eLife

Protein helps precursor cells mature in aged mice

In aged mice with spinal cord injuries, boosting the protein increased the maturation of precursor cells into nerve-insulating cells inside tissue lesions.

Paper by Tanay Ghosh, Roey Baror, Chao Zhao, +4 more authorsRobin J.M. Franklin · Wellcome/MRC Cambridge Stem Cell Institute
Figure 1. Dynamic regulation of genes during oligodendrocyte lineage progression.
Open the figure at full size
Figure 1. Dynamic regulation of genes during oligodendrocyte lineage progression.Dynamic regulation of genes during oligodendrocyte lineage progression.Ghosh et al.
Studied:
Experiments in aged mice with spinal cord demyelination, against Gfp-only vector-treated aged mice
What changed:
Aged mice given Bcl11a had more maturing cells in spinal cord lesions than mice given the control vector
The catch:
Cell maturation was inferred from Plp1 expression rather than direct measurement of myelin formation
In the record:
One of 10 papers on BCL11A on record: 2 with results in people, 4 in animals.
Why it’s aging research:
It studies organisms or tissues that aged naturally.

Editor of record: Boris Djordjevic · AgingResearch.News

Follow @agingbrief

In experiments in oligodendrocyte progenitor cells and aged mice, researchers investigated why aging reduces these cells’ ability to mature. In the central nervous system, these precursor cells mature into oligodendrocytes, cells that produce myelin, the insulation around nerve fibers. Aging reduces this maturation capacity. Using a computational tool to compare gene activity in young and aged precursor cells, the researchers identified Bcl11a, a protein that regulates gene activity, as a potential master regulator whose production declines with age.

In progenitor cells, inhibiting Bcl11a reduced maturation into oligodendrocytes. Increasing Bcl11a production in aged progenitor cells enhanced their maturation without affecting cell division. In aged mice with injuries that damaged myelin in the spinal cord’s white matter, increasing Bcl11a production increased progenitor cell maturation within the damaged areas.

Why it matters

As the central nervous system ages, progenitor cells become less able to mature into myelin-producing cells, impairing repair after injury. The study addresses whether restoring a regulatory protein that declines with age can restore this maturation capacity.

Caveats

The reported increase in cell maturation does not establish functional nerve repair or behavioral recovery. The spinal cord injury findings came from aged mice, not people.

Comments

Be the first to comment.