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Biomedicines
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Angiogenesis and Inflammation in Biological Barriers 2.0
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Angiogenesis and Inflammation in Biological Barriers 2.0

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

Deadline for manuscript submissions: closed (15 August 2022) | Viewed by 24450

Special Issue Editor

Dr. Nadia Alfaidy

E-Mail Website
Guest Editor
Biology and Biotechnology for Health, Biosanté, INSERM U1292, Grenoble, France
Interests: pregnancy pathologies; biological barriers; inflammasomes; angiogenesis; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Owing to the success of our first issue on angiogenesis and inflammation in biological barriers, I am pleased to announce the launch of a second volume. This Special Issue will gather publications that focus on two key processes, angiogenesis and inflammation, which strongly contribute to the functioning of highly vascularized biological barriers (BB). The scope of Volume 2 will be more focused on BB-associated pathologies. Biological barriers are essential for the integrity and proper function of many vertebrate organs and are critical for the regulation of tissue homeostasis and protection against pathogens or other tissue-damaging agents. BB separate internal and external compartments and are formed by specialized cell types, such as epithelial and endothelial cells, that interface the body and the external environment. Recent studies have uncovered the role of new inflammatory and angiogenic proteins in the control of the integrity of these BB as well as their physiological functioning. Deregulations in the expression and/or function of these proteins may explain BB-associated pathologies, such as infections, exacerbated inflammation, tissue injury, and cancer. This Special Issue welcomes original articles and reviews focused on pathological angiogenesis and inflammation in highly vascularized biological barriers.

Dr. Nadia Alfaidy
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

  • biological barriers
  • inflammasome
  • angiogenesis
  • inflammation
  • vascularization
  • angiogenic factors
  • oxidative stress
  • cancer

Related Special Issue

Published Papers (7 papers)

