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Wound Repair and Regeneration 2023
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Wound Repair and Regeneration 2023

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 5053

Special Issue Editor

Prof. Dr. Sadanori Akita

E-Mail Website
Guest Editor
Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima 9601247, Japan
Interests: wound healing; inflammation; scarring; extracellular matrix; regeneration; biomaterials; chronic wounds; remodeling; stem cells; growth factors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

This Special Issue is a continuation of our 2019 Special Issue “Wound Repair and Regeneration: Mechanisms, Signaling”, our 2020 Special Issue “Wound Repair and Regeneration 2.0”, and our 2022 Special Issue “Wound Repair and Regeneration 2022”.

Wound healing plays an integral part in cellular and molecular events. This process is implicated in regeneration. The regeneration process involves restoring defects and disfigurement towards the original or more ideal states via cells, molecules, and environmental factors. Cellular and molecular events are orchestrated both spatially and temporally. When targeting each disease, an understanding of wound healing and the regeneration process, as well as the findings of pathophysiology, will deliver new insights into realistic novel therapeutic options.

This Special Issue, “Wound Repair and Regeneration 2023”, calls for original articles, reviews, and perspectives that address the current knowledge and developments in the field of wound healing and regeneration using conventional approaches, as well as highly technologically advanced approaches. These include, but are not limited to, the fields mentioned in the keywords.

Prof. Dr. Sadanori Akita
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • wound healing
  • inflammation
  • scarring
  • extracellular matrix
  • regeneration
  • biomaterials
  • chronic wounds
  • remodeling
  • stem cells
  • growth factors
  • disease
  • pathophysiology
  • therapy
  • tissue engineering

Published Papers (4 papers)

