2016

DOI: 10.17116/patol201678219-28

|View full text |Cite

|

Sign up to set email alerts

|

Immunohistochemical study of the role of mast cells and macrophages in the process of angiogenesis in the atherosclerotic plaques in patients with metabolic syndrome

Anamaria Munteanu

¹

,

²

,

³

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Introduction2

Pathological Process Of Atherosclerosis1

Mast Cells and Endoglin1

Citation Types

Supporting

0

Mentioning

4

Contrasting

0

Year Published

2017

2017

2024

2024

Publication Types

Select...

Article6

Relationship

Self Cite0

Independent6

Authors

Journals

Cited by 7 publications

(4 citation statements)

References 24 publications

Supporting

0

Mentioning

4

Contrasting

0

Order By: Relevance

“…Then, blood monocytes and various types of leukocytes adhere to the endothelium and take up oxidized LDL (OxLDL) leading to the formation of cholesterol-laden foam cells and atherosclerotic plaques. The subsequent activities including cellular signaling, cellular recruitment, enzyme production, and protein modification ignite a flurry of activity that serves to further progress atherosclerotic plaque development [8, 9].…”

Section: Pathological Process Of Atherosclerosismentioning

confidence: 99%

Inflammation: A Novel Therapeutic Target/Direction in Atherosclerosis

¹

,

²

,

³

et al. 2017

View full text Add to dashboard Cite

Over the past two decades, the viewpoint of atherosclerosis has been replaced gradually by a lipiddriven, chronic, low-grade inflammatory disease of the arterial wall. Current treatment of atherosclerosis is focused on limiting its risk factors, such as hyperlipidemia or hypertension. However, treatment targeting the inflammatory nature of atherosclerosis is still very limited and deserves further attention to fight atherosclerosis successfully. Here, we review the current development of inflammation and atherosclerosis to discuss novel insights and potential targets in atherosclerosis, and to address drug discovery based on anti-inflammatory strategy in atherosclerotic disease.

“…Then, blood monocytes and various types of leukocytes adhere to the endothelium and take up oxidized LDL (OxLDL) leading to the formation of cholesterol-laden foam cells and atherosclerotic plaques. The subsequent activities including cellular signaling, cellular recruitment, enzyme production, and protein modification ignite a flurry of activity that serves to further progress atherosclerotic plaque development [8, 9].…”

Section: Pathological Process Of Atherosclerosismentioning

confidence: 99%

Inflammation: A Novel Therapeutic Target/Direction in Atherosclerosis

¹

,

²

,

³

et al. 2017

View full text Add to dashboard Cite

Over the past two decades, the viewpoint of atherosclerosis has been replaced gradually by a lipiddriven, chronic, low-grade inflammatory disease of the arterial wall. Current treatment of atherosclerosis is focused on limiting its risk factors, such as hyperlipidemia or hypertension. However, treatment targeting the inflammatory nature of atherosclerosis is still very limited and deserves further attention to fight atherosclerosis successfully. Here, we review the current development of inflammation and atherosclerosis to discuss novel insights and potential targets in atherosclerosis, and to address drug discovery based on anti-inflammatory strategy in atherosclerotic disease.

“…Phosphorylation of Flt3 receptor activates the intracellular signaling pathways responsible for cell proliferation [ 18 ]. Mounting evidence indicates that inflammation, involving dendritic cells (DC) or macrophages (Mphi), accounts for important in neovascularization (NV) [ 19 – 21 ]. Whiteley et al demonstrated that mesenchymal stromal and circulating angiogenic cells repair the tissues by expanding CD34+ cells [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Flt3 Regulation in the Mononuclear Phagocyte System Promotes Ocular Neovascularization

