innate immune stimuli and are susceptible to infections with various avian pathogens

et al. 2019

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It is well established that the endothelium plays a prominent role in the pathogenesis of various infectious diseases in mammals. However, little is known about the role of endothelial cells (EC) as targets for avian pathogens and their contribution to the pathogenesis of infectious diseases in galliform birds. First, we explored the innate immune response of primary chicken aortic endothelial cells (pchAEC), obtained from 18-day-old embryos, to stimulation with pathogen-associated molecular patterns or recombinant chicken interferons (type I, II and III IFNs). In spite of the abundant expression of a number of innate immune receptors, marked cytokine responses to stimulation with pathogenassociated molecular patterns were only seen in pchAEC treated with the TLR3 agonist polyI:C (pI:C) and the MDA5 agonist liposome-complexed polyI:C (L-pI:C), as was assessed by quantitative PCR and luciferase-based IFN-I/NFκB reporter assays. Treatments of pchAEC with IFN-α, IFN-γ and IFN-λ resulted in STAT1-phosphorylation/activation, as was revealed by immunoblotting. Next, we demonstrated that pchAEC are susceptible to infection with a variety of poultry pathogens, including Marek's disease virus (MDV), infectious bursal disease virus (IBDV), avian pathogenic Escherichia coli (APEC) and Eimeria tenella. Our data highlight that chicken EC are potential targets for viral, bacterial and protozoan pathogens in gallinaceous poultry and may partake in the inflammatory and antimicrobial response. The pchAEC infection model used herein will allow further studies interrogating avian pathogen interactions with vascular EC. RESEARCH HIGHLIGHTS. Use of a well-defined primary chicken aortic endothelial cell (pchAEC) culture model for studying avian host-pathogen interactions.. pchAEC are responsive to innate immune stimulation with viral pathogen-associated molecular patterns and chicken type I, II and III interferons.. pchAEC are susceptible to infections with economically important poultry pathogens, including MDV, IBDV, APEC and Eimeria tenella.

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Section: Discussionmentioning

confidence: 70%

Chicken endothelial cells are highly responsive to viral innate immune stimuli and are susceptible to infections with various avian pathogens

et al. 2019

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“…The cDNA was subjected to PCR amplification as previously described. 29 The oligonucleotide primers are presented in Table S1 . PCR products were separated by electrophoresis with 1.2% agarose gel and visualized with GoldView (Yeasen Biotechnology, Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

MSC Transplantation Attenuates Inflammation, Prevents Endothelial Damage and Enhances the Angiogenic Potency of Endogenous MSCs in a Model of Pulmonary Arterial Hypertension

Shao¹,

Li²,

Tan³

et al. 2022

JIR

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“…Ex vivo expansion of eEPCs were performed exactly as described in our previous work [ 44 ]. Briefly, mononuclear cell fraction of the peripheral blood (PBMC) from 4-week-old healthy birds was cultured in Endothelial cell growth medium (EGM)-2 (Lonza, Walkersvil, MD, USA) containing 2% fetal bovine serum (FBS), 100 U/ml penicillin, and 100 μg/ml streptomycin at 39 °C in 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Potential contribution of early endothelial progenitor cell (eEPC)-to-macrophage switching in the development of pulmonary plexogenic lesion

Shao

Guo

et al. 2022

Respir Res

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Background Plexiform lesions, which have a dynamic appearance in structure and cellular composition, are the histological hallmark of severe pulmonary arterial hypertension in humans. The pathogenesis of the lesion development remains largely unknown, although it may be related to local inflammation and dysfunction in early progenitor endothelial cells (eEPCs). We tested the hypothesis that eEPCs contribute to the development of plexiform lesions by differentiating into macrophages in the setting of chronic inflammation. Methods The eEPC markers CD133 and VEGFR-2, macrophage lineage marker mannose receptor C-type 1 (MRC1), TNFα and nuclear factor erythroid 2-related factor 2 (Nrf2) in plexiform lesions in a broiler model were determined by immunohistochemistry. eEPCs derived from peripheral blood mononuclear cells were exposed to TNFα, and macrophage differentiation and angiogenic capacity of the cells were evaluated by phagocytotic and Matrigel plug assays, respectively. The role of Nrf2 in eEPC-to-macrophage transition as well as in MRC1 expression was also evaluated. Intratracheal installation of TNFα was conducted to determine the effect of local inflammation on the formation of plexiform lesions. Results Cells composed of the early lesions have a typical eEPC phenotype whereas those in more mature lesions display molecular and morphological characteristics of macrophages. Increased TNFα production in plexiform lesions was observed with lesion progression. In vitro studies showed that chronic TNFα challenge directed eEPCs to macrophage differentiation accompanied by hyperactivation of Nrf2, a stress-responsive transcription factor. Nrf2 activation (Keap1 knockdown) caused a marked downregulation in CD133 but upregulation in MRC1 mRNA. Dual luciferase reporter assay demonstrated that Nrf2 binds to the promoter of MRC1 to trigger its expression. In good agreement with the in vitro observation, TNFα exposure induced macrophage differentiation of eEPCs in Matrigel plugs, resulting in reduced neovascularization of the plugs. Intratracheal installation of TNFα resulted in a significant increase in plexiform lesion density. Conclusions This work provides evidence suggesting that macrophage differentiation of eEPCs resulting from chronic inflammatory stimulation contributes to the development of plexiform lesions. Given the key role of Nrf2 in the phenotypic switching of eEPCs to macrophages, targeting this molecular might be beneficial for intervention of plexiform lesions.

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Isolation and characterization of peripheral blood-derived endothelial progenitor cells from broiler chickens

Cited by 10 publications

References 10 publications

Chicken endothelial cells are highly responsive to viral innate immune stimuli and are susceptible to infections with various avian pathogens

Chicken endothelial cells are highly responsive to viral innate immune stimuli and are susceptible to infections with various avian pathogens

MSC Transplantation Attenuates Inflammation, Prevents Endothelial Damage and Enhances the Angiogenic Potency of Endogenous MSCs in a Model of Pulmonary Arterial Hypertension

Potential contribution of early endothelial progenitor cell (eEPC)-to-macrophage switching in the development of pulmonary plexogenic lesion

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