Loureirin B inhibits fibroblast proliferation and extracellular matrix deposition in hypertrophic scar via TGF-β/Smad pathway

2015 ◽  
Vol 24 (5) ◽  
pp. 355-360 ◽  
Author(s):  
Xiaozhi Bai ◽  
Ting He ◽  
Jiaqi Liu ◽  
Yunchuan Wang ◽  
Lei Fan ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Hypertrophic Scar ◽  
Fibroblast Proliferation ◽  
Smad Pathway ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
Loureirin B

Hsa-miR-425-5p Inhibits Hypertrophic Scar Formation Through Suppressing the Growth of Human Hypertrophic Scar Fibroblasts and Extracellular Matrix Deposition by Targeting Smad2

2020 ◽  
Vol 10 (3) ◽  
pp. 352-359
Author(s):  
Pengju Fan ◽  
Zhen Li ◽  
Wuyuan Tan ◽  
Man Fang
Keyword(s):  
Extracellular Matrix ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Hypertrophic Scar ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Matrix Deposition ◽  
Qrt Pcr ◽  
Apoptosis Protein ◽  
Extracellular Matrix Deposition

The current study aimed to explore the role and mechanism of microRNA-425-5p (miR-425-5p) in hypertrophic scar (HS) development. Firstly, we used reverse transcription-quantitative polymerase chain reaction (qRT-PCR)to detect the expression of miR-425-5p in human hypertrophic scar fibroblasts (hHSFs) and HS tissues. qRT-PCR assay showed that miR-425-5p level significantly down-regulated in HS tissues and hHSFs. Next, we performed TargetScan and dual-luciferase reporter assay to predict and verify Smad2 was the target gene of miR-425-5p. In order to determine the role of miR-425-5p in HS formation, miR-425-5p was over-expressed or knockdown in hHSFs through transfection with miR-425-5p mimic or miR-425-5p inhibitor. CCK-8 assay and cell apoptosis analysis were carried out to measure cell viability and apoptosis. Protein expression was assessed by Western blotting. The findings indicated that miR-425-5p mimic transfection inhibited cell viability, promoted cell apoptosis and repressed Smad2, Col I, and Col III expression in hHSFs. Notably, the transfection of Smad2-plasmid eliminated the effects of miR-425-5p mimic on hHSFs. However, miR-425-5p inhibitor transfection had opposite effects on hHSFs, and were eliminated by the transfection of Smad2-siRNA. In conclusion, these findings suggested that miR-425-5p inhibited the hHSFs viability, induced hHSFs apoptosis and repressed extracellular matrix deposition of hHSFs through regulating Smad2. Therefore, miR-425-5p might be a novel therapeutic target for HS treatment.

scholarly journals A three-dimensional in vitro dynamic micro-tissue model of cardiac scar formation

2018 ◽  
Vol 10 (3) ◽  
pp. 174-183 ◽  
Author(s):  
Paola Occhetta ◽  
Giuseppe Isu ◽  
Marta Lemme ◽  
Chiara Conficconi ◽  
Philipp Oertle ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Three Dimensional ◽  
Scar Formation ◽  
Fibroblast Proliferation ◽  
Tissue Model ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
Mechanical Stretching

Our 3D-scar-on-a-chip model resembles fibroblast proliferation and activation, extracellular matrix deposition and stiffening upon application of only cyclic mechanical stretching.

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.

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....

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