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

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....

Download Full-text

Hyaluronan in intestinal homeostasis and inflammation: implications for fibrosis

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00063.2011 ◽

2011 ◽

Vol 301 (6) ◽

pp. G945-G949 ◽

Cited By ~ 45

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.

Download Full-text

The molecular basis of hypertrophic scars

Burns & Trauma ◽

10.1186/s41038-015-0026-4 ◽

2016 ◽

Vol 4 ◽

pp. 1-12 ◽

Cited By ~ 36

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.

Download Full-text

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2020-0219 ◽

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.

Download Full-text