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Mesenchymal Stem Cells

Mesenchymal Stem Cells

Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into most connective tissue cell types, except for hematopoietic cells, depending upon the source of MSCs. For example, bone-marrow-derived MSCs (BM-MSCs) can differentiate into osteocytes, hepatocytes, and pancreatic and neuronal cells. MSCs can be isolated from various sources such as bone marrow, placenta, adipose tissue, teeth, and Wharton’s jelly, a gelatinous substance in the umbilical cord. The ease of their...

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Updated: Jun 29, 2025

Isolation of Human Mesenchymal Stem Cells and their Cultivation on the Porous Bone Matrix

Isolation of Human Mesenchymal Stem Cells and their Cultivation on the Porous Bone Matrix

Published on: February 9, 2015

High glucose microenvironment and human mesenchymal stem cell behavior.

Muhammad Abdul Mateen¹, Nouralsalhin Alaagib¹, Khawaja Husnain Haider²

¹Basic Sciences, Sulaiman AlRajhi University, AlQaseem 52736, Saudi Arabia.

World Journal of Stem Cells

|April 5, 2024

Summary

This summary is machine-generated.

High glucose negatively impacts mesenchymal stem cells (MSCs) by disrupting signaling pathways and mitochondrial function, leading to reduced survival. Restoring mitochondrial membrane potential (MtMP) may improve MSC function in diabetic patients.

Keywords:

Adipose tissue Apoptosis Bioenergetics Cell survival Cell therapy Hyperglycemia Mesenchymal stem cells Mitochondria Stem cells

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Last Updated: Jun 29, 2025

Isolation of Human Mesenchymal Stem Cells and their Cultivation on the Porous Bone Matrix

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Area of Science:

Biomedical Sciences
Cell Biology
Metabolic Research

Background:

High glucose (HG) conditions and hyperglycemia impair mesenchymal stem cell (MSC) survival and function.
This impairment involves dysregulation of mammalian target of rapamycin (mTOR)-phosphoinositide 3-kinase (PI3K)-Akt signaling pathways.
Cellular dysfunction is exacerbated by mitochondrial malfunctioning, including defective mitochondrial membrane potential (MtMP) and reduced ATP production.

Discussion:

HG exposure leads to mitochondrial electron transport chain disruption, altering the NAD+/NADH ratio and increasing oxidative stress.
Mitochondrial homeostasis is further perturbed by altered membrane polarity and reduced mitochondrial mass.
These ultrastructural and functional changes in mitochondria compromise MSC bioenergetics and ATP generation.

Key Insights:

HG dysregulates critical signaling pathways and impairs mitochondrial function in MSCs.
Defective mitochondrial membrane potential (MtMP) is a key factor in reduced ATP production and cell survival under high glucose.
Altered mitochondrial NAD+/NADH redox state contributes significantly to decreased MSC survival in hyperglycemic conditions.

Outlook:

MSCs from hyperglycemic donors require cautious use in cell-based therapies due to poor survival and proliferation rates.
Targeting and rectifying the loss of mitochondrial membrane potential (MtMP) presents a promising therapeutic strategy.
Restoring normal MSC function in hyperglycemic patients through mitochondrial interventions is a key area for future research.