scholarly journals Regeneration of Dermis: Scarring and Cells Involved

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 607 ◽  
Author(s):  
Alexandra L. Rippa ◽  
Ekaterina P. Kalabusheva ◽  
Ekaterina A. Vorotelyak
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Hair Follicle ◽  
Scar Formation ◽  
Population Characteristics ◽  
Matrix Composition ◽  
Skin Substitutes ◽  
Skin Repair ◽  
Dermal Cell

There are many studies on certain skin cell specifications and their contribution to wound healing. In this review, we provide an overview of dermal cell heterogeneity and their participation in skin repair, scar formation, and in the composition of skin substitutes. The papillary, reticular, and hair follicle associated fibroblasts differ not only topographically, but also functionally. Human skin has a number of particular characteristics that are different from murine skin. This should be taken into account in experimental procedures. Dermal cells react differently to skin wounding, remodel the extracellular matrix in their own manner, and convert to myofibroblasts to different extents. Recent studies indicate a special role of papillary fibroblasts in the favorable outcome of wound healing and epithelial-mesenchyme interactions. Neofolliculogenesis can substantially reduce scarring. The role of hair follicle mesenchyme cells in skin repair and possible therapeutic applications is discussed. Participation of dermal cell types in wound healing is described, with the addition of possible mechanisms underlying different outcomes in embryonic and adult tissues in the context of cell population characteristics and extracellular matrix composition and properties. Dermal white adipose tissue involvement in wound healing is also overviewed. Characteristics of myofibroblasts and their activity in scar formation is extensively discussed. Cellular mechanisms of scarring and possible ways for its prevention are highlighted. Data on keloid cells are provided with emphasis on their specific characteristics. We also discuss the contribution of tissue tension to the scar formation as well as the criteria and effectiveness of skin substitutes in skin reconstruction. Special attention is given to the properties of skin substitutes in terms of cell composition and the ability to prevent scarring.

scholarly journals Wound Healing Versus Regeneration: Role of the Tissue Environment in Regenerative Medicine

MRS Bulletin ◽  
2010 ◽  
Vol 35 (8) ◽  
pp. 597-606 ◽  
Author(s):  
Anthony Atala ◽  
Darrell J. Irvine ◽  
Marsha Moses ◽  
Sunil Shaunak
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Regenerative Medicine ◽  
Tissue Regeneration ◽  
Normal Tissue ◽  
Disease Process ◽  
Scar Formation ◽  
The Body ◽  
Mechanistic Basis

AbstractOne of the major challenges in the field of regenerative medicine is how to optimize tissue regeneration in the body by therapeutically manipulating its natural ability to form scar at the time of injury or disease. It is often the balance between tissue regeneration, a process that is activated at the onset of disease, and scar formation, which develops as a result of the disease process that determines the ability of the tissue or organ to be functional. Using biomaterials as scaffolds often can provide a “bridge” for normal tissue edges to regenerate over small distances, usually up to 1 cm. Larger tissue defect gaps typically require both scaffolds and cells for normal tissue regeneration to occur without scar formation. Various strategies can help to modulate the scar response and can potentially enhance tissue regeneration. Understanding the mechanistic basis of such multivariate interactions as the scar microenvironment, the immune system, extracellular matrix, and inflammatory cytokines may enable the design of tissue engineering and wound healing strategies that directly modulate the healing response in a manner favorable to regeneration.

scholarly journals Invasive Techniques in Scar Management: Skin Substitutes

2020 ◽  
pp. 317-323
Author(s):  
F. W. Timmermans ◽  
E. Middelkoop
Keyword(s):  
Wound Healing ◽  
Scar Formation ◽  
Wound Management ◽  
Skin Substitutes ◽  
Current State ◽  
Scar Management ◽  
Scar Quality ◽  
Engineered Skin Substitutes ◽  
Invasive Techniques

AbstractIn the last decades, skin substitutes have emerged as an important innovation in improving scar quality. They can be applied during the initial wound management but also during scar reconstruction procedures. This chapter provides an overview on the development, current state, and future of cell-seeded and tissue-engineered skin substitutes. We will discuss some of the most important varieties of skin substitutes in the context of scar formation and wound healing.

scholarly journals Role of periostin in skin wound healing and pathologic scar formation

2020 ◽  
Vol 133 (18) ◽  
pp. 2236-2238
Author(s):  
Shi-Lu Yin ◽  
Ze-Lian Qin ◽  
Xin Yang
Keyword(s):  
Wound Healing ◽  
Skin Wound ◽  
Scar Formation ◽  
Skin Wound Healing

scholarly journals LncRNA XIST promotes extracellular matrix synthesis, proliferation and migration by targeting miR-29b-3p/COL1A1 in human skin fibroblasts after thermal injury

