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Replicative Cell Senescence

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...

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Related Experiment Video

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Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

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Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype.

Asif Manzoor Khan¹, Alicia A Babcock¹, Hamid Saeed²

¹Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense C, Denmark.

Neurobiology of Aging

|April 21, 2015

Summary

Cellular aging of microglia, induced by telomere shortening in TERC knockout mice, reduced microglial numbers but increased density. These aged microglia exhibited distinct morphology and impaired spatial learning, suggesting aging impacts brain cell function.

Keywords:

Cellular apoptosis Dentate gyrus Global spatial sampling Optical fractionator Replicative senescence Spatial learning

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Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

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Published on: April 13, 2017

Area of Science:

Neuroscience
Cell Biology
Aging Research

Background:

The aging brain is susceptible to neurodegenerative diseases.
Microglia, the brain's immune cells, undergo cellular aging.
Telomere shortening is a hallmark of cellular aging.

Purpose of the Study:

To investigate the impact of telomere shortening-induced cellular aging on microglia.
To analyze the effects of telomerase RNA component (TERC) deficiency on microglial populations and function.

Main Methods:

Utilized TERC knockout (KO) mice to induce telomere shortening and cellular aging.
Employed design-based stereology to quantify microglia in the dentate gyrus.
Assessed microglial morphology, distribution, and expression of markers (CD45, CD68, ferritin).
Evaluated cellular apoptosis and spatial learning in TERC KO mice.

Main Results:

TERC KO mice showed a reduced number of CD11b(+) microglia in the dentate gyrus.
Despite reduced numbers, microglial density increased due to a greater reduction in dentate gyrus volume.
Microglia in TERC KO mice displayed distinct morphology compared to wild-type mice.
TERC KO mice exhibited increased cellular apoptosis and impaired spatial learning.

Conclusions:

Individual microglia show relative resistance to telomerase deficiency under steady-state conditions.
Telomere deficiency leads to reduced microglial numbers but altered morphology and function.
Cellular aging and natural aging may induce distinct changes in microglial phenotype and morphology.