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Research

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15 pages, 3074 KiB  
Article
Angiopoietin-like 4-Induced 3D Capillary Morphogenesis Correlates to Stabilization of Endothelial Adherens Junctions and Restriction of VEGF-Induced Sprouting
by Athanasia Liabotis, Corinne Ardidie-Robouant, Philippe Mailly, Samaher Besbes, Charly Gutierrez, Yoann Atlas, Laurent Muller, Stéphane Germain and Catherine Monnot
Biomedicines 2022, 10(2), 206; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10020206 - 18 Jan 2022
Cited by 3 | Viewed by 2179
Abstract
Angiopoietin-like 4 (ANGPTL4) is a target of hypoxia that accumulates in the endothelial extracellular matrix. While ANGPTL4 is known to regulate angiogenesis and vascular permeability, its context-dependent role related to vascular endothelial growth factor (VEGF) has been suggested in capillary morphogenesis. We here [...] Read more.
Angiopoietin-like 4 (ANGPTL4) is a target of hypoxia that accumulates in the endothelial extracellular matrix. While ANGPTL4 is known to regulate angiogenesis and vascular permeability, its context-dependent role related to vascular endothelial growth factor (VEGF) has been suggested in capillary morphogenesis. We here thus develop in vitro 3D models coupled to imaging and morphometric analysis of capillaries to decipher ANGPTL4 functions either alone or in the presence of VEGF. ANGPTL4 induces the formation of barely branched and thin endothelial capillaries that display linear adherens junctions. However, ANGPTL4 counteracts VEGF-induced formation of abundant ramified capillaries presenting cell–cell junctions characterized by VE-cadherin containing reticular plaques and serrated structures. We further deciphered the early angiogenesis steps regulated by ANGPTL4. During the initial activation of endothelial cells, ANGPTL4 alone induces cell shape changes but limits the VEGF-induced cell elongation and unjamming. In the growing sprout, ANGPTL4 maintains cohesive VE-cadherin pattern and sustains moderate 3D cell migration but restricts VEGF-induced endothelium remodeling and cell migration. This effect is mediated by differential short- and long-term regulation of P-Y1175-VEGFR2 and ERK1-2 signaling by ANGPTL4. Our in vitro 3D models thus provide the first evidence that ANGPTL4 induces a specific capillary morphogenesis but also overcomes VEGF effect. Full article
(This article belongs to the Special Issue Angiogenesis and Inflammation in Biological Barriers 2.0)
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12 pages, 3292 KiB  
Communication
VEGF-Trap Modulates Retinal Inflammation in the Murine Oxygen-Induced Retinopathy (OIR) Model
by Jesús Eduardo Rojo Arias, Vanessa Elisabeth Englmaier and József Jászai
Biomedicines 2022, 10(2), 201; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10020201 - 18 Jan 2022
Cited by 7 | Viewed by 2132
Abstract
Anti-Vascular Endothelial Growth Factor (VEGF) agents are the first-line treatment for retinal neovascular diseases, which represent the most prevalent causes of acquired vision loss world-wide. VEGF-Trap (Aflibercept, AFL), a recombinant decoy receptor recognizing ligands of both VEGFR-1 and -2, was recently reported to [...] Read more.
Anti-Vascular Endothelial Growth Factor (VEGF) agents are the first-line treatment for retinal neovascular diseases, which represent the most prevalent causes of acquired vision loss world-wide. VEGF-Trap (Aflibercept, AFL), a recombinant decoy receptor recognizing ligands of both VEGFR-1 and -2, was recently reported to be highly efficient in improving visual acuity and preserving retinal anatomy in individuals affected by diabetic macular edema. However, the precise molecular and cell biological mechanisms underlying the beneficial effects of this novel tool have yet to be elucidated. Using the mouse oxygen-induced retinopathy (OIR) model as a surrogate of retinopathies with sterile post-ischemic inflammation, such as late proliferative diabetic retinopathy (PDR), retinopathy of prematurity (ROP), and diabetic macular edema (DME), we provide evidence that AFL modulates inflammation in response to hypoxia by regulating the morphology of microglial cells, a parameter commonly used as a proxy for changes in their activation state. We show that AFL administration during the hypoxic period of OIR leads to an increased number of ramified Iba1+ microglial cells/macrophages while subsequently limiting the accumulation of these cells in particular retinal layers. Our results suggest that, beyond its well-documented beneficial effects on microvascular regeneration, AFL might exert important modulatory effects on post-ischemic retinal inflammation. Full article
(This article belongs to the Special Issue Angiogenesis and Inflammation in Biological Barriers 2.0)
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18 pages, 7219 KiB  
Article
IL-17A Damages the Blood–Retinal Barrier through Activating the Janus Kinase 1 Pathway
by Eimear M. Byrne, María Llorián-Salvador, Miao Tang, Andriana Margariti, Mei Chen and Heping Xu
Biomedicines 2021, 9(7), 831; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9070831 - 16 Jul 2021
Cited by 19 | Viewed by 2812
Abstract
Blood–retinal barrier (BRB) dysfunction underlies macular oedema in many sight-threatening conditions, including diabetic macular oedema, neovascular age-related macular degeneration and uveoretinitis. Inflammation plays an important role in BRB dysfunction. This study aimed to understand the role of the inflammatory cytokine IL-17A in BRB [...] Read more.
Blood–retinal barrier (BRB) dysfunction underlies macular oedema in many sight-threatening conditions, including diabetic macular oedema, neovascular age-related macular degeneration and uveoretinitis. Inflammation plays an important role in BRB dysfunction. This study aimed to understand the role of the inflammatory cytokine IL-17A in BRB dysfunction and the mechanism involved. Human retinal pigment epithelial (RPE) cell line ARPE19 and murine brain endothelial line bEnd.3 were cultured on transwell membranes to model the outer BRB and inner BRB, respectively. IL-17A treatment (3 days in bEnd.3 cells and 6 days in ARPE19 cells) disrupted the distribution of claudin-5 in bEnd.3 cells and ZO-1 in ARPE19 cells, reduced the transepithelial/transendothelial electrical resistance (TEER) and increased permeability to FITC-tracers in vitro. Intravitreal (20 ng/1 μL/eye) or intravenous (20 ng/g) injection of recombinant IL-17A induced retinal albumin leakage within 48 h in C57BL/6J mice. Mechanistically, IL-17A induced Janus kinase 1 (JAK1) phosphorylation in bEnd.3 but not ARPE19 cells. Blocking JAK1 with Tofacitinib prevented IL-17A-mediated claudin-5 dysmorphia in bEnd.3 cells and reduced albumin leakage in IL-17A-treated mice. Our results suggest that IL-17A can damage the BRB through the activating the JAK1 signaling pathway, and targeting this pathway may be a novel approach to treat inflammation-induced macular oedema. Full article
(This article belongs to the Special Issue Angiogenesis and Inflammation in Biological Barriers 2.0)
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Review

