Mechanisms underlying cytokine-mediated cell-fate regulation in the nervous system

Kinichi Nakashima, Tetsuya Taga

Research output: Contribution to journalArticle

66 Citations (Scopus)

Abstract

Neurons, astrocytes, and oligodendrocytes, the three major cell types in the nervous system, are generated from common neural stem cells during development. Recent studies have provided evidence that neural stem cells are preserved in the adult brain, where, until recently, neurogenesis had not been considered to take place. The mechanisms that govern the fate of neural stem-cell determination have yet to be clarified. It is becoming apparent that soluble protein mediators referred to as cytokines play critical roles in cell-fate determination. For instance, bone morphogenetic proteins (BMrs) alter the fate of developing brain cells from a neurogenic differentiation to an astrocytic one. Different types of cytokines sometimes cooperate to modulate differentiation. For example, the interleukin-6 (IL-6) family cytokines and the BMP family cytokines act in synergy to elaborate astrocyte differentiation. In this review, we focus on recent progress that addresses the molecular mechanisms whereby cytokines regulate the fate of cells in neural lineages. We also discuss possible clinical applications of these findings to minimize the undesirable gliogenesis that occurs after neural stem-cell implantation and nerve injury.

Original languageEnglish
Pages (from-to)233-244
Number of pages12
JournalMolecular Neurobiology
Volume25
Issue number3
DOIs
Publication statusPublished - Jan 1 2002
Externally publishedYes

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Neural Stem Cells
Nervous System
Cytokines
Astrocytes
Bone Morphogenetic Proteins
Neurogenesis
Oligodendroglia
Brain
Interleukin-6
Neurons
Wounds and Injuries
Proteins

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience

Cite this

Mechanisms underlying cytokine-mediated cell-fate regulation in the nervous system. / Nakashima, Kinichi; Taga, Tetsuya.

In: Molecular Neurobiology, Vol. 25, No. 3, 01.01.2002, p. 233-244.

Research output: Contribution to journalArticle

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