scholarly journals Redox Signaling in Diabetic Wound Healing Regulates Extracellular Matrix Deposition

2017 ◽  
Vol 27 (12) ◽  
pp. 823-838 ◽  
Author(s):  
Britta Kunkemoeller ◽  
Themis R. Kyriakides
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Redox Signaling ◽  
Diabetic Wound ◽  
Matrix Deposition ◽  
Diabetic Wound Healing ◽  
Extracellular Matrix Deposition

scholarly journals Insulin-Containing Wound Dressing Promotes Diabetic Wound Healing Through Stabilizing HIF-1α

2020 ◽  
Vol 8 ◽  
Author(s):  
Peilang Yang ◽  
Di Wang ◽  
Yan Shi ◽  
Mingzhong Li ◽  
Min Gao ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Wound Dressing ◽  
Control Group ◽  
Unstable State ◽  
Diabetic Wound ◽  
Diabetic State ◽  
Matrix Deposition ◽  
Diabetic Wound Healing

HIF-1α is seen as a major regulator during wound healing and controls many wound healing processes, such as angiogenesis, extracellular deposition, and reepithelialization. A diabetic state plays a vicious effect on wound healing, and the destabilization of HIF-1α is a non-negligible factor. Insulin-loaded silk fibroin microparticles were prepared to release insulin by covering the wounds, and this material was proven to promote wound healing in both in vitro and in vivo studies. In this work, we found that this insulin-containing wound dressing could accelerate diabetic wound healing by promoting reepithelialization, angiogenesis, and extracellular matrix, especially collagen deposition. Meanwhile, HIF-1α was stable and accumulated in insulin-containing dressing to group wound cells, which was significantly unstable in the control group. In further studies, we showed that methylglyoxal (MGO), the main form of advanced glycation end products (AGEs), accumulated significantly and caused the destabilization of HIF-1α in the diabetic state. Insulin could alleviate the MGO-induced HIF-1α unstable state and promote HIF-1α target gene expression and its downstream biological effect such as angiogenesis and wound extracellular matrix deposition.

A multifunctional substance P-conjugated chitosan hydrochloride hydrogel accelerates full-thickness wound healing by enhancing synchronized vascularization, extracellular matrix deposition, and nerve regeneration

2021 ◽  
Author(s):  
Hao Li ◽  
Mengna Li ◽  
Pei Liu ◽  
Kai-Yang Wang ◽  
Haoyu Fang ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Full Thickness ◽  
Matrix Deposition ◽  
Chitosan Hydrochloride ◽  
Reconstructive Microsurgery ◽  
Extracellular Matrix Deposition ◽  
Advanced Biomaterials ◽  
Native Skin ◽  
Full Thickness Wound

Due to the native skin limitations and the complexity of reconstructive microsurgery, advanced biomaterials are urgently required to promote wound healing for severe skin defects caused by accidents and disasters....

scholarly journals Hyaluronan in intestinal homeostasis and inflammation: implications for fibrosis

2011 ◽  
Vol 301 (6) ◽  
pp. G945-G949 ◽  
Author(s):  
Carol A. de la Motte
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Intestinal Inflammation ◽  
Cellular Mechanisms ◽  
Matrix Component ◽  
Matrix Deposition ◽  
Fibrotic Tissue ◽  
Myofibroblast Phenotype ◽  
Extracellular Matrix Deposition ◽  
Chronic Intestinal Inflammation

The causes of fibrosis, or the inappropriate wound healing, that follows chronic intestinal inflammation are not well defined and likely involve the contributions of multiple cellular mechanisms. As other articles in this series confirm, inflammatory cytokines clearly play a role in driving cell differentiation to the myofibroblast phenotype, promoting proliferation and extracellular matrix deposition that are characteristic of fibrotic tissue. However, controlling the balance of cytokines produced and process of myofibroblast differentiation appears to be more complex. This review considers ways in which hyaluronan, an extracellular matrix component that is remodeled during the progression of colitis, may provide indirect as well as direct cues that influence the balancing act of intestinal wound healing.