¹

,

²

,

³

et al. 2018

Journal of Ophthalmology

View full text Add to dashboard Cite

Fms-like tyrosine kinase 3 (Flt3), a tyrosine kinase receptor expressed in CD34+ hematopoietic stem/progenitor cells, is important for both normal myeloid and lymphoid differentiation. It has been implicated in mice and humans for potential multilineage differentiation. We found that mice deficient in Flt3 or mice that received an Flt3 inhibitor (AC220) showed significantly reduced areas of ischemia-induced retinal neovascularization (RNV) and laser-induced choroidal NV (CNV) (P < 0.05). Increased Flt3 expression at the protein level was detected in retinas of oxygen-induced retinopathy (OIR) mice at P15 and P18 during retinal NV (RNV) progression. We subsequently found that macrophages (Mphi) polarization was regulated at the site of CNV in Flt3-deficient mice. Flow cytometry analysis demonstrated that Flt3 deficiency shifted Mphi polarization towards an M2 phenotype during RNV with significant reduction in M1 cytokine expression when compared to the wild-type controls (P < 0.05). Based on the above findings, we concluded that Flt3 inhibition alleviated ocular NV by promoting a Mphi polarization shift towards the M2 phenotype. Therapies targeting Flt3 may provide a new approach for the treatment of ocular NV.

“…In most of the studies dealing with MCs and Endoglin, the effect of MCs on microvessel density (angiogenesis) was analyzed. Therefore, tryptase (MCs) and endoglin (ECs) were correlated [155][156][157][158][159]. Because MCs are located mostly close to vessels and ECs it is assumed that the increase in MCs observed under different pathological conditions stimulate via release of pro-angiogenic mediators EC activation.…”

Section: Mast Cells and Endoglinmentioning

confidence: 99%

Endoglin: An ‘Accessory’ Receptor Regulating Blood Cell Development and Inflammation

¹

,

²

2020

View full text Add to dashboard Cite

Transforming growth factor-β1 (TGF-β1) is a pleiotropic factor sensed by most cells. It regulates a broad spectrum of cellular responses including hematopoiesis. In order to process TGF-β1-responses in time and space in an appropriate manner, there is a tight regulation of its signaling at diverse steps. The downstream signaling is mediated by type I and type II receptors and modulated by the ‘accessory’ receptor Endoglin also termed cluster of differentiation 105 (CD105). Endoglin was initially identified on pre-B leukemia cells but has received most attention due to its high expression on activated endothelial cells. In turn, Endoglin has been figured out as the causative factor for diseases associated with vascular dysfunction like hereditary hemorrhagic telangiectasia-1 (HHT-1), pre-eclampsia, and intrauterine growth restriction (IUPR). Because HHT patients often show signs of inflammation at vascular lesions, and loss of Endoglin in the myeloid lineage leads to spontaneous inflammation, it is speculated that Endoglin impacts inflammatory processes. In line, Endoglin is expressed on progenitor/precursor cells during hematopoiesis as well as on mature, differentiated cells of the innate and adaptive immune system. However, so far only pro-monocytes and macrophages have been in the focus of research, although Endoglin has been identified in many other immune system cell subsets. These findings imply a functional role of Endoglin in the maturation and function of immune cells. Aside the functional relevance of Endoglin in endothelial cells, CD105 is differentially expressed during hematopoiesis, arguing for a role of this receptor in the development of individual cell lineages. In addition, Endoglin expression is present on mature immune cells of the innate (i.e., macrophages and mast cells) and the adaptive (i.e., T-cells) immune system, further suggesting Endoglin as a factor that shapes immune responses. In this review, we summarize current knowledge on Endoglin expression and function in hematopoietic precursors and mature hematopoietic cells of different lineages.

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Product

Browser Extension Assistant by scite Citation Statement Search Reference Check Visualizations Dashboards Explore Journals Explore Organizations Explore Funders Embedding Badge Embedding Citation Search Pricing

Resources

Blog Help & FAQ Accessibility Statement API Terms For Universities & Governments For Researchers For Publishers For Corporate, Pharma & Enterprise Author Marketing Become an Affiliate Get an organization trial or quote scite Data & Services

About

News & Press Careers Read our Paper Coverage

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Copyright © 2025 scite LLC. All rights reserved.

Made with 💙 for researchers

Part of the Research Solutions Family.