scholarly journals Simple Modelling of Extracellular Matrix Alignment in Dermal Wound Healing I. Cell Flux Induced Alignment

1998 ◽  
Vol 1 (3) ◽  
pp. 175-192 ◽  
Author(s):  
Luke Olsen ◽  
Philip K. Maini ◽  
Jonathan A. Sherratt ◽  
Ben Marchant
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Cell Movement ◽  
Collagen Fibre ◽  
Cell Types ◽  
Travelling Wave ◽  
Generic Model ◽  
Dimensional Version ◽  
Healing Wounds ◽  
Dermal Wound

We present a generic model to investigate alignment due to cell movement with spefic application to collagen fibre alignment in wound healing. In particular, alignment in two orthogonal directions is considered. Numerical simulation are presented to show how alignment is affected by key parameter min the model. from a travelling wave analysis of a simplified one-dimensional version of the model we derive a first order ordinary differential equation to describe the time evolution of aligment. We conclude that in the wound healing context,faster healing wounds result in more aligment and hence more serve scarring. It is shown how the model can be extended to included orientation dependent Kinetics,multipkle cell types and several extracellular matrix materials.

scholarly journals Augmentation of Dermal Wound Healing by Adipose Tissue-Derived Stromal Cells (ASC)

2018 ◽  
Vol 5 (4) ◽  
pp. 91 ◽  
Author(s):  
Joris van Dongen ◽  
Martin Harmsen ◽  
Berend van der Lei ◽  
Hieronymus Stevens
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Adipose Tissue ◽  
Stromal Cells ◽  
Randomized Clinical Trials ◽  
Cell Types ◽  
Matrix Remodeling ◽  
Skin Wound Healing ◽  
Dermal Wound Healing ◽  
Dermal Wound

The skin is the largest organ of the human body and is the first line of defense against physical and biological damage. Thus, the skin is equipped to self-repair and regenerates after trauma. Skin regeneration after damage comprises a tightly spatial-temporally regulated process of wound healing that involves virtually all cell types in the skin. Wound healing features five partially overlapping stages: homeostasis, inflammation, proliferation, re-epithelization, and finally resolution or fibrosis. Dysreguled wound healing may resolve in dermal scarring. Adipose tissue is long known for its suppressive influence on dermal scarring. Cultured adipose tissue-derived stromal cells (ASCs) secrete a plethora of regenerative growth factors and immune mediators that influence processes during wound healing e.g., angiogenesis, modulation of inflammation and extracellular matrix remodeling. In clinical practice, ASCs are usually administered as part of fractionated adipose tissue i.e., as part of enzymatically isolated SVF (cellular SVF), mechanically isolated SVF (tissue SVF), or as lipograft. Enzymatic isolation of SVF obtained adipose tissue results in suspension of adipocyte-free cells (cSVF) that lack intact intercellular adhesions or connections to extracellular matrix (ECM). Mechanical isolation of SVF from adipose tissue destructs the parenchyma (adipocytes), which results in a tissue SVF (tSVF) with intact connections between cells, as well as matrix. To date, due to a lack of well-designed prospective randomized clinical trials, neither cSVF, tSVF, whole adipose tissue, or cultured ASCs can be indicated as the preferred preparation procedure prior to therapeutic administration. In this review, we present and discuss current literature regarding the different administration options to apply ASCs (i.e., cultured ASCs, cSVF, tSVF, and lipografting) to augment dermal wound healing, as well as the available indications for clinical efficacy.

scholarly journals Novel formulation approaches for wound healing

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 937-948
Author(s):  
Tanaji D Nandgude ◽  
Syed Nateque Naser
Keyword(s):  
Wound Healing ◽  
Healing Process ◽  
Cell Types ◽  
Wound Management ◽  
Wound Healing Process ◽  
Anatomic Structure ◽  
Tissue Integrity ◽  
Molecular Events ◽  
Acute Injuries ◽  
Healing Wounds