A Mussel-Inspired Extracellular Matrix-Mimicking Composite Scaffold for Diabetic Wound Healing

2020 ◽  
Vol 3 (7) ◽  
pp. 4052-4061 ◽  
Author(s):  
Yuqi Jiang ◽  
You Li ◽  
Jiankai Li ◽  
Yiming Han ◽  
Pengju Zhang ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Composite Scaffold ◽  
Diabetic Wound ◽  
Diabetic Wound Healing

Cross-linked antifouling polysaccharide hydrogel coating as extracellular matrix mimics for wound healing

2017 ◽  
Vol 5 (16) ◽  
pp. 2989-2999 ◽  
Author(s):  
Yuqin Tang ◽  
Xueqin Cai ◽  
Yingying Xiang ◽  
Yu Zhao ◽  
Xinge Zhang ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Diabetic Wound ◽  
Natural Polysaccharide ◽  
Diabetic Wound Healing ◽  
Polysaccharide Hydrogel ◽  
Hydrogel Coating

Antifouling hydrogel coating based on natural polysaccharide could effectively promote diabetic wound healing.

scholarly journals A Novel Composite Hydrogel Composed of Formic Acid-Decellularized Pepsin-Soluble Extracellular Matrix Hydrogel and Sacchachitin Hydrogel as Wound Dressing to Synergistically Accelerate Diabetic Wound Healing

Pharmaceutics ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 538
Author(s):  
Chien-Ming Hsieh ◽  
Weu Wang ◽  
Ying-Hsuan Chen ◽  
Pu-Sheng Wei ◽  
Yu-Hsuan Liu ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Formic Acid ◽  
Cell Viability ◽  
Hair Follicles ◽  
Composite Hydrogel ◽  
Sweat Glands ◽  
Diabetic Wound ◽  
Porcine Skin ◽  
Diabetic Wound Healing

Extracellular matrix (ECM) hydrogel can create a favorable regenerative microenvironment and act as a promising dressing for accelerating the healing of diabetic wound. In this study, a simple and effective decellularization technique was developed and optimized to obtain acellular extracellular matrix (aECM) from porcine skin. It was found that decellularization at 30% formic acid for 72 h effectively decellularized porcine skin while retaining >75% collagen and ~37% GAG in the aECM with no presence of nuclei of cellular remnants. aECM hydrogel was fabricated by digesting aECM with pepsin in various acidic solutions (0.1 N HCl, glycolic acid (GA) and 2-pyrrolidone-5-carboxylic acid (PCA)) and then treated with a pH-controlled neutralization and temperature-controlled gelation procedure. Based on physical characterizations, including SDS-PAGE, rheological analysis and SEM analysis, aECMHCl hydrogels fabricated at 25 mg/mL in 0.1 N HCl were selected. Four polymeric ECM-mimic hydrogels, including sacchachitin (SC), hyaluronic acid (HA) and chitosan (CS) and three composite hydrogels of combining SC either with aECMHCl,25 (aECMHCl/SC), HA (HA/SC) or CS (SC/CS) were prepared and evaluated for WS-1 cell viability and wound-healing effectiveness. Cell viability study confirmed that no hydrogel dressings possessed any toxicity at all concentrations examined and ECMHCl, HA and ECMHCl/SC at higher concentrations (>0.05%) induced statistically significant proliferation. Diabetic wound healing study and histological examinations revealed that ECMHCl/SC hydrogel was observed to synergistically accelerate wound healing and ultimately stimulated the growth of hair follicles and sweat glands in the healing wound indicating the wound had healed as functional tissues. The results support the great potential of this newly produced ECMHCl/SC composite hydrogel for healing and regeneration of diabetic wounds.

scholarly journals The molecular basis of hypertrophic scars

2016 ◽  
Vol 4 ◽  
pp. 1-12 ◽  
Author(s):  
Zhensen Zhu ◽  
Jie Ding ◽  
Edward E. Tredget
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Growth Factors ◽  
Molecular Basis ◽  
Hypertrophic Scars ◽  
Deep Dermis ◽  
Matrix Deposition ◽  
Prevention And Treatment ◽  
Extracellular Matrix Deposition ◽  
Current Advance

Abstract Hypertrophic scars (HTS) are caused by dermal injuries such as trauma and burns to the deep dermis, which are red, raised, itchy and painful. They can cause cosmetic disfigurement or contractures if craniofacial areas or mobile region of the skin are affected. Abnormal wound healing with more extracellular matrix deposition than degradation will result in HTS formation. This review will introduce the physiology of wound healing, dermal HTS formation, treatment and difference with keloids in the skin, and it also review the current advance of molecular basis of HTS including the involvement of cytokines, growth factors, and macrophages via chemokine pathway, to bring insights for future prevention and treatment of HTS.

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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