Effects of dexamethasone on cell sheet-based tissue engineering of mesenchymal stem cells for the regeneration of bone and cartilage tissues
Scaffold-free Tissue Engineering, specifically Cell Sheet Engineering, has been gaining traction due to the preserved extracellular matrix and vital supporting proteins within the cell sheet that can improve physiological imitation and overcome the limitations of conventional scaffolds. However,...
Saved in:
Main Author: | |
---|---|
Other Authors: | |
Format: | Final Year Project |
Language: | English |
Published: |
2017
|
Subjects: | |
Online Access: | http://hdl.handle.net/10356/71948 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Institution: | Nanyang Technological University |
Language: | English |
Summary: | Scaffold-free Tissue Engineering, specifically Cell Sheet Engineering, has been
gaining traction due to the preserved extracellular matrix and vital supporting proteins
within the cell sheet that can improve physiological imitation and overcome the
limitations of conventional scaffolds. However, there has been limited progress in the
regeneration of 3D tissues by this technique. In this study, we aim to study the impact of
culturing human bone marrow derived mesenchymal stem cell sheets with
dexamethasone on the subsequent induced osteogenesis and chondrogenesis. It was found
that dexamethasone-treated cell sheets resulted in lower cell proliferation, enhanced
calcium deposition and the upregulation of bone marker ALP and cartilage markers
AGG, COL1 and COL2 during induced differentiation. These findings suggest the
augmented osteogenic and chondrogenic properties by the dexamethasone-treated MSCs
and hence, be able to facilitate the regeneration of 3D tissues. Findings from this study
could influence future studies to examine the neural differentiation capacity of
dexamethasone-treated MSCs due to the consistent upregulation of ALP involved in the
development of the nervous system and the possible synergy from other additives that
can increase the gene expression of other bone markers or reduce the production of
fibrocartilage marker COL1. |
---|