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Biomedicines
Special Issues
Angiogenesis for Regeneration
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Angiogenesis for Regeneration

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 6790

Special Issue Editor

Dr. Jaw-Wen Chen

E-Mail Website
Guest Editor
1. Institute of Pharmacology, National Yang-Ming University School of Medicine, Taipei, Taiwan
2. Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan
Interests: vascular medicine; atherosclerosis; angiogenesis

Special Issue Information

Dear Colleagues,

Angiogenesis is impaired with micro- and macrovasculopathy for peripheral vascular complications, which is frequently seen in patients with chronic diseases including type II diabetes mellitus (DM), hypertension, and kidney disease. Meanwhile, impaired angiogenesis and neovascularization may be one of the major causes of unhealed wounds leading to morbidity and mortality. This Special Issue aims to showcase the latest scientific advances in angiogenesis for regeneration. Accordingly, there is an urgent clinical need to facilitate angiogenesis and neovascularization to improve peripheral vascular complications.

We invite all scientists working on angiogenesis-related conditions or diseases to participate in this Special Issue. Original research articles, reviews, or shorter perspective articles on all aspects related to angiogenesis for regeneration are welcome. Potential topics include but are not limited to the following research areas:

  • Ischemia;
  • Peripheral arterial disease;
  • Angiogenesis;
  • Neovasculogenesis;
  • Neovascularization;
  • Wound healing;
  • Endothelial cell.

Dr. Jaw-Wen Chen
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.

