Submit to Cells Review for Cells Propose a Special Issue

Journal Menu

Journal Browser

► Journal Browser

Toward Understanding Wound Repair Mechanism

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

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

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 11786

Share This Special Issue

Special Issue Editor

Dr. Shigehiko Yumura

E-Mail Website
Guest Editor

Graduate School of Sciences and Technology for Innovation, Yamaguchi University, Yamaguchi 753-8511, Japan
Interests: wound repair of cell membrane; cytokinesis; cell migration; cytoskeleton; cell polarity; mechanical force; membrane trafficking; Dictyostelium
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In our body, cells and tissues are frequently wounded by chemical and physical damages. In addition, the stretch and contraction in muscles and hydrostatic pressure in the cardiovascular system frequently injure the cell membrane. A wounded cell membrane loses its barrier function, resulting in an influx of undesirable substances into the cell as well as a loss of cytoplasm. However, cells can rapidly detect and repair the wounded cell membrane. Defects in cell membrane repair may cause muscular dystrophy, diabetes, vitamin deficiencies, and inflammatory myopathy. Plant cells can also repair cell membranes. Thus, like DNA repair, wound repair is a physiologically vital phenomenon for living cells. The molecular mechanism of wound repair is highly regulated temporally and spatially, involving intracellular signaling, membrane remodeling, membrane trafficking, and cytoskeletal dynamics. Historically, on a cellular level, repair of the wounded cell membrane has been mainly studied, but recent studies have revealed that intracellular organelles also have repair mechanisms. Wound repair in the level of multicellular tissue has a common feature to single cells but also involves cell migration, cell division, and cell adhesion. This Special Issue of Cells intends to accept a wide range of wound repair mechanisms, their related interesting phenomena, and techniques for research.

Dr. Shigehiko Yumura
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. 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

membrane resealing
multicellular wound repair
wound repair
wound healing
wound closure
lesion removal

Published Papers (6 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review, Other

13 pages, 3645 KiB

Open AccessArticle

MG53 Mitigates Nitrogen Mustard-Induced Skin Injury

by Haichang Li, Zhongguang Li, Xiuchun Li, Chuanxi Cai, Serena Li Zhao, Robert E. Merritt, Xinyu Zhou, Tao Tan, Valerie Bergdall and Jianjie Ma

Cells 2023, 12(14), 1915; https://doi.org/10.3390/cells12141915 - 23 Jul 2023

Cited by 3 | Viewed by 1461

Abstract

Sulfur mustard (SM) and nitrogen mustard (NM) are vesicant agents that cause skin injury and blistering through complicated cellular events, involving DNA damage, free radical formation, and lipid peroxidation. The development of therapeutic approaches targeting the multi-cellular process of tissue injury repair can potentially provide effective countermeasures to combat vesicant-induced dermal lesions. MG53 is a vital component of cell membrane repair. Previous studies have demonstrated that topical application of recombinant human MG53 (rhMG53) protein has the potential to promote wound healing. In this study, we further investigate the role of MG53 in NM-induced skin injury. Compared with wild-type mice, mg53^−/− mice are more susceptible to NM-induced dermal injuries, whereas mice with sustained elevation of MG53 in circulation are resistant to dermal exposure of NM. Exposure of keratinocytes and human follicle stem cells to NM causes elevation of oxidative stress and intracellular aggregation of MG53, thus compromising MG53′s intrinsic cell membrane repair function. Topical rhMG53 application mitigates NM-induced dermal injury in mice. Histologic examination reveals the therapeutic benefits of rhMG53 are associated with the preservation of epidermal integrity and hair follicle structure in mice with dermal NM exposure. Overall, these findings identify MG53 as a potential therapeutic agent to mitigate vesicant-induced skin injuries. Full article

(This article belongs to the Special Issue Toward Understanding Wound Repair Mechanism)

► Show Figures

Figure 1

21 pages, 3788 KiB

Open AccessArticle

Dynamics of Actin Cytoskeleton and Their Signaling Pathways during Cellular Wound Repair

by Shigehiko Yumura, Md. Shahabe Uddin Talukder, Mst. Shaela Pervin, Md. Istiaq Obaidi Tanvir, Takashi Matsumura, Koushiro Fujimoto, Masahito Tanaka and Go Itoh

Cells 2022, 11(19), 3166; https://doi.org/10.3390/cells11193166 - 09 Oct 2022

Cited by 4 | Viewed by 2185

Abstract

The repair of wounded cell membranes is essential for cell survival. Upon wounding, actin transiently accumulates at the wound site. The loss of actin accumulation leads to cell death. The mechanism by which actin accumulates at the wound site, the types of actin-related proteins participating in the actin remodeling, and their signaling pathways are unclear. We firstly examined how actin accumulates at a wound site in Dictyostelium cells. Actin assembled de novo at the wound site, independent of cortical flow. Next, we searched for actin- and signal-related proteins targeting the wound site. Fourteen of the examined proteins transiently accumulated at different times. Thirdly, we performed functional analyses using gene knockout mutants or specific inhibitors. Rac, WASP, formin, the Arp2/3 complex, profilin, and coronin contribute to the actin dynamics. Finally, we found that multiple signaling pathways related to TORC2, the Elmo/Doc complex, PIP2-derived products, PLA2, and calmodulin are involved in the actin dynamics for wound repair. Full article