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Wei Cao ◽  
Youping Feng
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Western Blot ◽  
Thermal Injury ◽  
Human Skin Fibroblasts ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Long noncoding RNAs (lncRNAs) have been reported to be associated with dermis process during burn wound healing. This study aimed to investigate the role of lncRNA X-inactive specific transcript (XIST) in human skin fibroblasts (HSF) and extracellular matrix (ECM) as well as the regulatory network of XIST/microRNA-29b-3p (miR-29b-3p)/collagen 1 alpha 1 (COL1A1). Methods The wound samples were collected from 25 patients with deep partial thickness burn at day 5 after burn. The thermal injured model was established using HSF cells. The expressions of XIST, miR-29b-3p and COL1A1 were measured by quantitative real-time polymerase chain reaction and western blot. ECM synthesis, cell proliferation and migration were detected by western blot, cell counting kit-8 and trans-well assays, respectively. The interaction between miR-29b-3p and XIST or COL1A1 was explored by bioinformatics analysis and luciferase reporter assay. Results The expressions of XIST and COL1A1 were enhanced but miR-29b-3p expression was decreased after thermal injury. XIST overexpression promoted ECM synthesis, cell proliferation and migration in thermal injured HSF cells. However, XIST knockdown played an opposite effect. miR-29b-3p overexpression inhibited ECM synthesis, cell proliferation and migration, which was reversed by XIST. COL1A1 silence suppressed ECM synthesis, cell proliferation and migration by miR-29b-3p targeting. Moreover, COL1A1 up-regulation weakened the effect of XIST silence on ECM synthesis and HSF cell function. Conclusion XIST promoted ECM synthesis, cell proliferation and migration by sponging miR-29b-3p and targeting COL1A1 in HSF cells after thermal injury, indicating the promoting role of XIST in wound healing.

The extracellular matrix of lip wounds in fetal, neonatal and adult mice

Development ◽  
1991 ◽  
Vol 112 (2) ◽  
pp. 651-668
Author(s):  
D.J. Whitby ◽  
M.W. Ferguson
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Cell Migration ◽  
Inflammatory Response ◽  
Cell Function ◽  
Chondroitin Sulphate ◽  
Scar Formation ◽  
Collagen Types ◽  
Cellular Mechanisms ◽  
Collagen Formation

Wound healing in the fetus occurs rapidly, by a regenerative process and without an inflammatory response, resulting in complete restitution of normal tissue function. By contrast, in the adult, wounds heal with scar formation, which may impair function and inhibit further growth. The cellular mechanisms underlying these differing forms of wound healing are unknown but the extracellular matrix (ECM), through its effects on cell function, may play a key role. We have studied the ECM in upper lip wounds of adult, neonatal and fetal mice at days 14, 16 and 18 of gestation. The spatial and temporal distribution of collagen types I, III, IV, V and VI, fibronectin, tenascin, laminin, chondroitin and heparan sulphates were examined immunohistochemically. Results from the fetal groups were essentially similar whilst there were distinct differences between fetus, neonate and adult. Fibronectin was present at the surface of the wound in all groups at 1 h post-wounding. Tenascin was also present at the wound surface but the time at which it was first present differed between fetus (1 h), neonate (12 h) and adult (24 h). The time of first appearance paralleled the rate of wound healing which was most rapid in the fetus and slowest in the adult. Tenascin inhibits the cell adhesion effect of fibronectin and during development the appearance of tenascin correlates with the initiation of cell migration. During wound healing the appearance of tenascin preceded cell migration and the rapid closure of fetal wounds may be due to the early appearance of tenascin in the wound. Collagen types I, III, IV, V and VI were present in all three wound groups but the timing and pattern of collagen deposition differed, with restoration of the normal collagen pattern in the fetus and a scar pattern in the adult. This confirms that lack of scarring in fetal wounds is due to the organisation of collagen within the wound and not simply lack of collagen formation. The distribution of chondroitin sulphate differed between normal fetal and adult tissues and between fetal and adult wounds. Its presence in the fetal wound may alter collagen fibril formation. No inflammatory response was seen in the fetal wounds. The differences in the ECM of fetal and adult wounds suggests that it may be possible to alter the adult wound so that it heals by a fetal-like process without scar formation, loss of tissue function or restriction of growth.

scholarly journals Estrogen promotes cutaneous wound healing via estrogen receptor β independent of its antiinflammatory activities

2010 ◽  
Vol 207 (9) ◽  
pp. 1825-1833 ◽  
Author(s):  
Laura Campbell ◽  
Elaine Emmerson ◽  
Faith Davies ◽  
Stephen C. Gilliver ◽  
Andre Krust ◽  
...  
Keyword(s):  
Wound Healing ◽  
Antiinflammatory Activity ◽  
Hormone Replacement ◽  
Skin Wound ◽  
The Body ◽  
Estrogen Replacement ◽  
Skin Wound Healing ◽  
Skin Repair ◽  
Increased Risk

Post-menopausal women have an increased risk of developing a number of degenerative pathological conditions, linked by the common theme of excessive inflammation. Systemic estrogen replacement (in the form of hormone replacement therapy) is able to accelerate healing of acute cutaneous wounds in elderly females, linked to its potent antiinflammatory activity. However, in contrast to many other age-associated pathologies, the detailed mechanisms through which estrogen modulates skin repair, particularly the cell type–specific role of the two estrogen receptors, ERα and ERβ, has yet to be determined. Here, we use pharmacological activation and genetic deletion to investigate the role of both ERα and ERβ in cutaneous tissue repair. Unexpectedly, we report that exogenous estrogen replacement to ovariectomised mice in the absence of ERβ actually delayed wound healing. Moreover, healing in epidermal-specific ERβ null mice (K14-cre/ERβL2/L2) largely resembled that in global ERβ null mice. Thus, the beneficial effects of estrogen on skin wound healing are mediated by epidermal ERβ, in marked contrast to most other tissues in the body where ERα is predominant. Surprisingly, agonists to both ERα and ERβ are potently antiinflammatory during skin repair, indicating clear uncoupling of inflammation and overall efficiency of repair. Thus, estrogen-mediated antiinflammatory activity is not the principal factor in accelerated wound healing.

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