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21 pages, 1352 KiB  
Review
Animal Models of Chorioamnionitis: Considerations for Translational Medicine
by Tiphaine Raia-Barjat, Margaux Digonnet, Antoine Giraud, Taghreed Ayash, Seline Vancolen, Mohamed Benharouga, Céline Chauleur, Nadia Alfaidy and Guillaume Sébire
Biomedicines 2022, 10(4), 811; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10040811 - 30 Mar 2022
Cited by 4 | Viewed by 3114
Abstract
Preterm birth is defined as any birth occurring before 37 completed weeks of gestation by the World Health Organization. Preterm birth is responsible for perinatal mortality and long-term neurological morbidity. Acute chorioamnionitis is observed in 70% of premature labor and is associated with [...] Read more.
Preterm birth is defined as any birth occurring before 37 completed weeks of gestation by the World Health Organization. Preterm birth is responsible for perinatal mortality and long-term neurological morbidity. Acute chorioamnionitis is observed in 70% of premature labor and is associated with a heavy burden of multiorgan morbidities in the offspring. Unfortunately, chorioamnionitis is still missing effective biomarkers and early placento- as well as feto-protective and curative treatments. This review summarizes recent advances in the understanding of the underlying mechanisms of chorioamnionitis and subsequent impacts on the pregnancy outcome, both during and beyond gestation. This review also describes relevant and current animal models of chorioamnionitis used to decipher associated mechanisms and develop much needed therapies. Improved knowledge of the pathophysiological mechanisms underpinning chorioamnionitis based on preclinical models is a mandatory step to identify early in utero diagnostic biomarkers and design novel anti-inflammatory interventions to improve both maternal and fetal outcomes. Full article
(This article belongs to the Special Issue Angiogenesis and Inflammation in Biological Barriers 2.0)
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14 pages, 1808 KiB  
Review
Role of NLRP7 in Normal and Malignant Trophoblast Cells
by Roland Abi Nahed, Maya Elkhoury Mikhael, Deborah Reynaud, Constance Collet, Nicolas Lemaitre, Thierry Michy, Pascale Hoffmann, Frederic Sergent, Christel Marquette, Padma Murthi, Tiphaine Raia-Barjat, Nadia Alfaidy and Mohamed Benharouga
Biomedicines 2022, 10(2), 252; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10020252 - 24 Jan 2022
Cited by 14 | Viewed by 3427
Abstract
Gestational choriocarcinoma (CC) is an aggressive cancer that develops upon the occurrence of abnormal pregnancies such as Hydatidiform moles (HMs) or upon non-molar pregnancies. CC cells often metastasize in multiple organs and can cause maternal death. Recent studies have established an association between [...] Read more.
Gestational choriocarcinoma (CC) is an aggressive cancer that develops upon the occurrence of abnormal pregnancies such as Hydatidiform moles (HMs) or upon non-molar pregnancies. CC cells often metastasize in multiple organs and can cause maternal death. Recent studies have established an association between recurrent HMs and mutations in the Nlrp7 gene. NLRP7 is a member of a new family of proteins that contributes to innate immune processes. Depending on its level of expression, NLRP7 can function in an inflammasome-dependent or independent pathway. To date, the role of NLRP7 in normal and in malignant human placentation remains to be elucidated. We have recently demonstrated that NLRP7 is overexpressed in CC trophoblast cells and may contribute to their acquisition of immune tolerance via the regulation of key immune tolerance-associated factors, namely HLA family, βCG and PD-L1. We have also demonstrated that NLRP7 increases trophoblast proliferation and decreases their differentiation, both in normal and tumor conditions. Actual findings suggest that NLRP7 expression may ensure a strong tolerance of the trophoblast by the maternal immune system during normal pregnancy and may directly affect the behavior and aggressiveness of malignant trophoblast cells. The proposed review summarizes recent advances in the understanding of the significance of NLRP7 overexpression in CC and discusses its multifaceted roles, including its function in an inflammasome-dependent or independent pathways. Full article