(This article belongs to the Special Issue Toward Understanding Wound Repair Mechanism)

► Show Figures

Figure 1

17 pages, 2924 KiB

Open AccessArticle

Reduced Sarcolemmal Membrane Repair Exacerbates Striated Muscle Pathology in a Mouse Model of Duchenne Muscular Dystrophy

by Brian J. Paleo, Kevin E. McElhanon, Hannah R. Bulgart, Kassidy K. Banford, Eric X Beck, Kristina M. Sattler, Briana N. Goines, Shelby L. Ratcliff, Kelly E. Crowe and Noah Weisleder

Cells 2022, 11(9), 1417; https://doi.org/10.3390/cells11091417 - 22 Apr 2022

Cited by 1 | Viewed by 2625

Abstract

Duchenne muscular dystrophy (DMD) is a common X-linked degenerative muscle disorder that involves mutations in the DMD gene that frequently reduce the expression of the dystrophin protein, compromising the structural integrity of the sarcolemmal membrane and leaving it vulnerable to injury during cycles of muscle contraction and relaxation. This results in an increased frequency of sarcolemma disruptions that can compromise the barrier function of the membrane and lead to death of the myocyte. Sarcolemmal membrane repair processes can potentially compensate for increased membrane disruptions in DMD myocytes. Previous studies demonstrated that TRIM72, a muscle-enriched tripartite motif (TRIM) family protein also known as mitsugumin 53 (MG53), is a component of the cell membrane repair machinery in striated muscle. To test the importance of membrane repair in striated muscle in compensating for the membrane fragility in DMD, we crossed TRIM72/MG53 knockout mice into the mdx mouse model of DMD. These double knockout (DKO) mice showed compromised sarcolemmal membrane integrity compared to mdx mice, as measured by immunoglobulin G staining and ex vivo muscle laser microscopy wounding assays. We also found a significant decrease in muscle ex vivo contractile function as compared to mdx mice at both 6 weeks and 1.5 years of age. As the DKO mice aged, they developed more extensive fibrosis in skeletal muscles compared to mdx. Our findings indicate that TRIM72/MG53-mediated membrane repair can partially compensate for the sarcolemmal fragility associated with DMD and that the loss of membrane repair results in increased pathology in the DKO mice. Full article

(This article belongs to the Special Issue Toward Understanding Wound Repair Mechanism)

► Show Figures

Graphical abstract

Review

Jump to: Research, Other

15 pages, 928 KiB

Open AccessReview

Leveraging Plasma Membrane Repair Therapeutics for Treating Neurodegenerative Diseases

by Hannah R. Bulgart, Isabella Goncalves and Noah Weisleder

Cells 2023, 12(12), 1660; https://doi.org/10.3390/cells12121660 - 18 Jun 2023

Cited by 1 | Viewed by 1818

Abstract

Plasma membrane repair is an essential cellular mechanism that reseals membrane disruptions after a variety of insults, and compromised repair capacity can contribute to the progression of many diseases. Neurodegenerative diseases are marked by membrane damage from many sources, reduced membrane integrity, elevated intracellular calcium concentrations, enhanced reactive oxygen species production, mitochondrial dysfunction, and widespread neuronal death. While the toxic intracellular effects of these changes in cellular physiology have been defined, the specific mechanism of neuronal death in certain neurodegenerative diseases remains unclear. An abundance of recent evidence indicates that neuronal membrane damage and pore formation in the membrane are key contributors to neurodegenerative disease pathogenesis. In this review, we have outlined evidence supporting the hypothesis that membrane damage is a contributor to neurodegenerative diseases and that therapeutically enhancing membrane repair can potentially combat neuronal death. Full article

(This article belongs to the Special Issue Toward Understanding Wound Repair Mechanism)

► Show Figures

Figure 1

20 pages, 8624 KiB

Open AccessReview

Wrangling Actin Assemblies: Actin Ring Dynamics during Cell Wound Repair

by Justin Hui, Viktor Stjepić, Mitsutoshi Nakamura and Susan M. Parkhurst

Cells 2022, 11(18), 2777; https://doi.org/10.3390/cells11182777 - 06 Sep 2022

Cited by 8 | Viewed by 2368 | Correction

Abstract

To cope with continuous physiological and environmental stresses, cells of all sizes require an effective wound repair process to seal breaches to their cortex. Once a wound is recognized, the cell must rapidly plug the injury site, reorganize the cytoskeleton and the membrane to pull the wound closed, and finally remodel the cortex to return to homeostasis. Complementary studies using various model organisms have demonstrated the importance and complexity behind the formation and translocation of an actin ring at the wound periphery during the repair process. Proteins such as actin nucleators, actin bundling factors, actin-plasma membrane anchors, and disassembly factors are needed to regulate actin ring dynamics spatially and temporally. Notably, Rho family GTPases have been implicated throughout the repair process, whereas other proteins are required during specific phases. Interestingly, although different models share a similar set of recruited proteins, the way in which they use them to pull the wound closed can differ. Here, we describe what is currently known about the formation, translocation, and remodeling of the actin ring during the cell wound repair process in model organisms, as well as the overall impact of cell wound repair on daily events and its importance to our understanding of certain diseases and the development of therapeutic delivery modalities. Full article

(This article belongs to the Special Issue Toward Understanding Wound Repair Mechanism)

► Show Figures