A wound is damage to the typical anatomic structure. Wound healing is an immediate therapeutic response to injury. It is a creation of the combined response of some cell types towards injury. Wound healing takes place by a sequence of molecular events which cooperate to fix tissue integrity and cell work. In typical healthy individual under ordinary conditions, these physiological events take place smoothly. Though sometimes, these molecular events are arrested, this brings about in struggle to heal. There is an assortment of approaches for the way toward managing and controlling both acute injuries (acute wounds) and ceaseless non-mending wounds (chronic non-healing wounds). The principal objective of these two cases is to achieve better-wound healing. Ideal formulations of wound healing should not only enhance the healing process but also reduce pain, infection and loss of electrolytes, proteins and liquids from the injury. A broad scope of items typically introduced with target various parts of the wound healing process depends on numerous types of wounds and novel polymers utilised for the conveyance of medications to both acute and ceaseless injuries. These include alginate, hydrocolloids, hydrofibers, polyurethane, and hydrogels. This article gives particular importance to different novel approaches in the management of wound healing. This review draws out the data and hopes to provide understanding into traditional, current and imminent techniques and methods for wound management.

Rapid epithelialisation of fetal wounds is associated with the early deposition of tenascin

1991 ◽  
Vol 99 (3) ◽  
pp. 583-586 ◽  
Author(s):  
D.J. Whitby ◽  
M.T. Longaker ◽  
M.R. Harrison ◽  
N.S. Adzick ◽  
M.W. Ferguson
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Temporal Distribution ◽  
Cell Types ◽  
Skin Wound ◽  
Skin Wound Healing ◽  
Early Appearance ◽  
Complex Process ◽  
Healing Wounds ◽  
Fetal Wound

Wound healing is a complex process involving the interaction of many cell types with the extracellular matrix (ECM). Fetal skin wound healing differs from that in the adult in that it occurs rapidly and without scar formation. The mechanisms underlying these differing processes may be related to the fetal environment, the stage of differentiation of the fetal cells or the ECM deposited in the wound. The spatial and temporal distribution of two components of the ECM, fibronectin and tenascin, were studied by immunostaining of cryosections from trunk wounds of fetal and adult sheep. Epithelialisation was complete earlier in the fetal wound than in the adult. The distribution of fibronectin was similar in fetal and adult wounds but tenascin was present earlier in the fetal wound. Fibronectin has several roles in wound healing including acting as a substratum for cell migration and as a mediator of cell adhesion through cell surface integrins. The attachment of fibroblasts to fibronectin is inhibited by tenascin and during development the appearance of tenascin in the ECM of migratory pathways correlates with the initiation of cell migration. Similarly, the appearance of tenascin in healing wounds may initiate cell migration. Tenascin was present in these wounds prior to cell migration and the rapid epithelialisation of fetal wounds may be due to the early appearance of tenascin in the wound.

scholarly journals Toward understanding scarless skin wound healing and pathological scarring

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 787 ◽  
Author(s):  
Sanna-Maria Karppinen ◽  
Ritva Heljasvaara ◽  
Donald Gullberg ◽  
Kaisa Tasanen ◽  
Taina Pihlajaniemi
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Healing Process ◽  
Cell Types ◽  
Skin Wound ◽  
Skin Wounds ◽  
Medical Problems ◽  
Skin Wound Healing ◽  
Recent Developments ◽  
Acute Wound

The efficient healing of skin wounds is crucial for securing the vital barrier function of the skin, but pathological wound healing and scar formation are major medical problems causing both physiological and psychological challenges for patients. A number of tightly coordinated regenerative responses, including haemostasis, the migration of various cell types into the wound, inflammation, angiogenesis, and the formation of the extracellular matrix, are involved in the healing process. In this article, we summarise the central mechanisms and processes in excessive scarring and acute wound healing, which can lead to the formation of keloids or hypertrophic scars, the two types of fibrotic scars caused by burns or other traumas resulting in significant functional or aesthetic disadvantages. In addition, we discuss recent developments related to the functions of activated fibroblasts, the extracellular matrix and mechanical forces in the wound environment as well as the mechanisms of scarless wound healing. Understanding the different mechanisms of wound healing is pivotal for developing new therapies to prevent the fibrotic scarring of large skin wounds.

