2015 journal article

MARCKS-dependent mucin clearance and lipid metabolism in ependymal cells are required for maintenance of forebrain homeostasis during aging

AGING CELL, 14(5), 764–773.

By: N. Muthusamy n, L. Sommerville n, A. Moeser n, D. Stumpo *, P. Sannes n, K. Adler n, P. Blackshear *, J. Weimer *, H. Ghashghaei  n

author keywords: aging; barrier function; Clca3; cerebral cortex; ependymal cells; lipid droplets; mucin; oxidative stress
MeSH headings : Aging / metabolism; Animals; Ependyma / cytology; Ependyma / metabolism; Homeostasis; Intracellular Signaling Peptides and Proteins / deficiency; Intracellular Signaling Peptides and Proteins / metabolism; Lipid Metabolism; Membrane Proteins / deficiency; Membrane Proteins / metabolism; Mice; Mucins / metabolism; Myristoylated Alanine-Rich C Kinase Substrate; Oxidative Stress; Prosencephalon / metabolism
TL;DR: It is demonstrated that metabolic and barrier functions in ECs decline significantly during aging in mice, and this work constitutes a conceptually new paradigm in the potential role of ECs in the initiation of various conditions and diseases in the aging brain. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Source: Web Of Science
Added: August 6, 2018

SummaryEpendymal cells (ECs) form a barrier responsible for selective movement of fluids and molecules between the cerebrospinal fluid and the central nervous system. Here, we demonstrate that metabolic and barrier functions in ECs decline significantly during aging in mice. The longevity of these functions in part requires the expression of the myristoylated alanine‐rich protein kinase C substrate (MARCKS). Both the expression levels and subcellular localization of MARCKS in ECs are markedly transformed during aging. Conditional deletion of MARCKS in ECs induces intracellular accumulation of mucins, elevated oxidative stress, and lipid droplet buildup. These alterations are concomitant with precocious disruption of ependymal barrier function, which results in the elevation of reactive astrocytes, microglia, and macrophages in the interstitial brain tissue of young mutant mice. Interestingly, similar alterations are observed during normal aging in ECs and the forebrain interstitium. Our findings constitute a conceptually new paradigm in the potential role of ECs in the initiation of various conditions and diseases in the aging brain.