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Biomedicines
Special Issues
The Role of Macrophage and Neutrophils in Angiogenesis
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The Role of Macrophage and Neutrophils in Angiogenesis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 2655

Special Issue Editor

Dr. Miki Rahat

E-Mail Website
Guest Editor
Carmel Medical Center and Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel
Interests: immunotherapy; immunology; inflammation; EMMPRIN; macrophage

Special Issue Information

Dear Colleagues,

Angiogenesis is a critical process in the development of chronic inflammatory diseases and for the progression of cancer. It provides a delivery system for oxygen, nutrients and cells to arrive at a specific site of inflammation, tumor, or even metastases. Macrophages and neutrophils play a regulatory role in this process, and interactions with the tissue cells or with the tumor cells promote the activation of endothelial cells towards angiogenesis. In the generated microenvironment, macrophages and neutrophils exhibit high plasticity that allow them to orchestrate and fine-tune this crucial process. The regulation exerted by macrophages and neutrophils involves cross-talk with other cell types, including tissue cells, other immune cells, and stroma cells (e.g., endothelial cells and fibroblasts), that is yet not fully elucidated. Novel research techniques into deciphering events at the single-cell level help us to clarify and better understand such interactions.

In this Special Issue, we invite researchers to highlight how the cooperation between macrophages and neutrophils and their interactions with other types of cells help regulate angiogenesis during disease and promote autoimmune diseases, tumor growth, and metastasis. We welcome manuscripts that examine new ways of intervention, new targets, or new applications of known drugs that help disrupt such interactions in order to inhibit inflammation and angiogenesis and arrest disease progression.

Dr. Miki Rahat
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • angiogenesis
  • macrophages
  • neutrophils
  • endothelial cells
  • cancer
  • autoimmune diseases
  • interventions

Published Papers (1 paper)

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Research

20 pages, 5394 KiB  
Article
Knocking-Down CD147/EMMPRIN Expression in CT26 Colon Carcinoma Forces the Cells into Cellular and Angiogenic Dormancy That Can Be Reversed by Interactions with Macrophages
by Gabriele Feigelman, Elina Simanovich, Phillipp Brockmeyer and Michal A. Rahat
Biomedicines 2023, 11(3), 768; https://doi.org/10.3390/biomedicines11030768 - 2 Mar 2023
Cited by 4 | Viewed by 2155
Abstract
Metastasis in colorectal cancer is responsible for most of the cancer-related deaths. For metastasis to occur, tumor cells must first undergo the epithelial-to-mesenchymal transition (EMT), which is driven by the transcription factors (EMT-TFs) Snail, Slug twist1, or Zeb1, to promote their migration. In [...] Read more.
Metastasis in colorectal cancer is responsible for most of the cancer-related deaths. For metastasis to occur, tumor cells must first undergo the epithelial-to-mesenchymal transition (EMT), which is driven by the transcription factors (EMT-TFs) Snail, Slug twist1, or Zeb1, to promote their migration. In the distant organs, tumor cells may become dormant for years, until signals from their microenvironment trigger and promote their outgrowth. Here we asked whether CD147/EMMPRIN controls entry and exit from dormancy in the aggressive and proliferative (i.e., non-dormant) CT26 mouse colon carcinoma cells, in its wild-type form (CT26-WT cells). To this end, we knocked down EMMPRIN expression in CT26 cells (CT26-KD), and compared their EMT and cellular dormancy status (e.g., proliferation, pERK/pP38 ratio, vimentin expression, expression of EMT-TFs and dormancy markers), and angiogenic dormancy (e.g., VEGF and MMP-9 secretion, healing of the wounded bEND3 mouse endothelial cells), to the parental cells (CT26-WT). We show that knocking-down EMMPRIN expression reduced the pERK/pP38 ratio, enhanced the expression of vimentin, the EMT-TFs and the dormancy markers, and reduced the proliferation and angiogenic potential, cumulatively indicating that cells were pushed towards dormancy. When macrophages were co-cultured with both types of CT26 cells, the CT26-WT cells increased their angiogenic potential, but did not change their proliferation, state of EMT, or dormancy, whereas the CT26-KD cells exhibited values mostly similar to those of the co-cultured CT26-WT cells. Addition of recombinant TGFβ or EMMPRIN that simulated the presence of macrophages yielded similar results. Combinations of low concentrations of TGFβ and EMMPRIN had a minimal additive effect only in the CT26-KD cells, suggesting that they work along the same signaling pathway. We conclude that EMMPRIN is important as a gatekeeper that prevents cells from entering a dormant state, and that macrophages can promote an exit from dormancy. Full article
(This article belongs to the Special Issue The Role of Macrophage and Neutrophils in Angiogenesis)
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