(This article belongs to the Special Issue Angiogenesis and Inflammation in Biological Barriers 2.0)
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14 pages, 1240 KiB  
Review
Versatile Role of Prokineticins and Prokineticin Receptors in Neuroinflammation
by Roberta Lattanzi and Rossella Miele
Biomedicines 2021, 9(11), 1648; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9111648 - 09 Nov 2021
Cited by 17 | Viewed by 2735
Abstract
Prokineticins are a new class of chemokine-like peptides involved in a wide range of biological and pathological activities. In particular, prokineticin 2 (PK2), prokineticin receptor 1 (PKR1) and prokineticin receptor 2 (PKR2) play a central role in modulating neuroinflammatory processes. PK2 and PKRs, [...] Read more.
Prokineticins are a new class of chemokine-like peptides involved in a wide range of biological and pathological activities. In particular, prokineticin 2 (PK2), prokineticin receptor 1 (PKR1) and prokineticin receptor 2 (PKR2) play a central role in modulating neuroinflammatory processes. PK2 and PKRs, which are physiologically expressed at very low levels, are strongly upregulated during inflammation and regulate neuronal-glial interaction. PKR2 is mainly overexpressed in neurons, whereas PKR1 and PK2 are mainly overexpressed in astrocytes. Once PK2 is released in inflamed tissue, it is involved in both innate and adaptive responses: it triggers macrophage recruitment, production of pro-inflammatory cytokines, and reduction of anti-inflammatory cytokines. Moreover, it modulates the function of T cells through the activation of PKR1 and directs them towards a pro-inflammatory Th1 phenotype. Since the prokineticin system appears to be upregulated following a series of pathological insults leading to neuroinflammation, we will focus here on the involvement of PK2 and PKRs in those pathologies that have a strong underlying inflammatory component, such as: inflammatory and neuropathic pain, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, stroke, obesity, diabetes, and gastrointestinal inflammation. Full article
(This article belongs to the Special Issue Angiogenesis and Inflammation in Biological Barriers 2.0)
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20 pages, 2278 KiB  
Review
Pathophysiological Implication of Pattern Recognition Receptors in Fetal Membranes Rupture: RAGE and NLRP Inflammasome
by Helena Choltus, Marilyne Lavergne, Coraline De Sousa Do Outeiro, Karen Coste, Corinne Belville, Loïc Blanchon and Vincent Sapin
Biomedicines 2021, 9(9), 1123; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9091123 - 31 Aug 2021
Cited by 6 | Viewed by 6871
Abstract
Preterm prelabor ruptures of fetal membranes (pPROM) are a pregnancy complication responsible for 30% of all preterm births. This pathology currently appears more as a consequence of early and uncontrolled process runaway activation, which is usually implicated in the physiologic rupture at term: [...] Read more.
Preterm prelabor ruptures of fetal membranes (pPROM) are a pregnancy complication responsible for 30% of all preterm births. This pathology currently appears more as a consequence of early and uncontrolled process runaway activation, which is usually implicated in the physiologic rupture at term: inflammation. This phenomenon can be septic but also sterile. In this latter case, the inflammation depends on some specific molecules called “alarmins” or “damage-associated molecular patterns” (DAMPs) that are recognized by pattern recognition receptors (PRRs), leading to a microbial-free inflammatory response. Recent data clarify how this activation works and which receptor translates this inflammatory signaling into fetal membranes (FM) to manage a successful rupture after 37 weeks of gestation. In this context, this review focused on two PRRs: the receptor for advanced glycation end-products (RAGE) and the NLRP7 inflammasome. Full article
(This article belongs to the Special Issue Angiogenesis and Inflammation in Biological Barriers 2.0)
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