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

15 pages, 1651 KiB  
Article
GARP Regulates the Immune Capacity of a Human Autologous Platelet Concentrate
by Emily R. Trzeciak, Niklas Zimmer, Peer W. Kämmerer, Daniel Thiem, Bilal Al-Nawas, Andrea Tuettenberg and Sebastian Blatt
Biomedicines 2022, 10(12), 3136; https://doi.org/10.3390/biomedicines10123136 - 5 Dec 2022
Cited by 3 | Viewed by 1579
Abstract
Autologous platelet concentrates, like liquid platelet rich fibrin (iPRF), optimize wound healing; however, the underlying immunological mechanisms are poorly understood. Platelets, the main cellular component of iPRF, highly express the protein, Glycoprotein A repetitions predominant (GARP), on their surfaces. GARP plays a crucial [...] Read more.
Autologous platelet concentrates, like liquid platelet rich fibrin (iPRF), optimize wound healing; however, the underlying immunological mechanisms are poorly understood. Platelets, the main cellular component of iPRF, highly express the protein, Glycoprotein A repetitions predominant (GARP), on their surfaces. GARP plays a crucial role in maintaining peripheral tolerance, but its influence on the immune capacity of iPRF remains unclear. This study analyzed the interaction of iPRF with immune cells implicated in the wound healing process (human monocyte derived macrophages and CD4+ T cells) and evaluated the distinct influence of GARP on these mechanisms in vitro. GARP was determined to be expressed on the surface of platelets and to exist as a soluble factor in iPRF. Platelets derived from iPRF and iPRF itself induced a regulatory phenotype in CD4+ T cells, shown by increased expression of Foxp3 and GARP as well as decreased production of IL-2 and IFN-γ. Application of an anti-GARP antibody reversed these effects. Additionally, iPRF polarized macrophages to a “M0/M2-like” phenotype in a GARP independent manner. Altogether, this study demonstrated for the first time that the immune capacity of iPRF is mediated in part by GARP and its ability to induce regulatory CD4+ T cells. Full article
(This article belongs to the Special Issue Angiogenesis for Regeneration)
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14 pages, 4088 KiB  
Article
CCL4 Deletion Accelerates Wound Healing by Improving Endothelial Cell Functions in Diabetes Mellitus
by Ting-Ting Chang, Ching Chen, Liang-Yu Lin and Jaw-Wen Chen
Biomedicines 2022, 10(8), 1963; https://doi.org/10.3390/biomedicines10081963 - 12 Aug 2022
Cited by 2 | Viewed by 2131
Abstract
Chronic inflammation in diabetes mellitus (DM) is the leading cause of non-healing wounds. Chemokine CC motif ligand 4 (CCL4) is enhanced in the circulation and in the wounds of DM patients. This study aimed to investigate the effect of endogenous CCL4 inhibition on [...] Read more.
Chronic inflammation in diabetes mellitus (DM) is the leading cause of non-healing wounds. Chemokine CC motif ligand 4 (CCL4) is enhanced in the circulation and in the wounds of DM patients. This study aimed to investigate the effect of endogenous CCL4 inhibition on diabetic wound healing. Endothelial progenitor cells (EPCs) and human dermal microvascular endothelial cells (HDMECs) were used. Mice were injected with streptozotocin to generate hyperglycemia. An enhanced CCL4 level as well as decreased tube formation and migration abilities were observed in high-glucose-treated HDMECs and in EPCs from type 2 DM patients. CCL4 inhibition by siRNA restored the damaged cell function by upregulating the Akt/endothelial nitric oxide synthase/vascular endothelial growth factor/stromal cell-derived factor-1α pathways. Wild-type diabetic mice had delayed wound repair, whereas the CCL4-knockout diabetic mice showed an accelerated rate of wound closure. In a Matrigel plug assay, CCL4-knockout diabetic mice showed higher blood vessel and hemoglobin levels. Higher CD31 and Ki67 expression in the wound area and Matrigel plugs was detected in the CCL4-knockout diabetic mice. CCL4-knockout mice had upregulated angiogenic factors and downregulated inflammatory factors. This study might provide the theoretical basis for CCL4 inhibition as a therapeutic option for clinical diabetic wound treatment. Full article
(This article belongs to the Special Issue Angiogenesis for Regeneration)
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13 pages, 3993 KiB  
Article
Role of Chitinase-3-like Protein 1 in Cardioprotection and Angiogenesis by Post-Infarction Exercise Training
by Zhuo Li, Fangnan Wu, Lei Xi and Zhenjun Tian
Biomedicines 2022, 10(5), 1028; https://doi.org/10.3390/biomedicines10051028 - 29 Apr 2022
Cited by 2 | Viewed by 2518
Abstract
Chitinase-3-like protein 1 (CHI3L1) is a myokine involving tissue remodeling and inflammatory processes. CHI3L1 and its receptor protease-activated receptor 2 (PAR2) are induced by exercise in skeletal muscles. However, it remains unknown if CHI3L1/PAR2 signaling also mediates exercise-induced cardioprotection after myocardial infarction. Twenty-four [...] Read more.
Chitinase-3-like protein 1 (CHI3L1) is a myokine involving tissue remodeling and inflammatory processes. CHI3L1 and its receptor protease-activated receptor 2 (PAR2) are induced by exercise in skeletal muscles. However, it remains unknown if CHI3L1/PAR2 signaling also mediates exercise-induced cardioprotection after myocardial infarction. Twenty-four adult male rats were divided into three groups (n = 8/group), receiving: (1) a sham operation; (2) permanent ligation of left anterior descending coronary artery; and (3) post-MI exercise training with one-week adaptive treadmill exercise for seven days followed by four weeks of aerobic exercise. Left ventricular systolic and end-diastolic pressure indices were measured and cardiac fibrosis, and angiogenesis were examined. Furthermore, HUVEC cells were treated in vitro with AMPK agonist—AICAR (a putative pharmacological memetic of exercise), recombinant human CHI3L1, PAR2 receptor blocker (AZ3451), and PI3K inhibitor (LY294002), respectively. We found that post-MI exercise significantly upregulated CHI3L1, PAR2, pPI3K/PI3K, pAKT/AKT, pERK/ERK, improved cardiac function, and diminished fibrosis. AICAR increased HUVEC tubules formation and upregulated CHI3L1 and PAR2 and these changes were attenuated by PAR2 blocker. In conclusion, post-MI exercise training can effectively activate CHI3L1/PAR2 signaling, which led to the improved myocardial function and enhanced cardiac angiogenesis in the infarcted heart. Full article
(This article belongs to the Special Issue Angiogenesis for Regeneration)
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