scholarly journals The Role of Hypoxia in Corneal Extracellular Matrix Deposition and Cell Motility

2019 ◽  
Vol 303 (6) ◽  
pp. 1703-1716 ◽  
Author(s):  
Obianamma E. Onochie ◽  
Anwuli J. Onyejose ◽  
Celeste B. Rich ◽  
Vickery Trinkaus‐Randall
Keyword(s):  
Extracellular Matrix ◽  
Cell Motility ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

scholarly journals Role of Nampt-Sirt6 Axis in Renal Proximal Tubules in Extracellular Matrix Deposition in Diabetic Nephropathy

Cell Reports ◽  
2019 ◽  
Vol 27 (1) ◽  
pp. 199-212.e5 ◽  
Author(s):  
Hirokazu Muraoka ◽  
Kazuhiro Hasegawa ◽  
Yusuke Sakamaki ◽  
Hitoshi Minakuchi ◽  
Takahisa Kawaguchi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Diabetic Nephropathy ◽  
Proximal Tubules ◽  
Renal Proximal Tubules ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

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.

scholarly journals Characterization of the role of Activator Protein 1 signaling pathway on extracellular matrix deposition in uterine leiomyoma

F&S Science ◽  
2020 ◽  
Vol 1 (1) ◽  
pp. 78-89
Author(s):  
Justin Pilgrim ◽  
Jacquel Arismendi ◽  
Anthony DeAngelis ◽  
Terrence Lewis ◽  
Joy Britten ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Signaling Pathway ◽  
Uterine Leiomyoma ◽  
Activator Protein 1 ◽  
Matrix Deposition ◽  
Activator Protein ◽  
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....

Sign in / Sign up

Export Citation Format

Share Document