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Research

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13 pages, 5393 KiB  
Article
Investigating the Relevance of Cyclic Adenosine Monophosphate Response Element-Binding Protein to the Wound Healing Process: An In Vivo Study Using Photobiomodulation Treatment
by Sungyeon Kim, Jion Park, Younghoon Choi, Hongbae Jeon and Namkyu Lim
Int. J. Mol. Sci. 2024, 25(9), 4838; https://doi.org/10.3390/ijms25094838 - 29 Apr 2024
Viewed by 213
Abstract
Monitoring inflammatory cytokines is crucial for assessing healing process and photobiomodulation (PBM) enhances wound healing. Meanwhile, cAMP response element-binding protein (CREB) is a regulator of cellular metabolism and proliferation. This study explored potential links between inflammatory cytokines and the activity of CREB in [...] Read more.
Monitoring inflammatory cytokines is crucial for assessing healing process and photobiomodulation (PBM) enhances wound healing. Meanwhile, cAMP response element-binding protein (CREB) is a regulator of cellular metabolism and proliferation. This study explored potential links between inflammatory cytokines and the activity of CREB in PBM-treated wounds. A total of 48 seven-week-old male SD rats were divided into four groups (wound location, skin or oral; treatment method, natural healing or PBM treatment). Wounds with a 6 mm diameter round shape were treated five times with an 808 nm laser every other day (total 60 J). The wound area was measured with a caliper and calculated using the elliptical formula. Histological analysis assessed the epidermal regeneration and collagen expression of skin and oral tissue with H&E and Masson’s trichrome staining. Pro-inflammatory (TNF-α) and anti-inflammatory (TGF-β) cytokines were quantified by RT-PCR. The ratio of phosphorylated CREB (p-CREB) to unphosphorylated CREB was identified through Western blot. PBM treatment significantly reduced the size of the wounds on day 3 and day 7, particularly in the skin wound group (p < 0.05 on day 3, p < 0.001 on day 7). The density of collagen expression was significantly higher in the PBM treatment group (in skin wound, p < 0.05 on day 3, p < 0.001 on day 7, and p < 0.05 on day 14; in oral wound, p < 0.01 on day 7). The TGF-β/TNF-α ratio and the p-CREB/CREB ratio showed a parallel trend during wound healing. Our findings suggested that the CREB has potential as a meaningful marker to track the wound healing process. Full article
(This article belongs to the Special Issue Wound Repair and Regeneration 2023)
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16 pages, 2604 KiB  
Article
Mice Lacking PLAP-1/Asporin Show Alteration of Periodontal Ligament Structures and Acceleration of Bone Loss in Periodontitis
by Masaki Kinoshita, Satoru Yamada, Junichi Sasaki, Shigeki Suzuki, Tetsuhiro Kajikawa, Tomoaki Iwayama, Chiharu Fujihara, Satoshi Imazato and Shinya Murakami
Int. J. Mol. Sci. 2023, 24(21), 15989; https://doi.org/10.3390/ijms242115989 - 05 Nov 2023
Cited by 2 | Viewed by 1145
Abstract
Periodontal ligament-associated protein 1 (PLAP-1), also known as Asporin, is an extracellular matrix protein expressed in the periodontal ligament and plays a crucial role in periodontal tissue homeostasis. Our previous research demonstrated that PLAP-1 may inhibit TLR2/4-mediated inflammatory responses, thereby exerting a protective [...] Read more.
Periodontal ligament-associated protein 1 (PLAP-1), also known as Asporin, is an extracellular matrix protein expressed in the periodontal ligament and plays a crucial role in periodontal tissue homeostasis. Our previous research demonstrated that PLAP-1 may inhibit TLR2/4-mediated inflammatory responses, thereby exerting a protective function against periodontitis. However, the precise roles of PLAP-1 in the periodontal ligament (PDL) and its relationship to periodontitis have not been fully explored. In this study, we employed PLAP-1 knockout mice to investigate its roles and contributions to PDL tissue and function in a ligature-induced periodontitis model. Mandibular bone samples were collected from 10-week-old male C57BL/6 (WT) and PLAP-1 knockout (KO) mice. These samples were analyzed through micro-computed tomography (μCT) scanning, hematoxylin and eosin (HE) staining, picrosirius red staining, and fluorescence immunostaining using antibodies targeting extracellular matrix proteins. Additionally, the structure of the PDL collagen fibrils was examined using transmission electron microscopy (TEM). We also conducted tooth extraction and ligature-induced periodontitis models using both wild-type and PLAP-1 KO mice. PLAP-1 KO mice did not exhibit any changes in alveolar bone resorption up to the age of 10 weeks, but they did display an enlarged PDL space, as confirmed by μCT and histological analyses. Fluorescence immunostaining revealed increased expression of extracellular matrix proteins, including Col3, BGN, and DCN, in the PDL tissues of PLAP-1 KO mice. TEM analysis demonstrated an increase in collagen diameter within the PDL of PLAP-1 KO mice. In line with these findings, the maximum stress required for tooth extraction was significantly lower in PLAP-1 KO mice in the tooth extraction model compared to WT mice (13.89 N ± 1.34 and 16.51 N ± 1.31, respectively). In the ligature-induced periodontitis model, PLAP-1 knockout resulted in highly severe alveolar bone resorption, with a higher number of collagen fiber bundle tears and significantly more osteoclasts in the periodontium. Our results demonstrate that mice lacking PLAP-1/Asporin show alteration of periodontal ligament structures and acceleration of bone loss in periodontitis. This underscores the significant role of PLAP-1 in maintaining collagen fibrils in the PDL and suggests the potential of PLAP-1 as a therapeutic target for periodontal diseases. Full article
(This article belongs to the Special Issue Wound Repair and Regeneration 2023)
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20 pages, 3166 KiB  
Article
Procoagulant Activity of Umbilical Cord-Derived Mesenchymal Stromal Cells’ Extracellular Vesicles (MSC-EVs)
by Adrienne Wright, Orman (Larry) Snyder, Hong He, Lane K. Christenson, Sherry Fleming and Mark L. Weiss
Int. J. Mol. Sci. 2023, 24(11), 9216; https://doi.org/10.3390/ijms24119216 - 24 May 2023
Cited by 1 | Viewed by 1149
Abstract
Many cell types, including cancer cells, release tissue factor (TF)-exposing extracellular vesicles (EVs). It is unknown whether MSC-EVs pose a thromboembolism risk due to TF expression. Knowing that MSCs express TF and are procoagulant, we hypothesize that MSC-EVs also might. Here, we examined [...] Read more.
Many cell types, including cancer cells, release tissue factor (TF)-exposing extracellular vesicles (EVs). It is unknown whether MSC-EVs pose a thromboembolism risk due to TF expression. Knowing that MSCs express TF and are procoagulant, we hypothesize that MSC-EVs also might. Here, we examined the expression of TF and the procoagulant activity of MSC-EVs and the impact of EV isolation methods and cell culture expansion on EV yield, characterization, and potential risk using a design of experiments methodology. MSC-EVs were found to express TF and have procoagulant activity. Thus, when MSC-derived EVs are employed as a therapeutic agent, one might consider TF, procoagulant activity, and thromboembolism risk and take steps to prevent them. Full article
(This article belongs to the Special Issue Wound Repair and Regeneration 2023)
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Review

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21 pages, 2504 KiB  
Review
Targeting Signalling Pathways in Chronic Wound Healing
by Lian Bonnici, Sherif Suleiman, Pierre Schembri-Wismayer and Analisse Cassar
Int. J. Mol. Sci. 2024, 25(1), 50; https://doi.org/10.3390/ijms25010050 - 19 Dec 2023
Cited by 3 | Viewed by 1968
Abstract
Chronic wounds fail to achieve complete closure and are an economic burden to healthcare systems due to the limited treatment options and constant medical attention. Chronic wounds are characterised by dysregulated signalling pathways. Research has focused on naturally derived compounds, stem-cell-based therapy, small [...] Read more.
Chronic wounds fail to achieve complete closure and are an economic burden to healthcare systems due to the limited treatment options and constant medical attention. Chronic wounds are characterised by dysregulated signalling pathways. Research has focused on naturally derived compounds, stem-cell-based therapy, small molecule drugs, oligonucleotide delivery nanoparticles, exosomes and peptide-based platforms. The phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT), Wingless-related integration (Wnt)/β-catenin, transforming growth factor-β (TGF-β), nuclear factor erythroid 2–related factor 2 (Nrf2), Notch and hypoxia-inducible factor 1 (HIF-1) signalling pathways have critical roles in wound healing by modulating the inflammatory, proliferative and remodelling phases. Moreover, several regulators of the signalling pathways were demonstrated to be potential treatment targets. In this review, the current research on targeting signalling pathways under chronic wound conditions will be discussed together with implications for future studies. Full article
(This article belongs to the Special Issue Wound Repair and Regeneration 2023)
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