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Updated: Jun 23, 2026

Generation of Human Neurons and Oligodendrocytes from Pluripotent Stem Cells for Modeling Neuron-Oligodendrocyte Interactions

Generation of Human Neurons and Oligodendrocytes from Pluripotent Stem Cells for Modeling Neuron-Oligodendrocyte Interactions

Published on: November 9, 2020

Bone marrow stromal cells increase oligodendrogenesis after stroke.

Jing Zhang¹, Yi Li, Zheng Gang Zhang

¹Department of Neurology, Henry Ford Health System, Detroit, Michigan, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism

|April 23, 2009

Summary

Bone marrow stromal cells (BMSCs) promote recovery after stroke by stimulating oligodendrocyte production. This occurs through activating the Sonic hedgehog (Shh)/Gli1 pathway, crucial for brain repair.

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Area of Science:

Neuroscience
Regenerative Medicine
Cell Biology

Background:

Oligodendrocytes are vulnerable to ischemic injury, impacting brain function.
The Sonic hedgehog (Shh) pathway, with Gli1 as its effector, plays a key role in generating new oligodendrocytes.
Bone marrow stromal cells (BMSCs) show promise in improving functional recovery after stroke.

Purpose of the Study:

To investigate the impact of BMSC treatment on oligodendrogenesis and Shh/Gli1 pathway activation following stroke in a rat model.
To determine if BMSCs stimulate the production of oligodendrocytes and myelin in the affected brain regions.
To elucidate the role of the Shh/Gli1 pathway in mediating the effects of BMSCs post-stroke.

Main Methods:

Middle cerebral artery occlusion (MCAo) model in rats to induce stroke.
BMSC transplantation (3 x 10(6) cells) initiated 1 day post-MCAo.
Immunohistochemistry and gene expression analysis (mRNA and protein) of oligodendrocytes, myelin, Shh, and Gli1 at 2 and 14 days post-MCAo.
In vitro study using N20.1 oligodendrocyte precursor cells treated with BMSCs and a Shh inhibitor (cyclopamine).

Main Results:

BMSC treatment significantly increased the number of oligodendrocytes (O4+), myelin basic protein (MBP) expression, and oligodendrocyte progenitor cells (BrdU+, NG2+, BrdU+-NG2+) in the stroke-affected brain.
BMSC administration upregulated both mRNA and protein expression of Shh and Gli1 in the ipsilateral hemisphere post-MCAo.
In vitro, BMSCs enhanced N20.1 cell proliferation and Gli1 expression, effects blocked by cyclopamine, confirming Shh pathway involvement.

Conclusions:

BMSC treatment effectively stimulates oligodendrogenesis and remyelination after ischemic stroke in rats.
The therapeutic benefits of BMSCs in stroke appear to be mediated, at least in part, by the activation of the Shh/Gli1 signaling pathway.
Targeting the Shh/Gli1 pathway with BMSCs represents a potential therapeutic strategy for stroke recovery.