scholarly journals Ignoring matrix boundaries when the LKB1 master kinase is gone

2014 ◽  
Vol 207 (2) ◽  
pp. 167-169 ◽  
Author(s):  
Erik H.J. Danen
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Tumor Suppressor ◽  
Embryonic Development ◽  
Immune Responses ◽  
Cell Movement ◽  
Metastatic Spread ◽  
Ecm Proteins ◽  
The Many ◽  
Migration Of Cells

Gradients of soluble attractants as well as extracellular matrix (ECM) proteins serve as cues for directional cell movement. Such “chemotaxis” and “haptotaxis” steers migration of cells during embryonic development, wound healing, and immune responses. In this issue, Chan et al. (2014. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201404067) show that the tumor suppressor LKB1 controls haptotaxis through the microtubule affinity-regulating kinase (MARK) family, one of the many substrates of the LKB1 master kinase. In the absence of this pathway, melanoma cells migrate irrespective of ECM gradients, which may explain the increased metastatic spread observed in LKB1-deficient tumors.

scholarly journals Wound Healing: A Cellular Perspective

2019 ◽  
Vol 99 (1) ◽  
pp. 665-706 ◽  
Author(s):  
Melanie Rodrigues ◽  
Nina Kosaric ◽  
Clark A. Bonham ◽  
Geoffrey C. Gurtner
Keyword(s):  
Wound Healing ◽  
Single Cell ◽  
Wound Closure ◽  
Chronic Wounds ◽  
Cell Types ◽  
Skin Injury ◽  
Complex Processes ◽  
Cell Technologies ◽  
Cellular Recruitment ◽  
Healing Wounds

Wound healing is one of the most complex processes in the human body. It involves the spatial and temporal synchronization of a variety of cell types with distinct roles in the phases of hemostasis, inflammation, growth, re-epithelialization, and remodeling. With the evolution of single cell technologies, it has been possible to uncover phenotypic and functional heterogeneity within several of these cell types. There have also been discoveries of rare, stem cell subsets within the skin, which are unipotent in the uninjured state, but become multipotent following skin injury. Unraveling the roles of each of these cell types and their interactions with each other is important in understanding the mechanisms of normal wound closure. Changes in the microenvironment including alterations in mechanical forces, oxygen levels, chemokines, extracellular matrix and growth factor synthesis directly impact cellular recruitment and activation, leading to impaired states of wound healing. Single cell technologies can be used to decipher these cellular alterations in diseased states such as in chronic wounds and hypertrophic scarring so that effective therapeutic solutions for healing wounds can be developed.

scholarly journals VEGF-A, PDGF-BB and HB-EGF engineered for promiscuous super affinity to the extracellular matrix improve wound healing in a model of type 1 diabetes

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Michael J. V. White ◽  
Priscilla S. Briquez ◽  
David A. V. White ◽  
Jeffrey A. Hubbell
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Growth Factors ◽  
Growth Factor ◽  
Mouse Model ◽  
Triple Therapy ◽  
Nod Mouse ◽  
Heparin Binding ◽  
Healing Wounds

