The role of inflammation and extracellular matrix in the wound healing after glaucoma surgery

2014 ◽  
Vol 92 ◽  
pp. 0-0
Author(s):  
H UUSITALO
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Glaucoma Surgery

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.

scholarly journals The Versatile Role of Matrix Metalloproteinase for the Diverse Results of Fibrosis Treatment

Molecules ◽  
2019 ◽  
Vol 24 (22) ◽  
pp. 4188 ◽  
Author(s):  
Hong-Meng Chuang ◽  
Yu-Shuan Chen ◽  
Horng-Jyh Harn
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Cardiovascular Diseases ◽  
De Novo ◽  
Biological Processes ◽  
Tissue Formation ◽  
Ecm Degradation ◽  
Excessive Secretion ◽  
Wound Tissue

Fibrosis is a type of chronic organ failure, resulting in the excessive secretion of extracellular matrix (ECM). ECM protects wound tissue from infection and additional injury, and is gradually degraded during wound healing. For some unknown reasons, myofibroblasts (the cells that secrete ECM) do not undergo apoptosis; this is associated with the continuous secretion of ECM and reduced ECM degradation even during de novo tissue formation. Thus, matrix metalloproteinases (MMPs) are considered to be a potential target of fibrosis treatment because they are the main groups of ECM-degrading enzymes. However, MMPs participate not only in ECM degradation but also in the development of various biological processes that show the potential to treat diseases such as stroke, cardiovascular diseases, and arthritis. Therefore, treatment involving the targeting of MMPs might impede typical functions. Here, we evaluated the links between these MMP functions and possible detrimental effects of fibrosis treatment, and also considered possible approaches for further applications.

The Role of Extracellular Matrix in Corneal Wound Healing

Cornea ◽  
2013 ◽  
Vol 32 ◽  
pp. S43-S45 ◽  
Author(s):  
Osamu Yamanaka ◽  
Takayoshi Sumioka ◽  
Shizuya Saika
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Corneal Wound Healing ◽  
Corneal Wound

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.

The Role of Collagen, Fibronectin, Chondronectin and Laminin in Cell Adhesion

1982 ◽  
Vol 40 ◽  
pp. 102-105
Author(s):  
Hynda K. Kleinman ◽  
George R. Martin
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Blood Cells ◽  
Basement Membranes ◽  
Extracellular Matrices ◽  
Structural Support ◽  
Tissue Organization ◽  
Attachment Proteins ◽  
Surrounding Extracellular Matrix

Most cells other than blood cells interact with extracellular matrices composed of various types of collagens, proteoglycans and a newly described group of glycoproteins termed the attachment proteins. Variations in the composition of the extracellular matrix determine the uniqueness of tissues, such as cartilage, bone, dermis and basement membranes. These matrices have numerous functions, including providing structural support to rigid tissues (cartilage, tooth and bone), regulating the passage of macromolecules (kidney basement membrane), and allowing tissues to stretch (blood vessels and skin). In addition, these matrices have potent influences upon the cells which populate them. The anchorage, growth, differentiation, and motility of the resident cells are all determined by their surrounding extracellular matrix. Such matrices are critically important in embryonic development, tissue organization and wound healing.

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.

p75NTR silencing inhibits proliferation, migration and extracellular matrix deposition of hypertrophic scar fibroblasts by activating autophagy through inhibiting PI3K/Akt/mTOR pathway

2020 ◽  
Author(s):  
Wen Shi ◽  
Yan Wu ◽  
Donghui Bian
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Hypertrophic Scar ◽  
Mtor Pathway ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Inhibitory Effects ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

Hypertrophic scar (HS) results from abnormal wound healing, accompanied by excessive hypercellularity, migration and extracellular matrix (ECM) deposition. Autophagy dysregulation plays crucial roles during HS formation. The overexpressed p75 neurotrophin receptor (p75NTR) in injured skin tissue after wound healing becomes a factor aggravating scar. The study was designed to investigate the role of p75NTR and p75NTR-mediated autophagy in the process of HS. The results revealed that p75NTR expression was significantly upregulated while that of autophagy proteins was downregulated in cicatrix at 3 and 6 months after burn, which was recovered at 12 months. p75NTR silencing inhibited proliferation, migration and ECM deposition of hypertrophic scar fibroblasts (HSF), whereas p75NTR overexpression presented the opposite results. Silencing of p75NTR reduced the expression of PI3K/Akt/mTOR signaling molecules while enhanced that of autophagy proteins. Importantly, PI3K agonist (IGF-1) intervention notably decreased the levels of LC3B II/I and Beclin-1, and restored the inhibitory effects of p75NTR silencing on proliferation, migration and ECM deposition of HSF. Concurrently, autophagy inhibitor 3-methyladenine (3-MA) treatment exhibited the same variation trends with IGF-1. Taken together, these findings demonstrated that p75NTR silencing inhibits proliferation, migration and ECM deposition of HSF by activating autophagy through inhibiting PI3K/Akt/mTOR pathway.

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