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Cells
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Biomarkers in Inflammation and Angiogenesis
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Biomarkers in Inflammation and Angiogenesis

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 11177

Special Issue Editor

Prof. Dr. Domenico Ribatti

E-Mail Website
Guest Editor
Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari Medical School, Policlinico - Piazza G. Cesare, 11, 70124 Bari, Italy
Interests: angiogenesis; anti-angiogenesis; tumor progression; tumor vessel
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Both innate and adaptive immune cells are involved in the mechanisms of endothelial cell proliferation, migration and activation through the production and release of a large spectrum of pro-angiogenic mediators. These may create the specific microenvironment that favors an increased rate of tissue vascularization. The link between chronic inflammation and tumorigenesis was first proposed by Rudolf Virchow in 1863 after the observation that infiltrating leukocytes are a hallmark of tumors and first established a causative connection between the lymph reticular infiltrate at sites of chronic inflammation and the development of cancer. Tumors were described as wounds that never heal, and surgeons have long described the tendency of tumors to recur in the healing resection margin, and it has been reported that the wound healing environment provides an opportunistic matrix for tumor growth. This Special Issue will provide more recent literature data concerning biomarkers of inflammation and angiogenesis, and as angiogenesis is the result of a net balance between the activities exerted by positive and negative regulators, this Special Issue will  provide more recent information on some anti-angiogenic properties of immune cells that may be utilized for a potential pharmacological use as anti-angiogenic agents in inflammation as well as in cancer.

Prof. Dr. Domenico Ribatti
Guest Editor

Manuscript Submission Information

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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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • cancer biology
  • metastasis
  • cancer biomarkers
  • inflammation
  • tumors
  • cancer research
  • molecular biology
  • cell biology
  • cell proliferation
  • cancer
  • angiogenesis
  • anti-angiogenesis

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Published Papers (3 papers)

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Research

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12 pages, 3701 KiB  
Article
Tumor Microenvironment and Microvascular Density in Human Glioblastoma
by Roberto Tamma, Giuseppe Ingravallo, Tiziana Annese, Antonio d’Amati, Loredana Lorusso and Domenico Ribatti
Cells 2023, 12(1), 11; https://doi.org/10.3390/cells12010011 - 20 Dec 2022
Cited by 11 | Viewed by 2929
Abstract
Glioblastoma (GBM) is a very aggressive form of cancer affecting the central nervous system. Although it occurs almost exclusively in the brain, glioblastoma can also appear in the brainstem, cerebellum, and spinal cord. It is characterized by high rates of proliferation, invasion, and [...] Read more.
Glioblastoma (GBM) is a very aggressive form of cancer affecting the central nervous system. Although it occurs almost exclusively in the brain, glioblastoma can also appear in the brainstem, cerebellum, and spinal cord. It is characterized by high rates of proliferation, invasion, and necrosis. Moreover, GBM is a highly vascularized tumor and presents resistance to therapy. Recent data indicate that GBM cells are surrounded by a microenvironment (TME) which includes a complex network constituted of cellular/extracellular components and vessels able to influence both tumor growth and angiogenesis. In this retrospective study, we evaluated 30 bioptic specimens of adult patients diagnosed with IDH1 wild type GBM taken at the time of the first diagnosis. Each section has been divided into two experimental zones: the tumor side and the healthy surrounding tissue. We performed a series of immunohistochemical stainings with the purpose of evaluating the presence of total and M2 macrophages, CD4+-, CD8+-lymphocytes, and CD34+ microvessels. In addition, we have also evaluated the percentage of cells expressing bcl6 and p53 to determine any possible correlations with TME. Our data showed a significant increase in the total and M2 type macrophages, of CD4+ and CD8+ lymphocytes, and of CD34+ microvessels in the tumoral area respective to the healthy zone. We also confirmed our previous data showing the higher number of p53 and BCL6+ cells in the tumor area with a positive correlation between BCL6 and CD34+ microvessels. In conclusion, the data that came from this work support the important role played by microenvironment components in GBM progression. These results could contribute to the generation of new specific therapies useful in preventing GBM progression. Full article
(This article belongs to the Special Issue Biomarkers in Inflammation and Angiogenesis)
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22 pages, 4337 KiB  
Article
Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors
by Mohamed Adel, Hassan Reda Hassan Elsayed, Mohammad El-Nablaway, Shereen Hamed, Amira Eladl, Samah Fouad, Eman Mohamad El Nashar, Mohammed Lafi Al-Otaibi and Mohammed R. Rabei
Cells 2022, 11(16), 2500; https://doi.org/10.3390/cells11162500 - 11 Aug 2022
Cited by 8 | Viewed by 2215
Abstract
Long-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaHS) [...] Read more.
Long-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaHS) H2S donor, against Dexamethasone (Dex)-induced soleus muscle atrophy and microvascular rarefaction and on muscle endothelial progenitors and M2 macrophages. Rats received either; saline, Dex (0.6 mg/Kg/day), Dex + NaHS (5 mg/Kg/day), or Dex + Aminooxyacetic acid (AOAA), a blocker of H2S (10 mg/Kg/day) for two weeks. The soleus muscle was examined for contractile properties. mRNA expression for Myostatin, Mechano-growth factor (MGF) and NADPH oxidase (NOX4), HE staining, and immunohistochemical staining for caspase-3, CD34 (Endothelial progenitor marker), vascular endothelial growth factor (VEGF), CD31 (endothelial marker), and CD163 (M2 macrophage marker) was performed. NaHS could improve the contractile properties and decrease oxidative stress, muscle atrophy, and the expression of NOX4, caspase-3, Myostatin, VEGF, and CD31 and could increase the capillary density and expression of MGF with a significant increase in expression of CD34 and CD163 as compared to Dex group. However, AOAA worsened the studied parameters. Therefore, H2S can be a promising target to attenuate muscle atrophy and microvascular rarefaction. Full article
(This article belongs to the Special Issue Biomarkers in Inflammation and Angiogenesis)
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Review

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30 pages, 2088 KiB  
Review
Central Nervous System Pericytes Contribute to Health and Disease
by Francesco Girolamo, Mariella Errede, Antonella Bizzoca, Daniela Virgintino and Domenico Ribatti
Cells 2022, 11(10), 1707; https://doi.org/10.3390/cells11101707 - 20 May 2022
Cited by 10 | Viewed by 5480
Abstract
Successful neuroprotection is only possible with contemporary microvascular protection. The prevention of disease-induced vascular modifications that accelerate brain damage remains largely elusive. An improved understanding of pericyte (PC) signalling could provide important insight into the function of the neurovascular unit (NVU), and into [...] Read more.
Successful neuroprotection is only possible with contemporary microvascular protection. The prevention of disease-induced vascular modifications that accelerate brain damage remains largely elusive. An improved understanding of pericyte (PC) signalling could provide important insight into the function of the neurovascular unit (NVU), and into the injury-provoked responses that modify cell–cell interactions and crosstalk. Due to sharing the same basement membrane with endothelial cells, PCs have a crucial role in the control of endothelial, astrocyte, and oligodendrocyte precursor functions and hence blood–brain barrier stability. Both cerebrovascular and neurodegenerative diseases impair oxygen delivery and functionally impair the NVU. In this review, the role of PCs in central nervous system health and disease is discussed, considering their origin, multipotency, functions and also dysfunction, focusing on new possible avenues to modulate neuroprotection. Dysfunctional PC signalling could also be considered as a potential biomarker of NVU pathology, allowing us to individualize therapeutic interventions, monitor responses, or predict outcomes. Full article
(This article belongs to the Special Issue Biomarkers in Inflammation and Angiogenesis)
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