AbstractChronic non-healing wounds, frequently caused by diabetes, lead to lower quality of life, infection, and amputation. These wounds have limited treatment options. We have previously engineered growth factors to bind to exposed extracellular matrix (ECM) in the wound environment using the heparin-binding domain of placental growth factor-2 (PlGF-2123–144), which binds promiscuously to ECM proteins. Here, in the type 1 diabetic (T1D) NOD mouse model, engineered growth factors (eGFs) improved both re-epithelialization and granulation tissue formation. eGFs were even more potent in combination, and the “triple therapy” of vascular endothelial growth factor-A (VEGF-PlGF-2123–144), platelet-derived growth factor-BB (PDGF-BB-PlGF-2123–144), and heparin-binding epidermal growth factor (HB-EGF-PlGF-2123–144) both improved wound healing and remained at the site of administration for significantly longer than wild-type growth factors. In addition, we also found that changes in the cellular milieu of a wound, including changing amounts of M1 macrophages, M2 macrophages and effector T cells, are most predictive of wound-healing success in the NOD mouse model. These results suggest that the triple therapy of VEGF-PlGF-2123–144, PDGF-BB-PlGF-2123–144, and HB-EGF-PlGF-2123–144 may be an effective therapy for chronic non-healing wounds in that occur as a complication of diabetes.

scholarly journals A mathematical model for collagen fibre formation during foetal and adult dermal wound healing

1996 ◽  
Vol 263 (1370) ◽  
pp. 653-660 ◽  
Keyword(s):  
Mathematical Model ◽  
Wound Healing ◽  
Transforming Growth Factor ◽  
Collagen Fibre ◽  
Transforming Growth Factor Β ◽  
Scar Tissue ◽  
A Value ◽  
Fibre Formation ◽  
The Difference ◽  
Dermal Wound

Adult dermal wounds, in contrast to foetal wounds, heal with the formation of scar tissue. A crucial factor in determining the nature of the healed tissue is the ratio of collagen 1 to collagen 3, which regulates the diameter of collagen fibres. We develop a mathematical model which focuses on the stimulus for collagen synthesis due to the secretion of the different isoforms of the regulatory chemical transforming growth factor β. Numerical simulations of the model lead to a value of this ratio consistent with that of healthy tissue for the foetus but corresponding to scarring in adult wound healing. We investigate the effect of topical application of TGFβ isoforms during healing and determine the key parameters which control the difference between adult and foetal repair.

scholarly journals VEGF-A, PDGF-BB and HB-EGF engineered for promiscuous super affinity to the extracellular matrix improve wound healing in a model of type 1 diabetes

2021 ◽  
Author(s):  
MICHAEL John Victor WHITE ◽  
Priscilla Briquez ◽  
David Andrew Victor White ◽  
Jeffrey Hubbell
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Growth Factors ◽  
Growth Factor ◽  
Mouse Model ◽  
Triple Therapy ◽  
Nod Mouse ◽  
Heparin Binding ◽  
Healing Wounds

Chronic non-healing wounds, frequently caused by diabetes, lead to lower quality of life, infection, and amputation. These wounds have limited treatment options. We have previously engineered growth factors to bind to exposed extracellular matrix (ECM) in the wound environment using the heparin-binding domain of placental growth factor-2 (PlGF-2123-144), which binds promiscuously to ECM proteins. Here, in the type 1 diabetic (T1D) NOD mouse model, engineered growth factors improved both re-epithelialization and granulation tissue formation. Engineered growth factors were even more potent in combination, and the *triple therapy* of vascular endothelial growth factor-A (VEGF-PlGF-2123-144), platelet-derived growth factor-BB (PDGF-BB-PlGF-2123-144), and heparin-binding epidermal-growth factor (EGF-PlGF-2123-144) both improved wound healing and remained at the site of administration for significantly longer than wild-type growth factors. In addition, we also found that changes in the cellular milieu of a wound, including changing amounts of M1 macrophages, M2 macrophages and effector T cells, are most predictive of wound healing success in the NOD mouse model. These results suggest that the triple therapy of VEGF-PlGF-2123-144, PDGF-BB-PlGF-2123-144, and EGF-PlGF-2123-144 may be an effective therapy for chronic non-healing wounds in that occur as a complication of diabetes.

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