Citation

Sater AP, Rael LT, Tanner AH, Lieser MJ, Acuna DL, Mains CW, Bar-Or D. Clin. Chim. Acta 2018; 482: 149-154.

Affiliation

Trauma Research Dept, Swedish Medical Center, Englewood, CO 80113, United States; St. Anthony Hospital, Lakewood, CO 80228, United States; Medical City Plano, Plano, TX 75075, United States; Penrose Hospital, Colorado Springs, CO 80907, United States; Research Medical Center, Kansas City, MO 64132, United States; Wesley Medical Center, Wichita, KS 67214, United States. Electronic address: dbaror@ampiopharma.com.

Copyright

(Copyright © 2018, Elsevier Publishing)

DOI

10.1016/j.cca.2018.04.008

PMID

29627488

Abstract

Within the first few hours of a traumatic brain injury, the activity of extracellular matrix degradative enzymes increases. As a result, the blood brain barrier becomes disrupted as secondary white matter injury increases. Anoikis, a form of apoptosis, results from cells detaching from the extracellular matrix leading to cell death. This "homelessness" (anoikis) of cells hinders recovery progression, exacerbating brain injury while disrupting synaptic plasticity and other central nervous system functions. Here, we discuss the current knowledge of molecular pathways and proteins involved in both the activation and inhibition of anoikis.

Copyright © 2018. Published by Elsevier B.V.

Language: en

Keywords

Anoikis; Apoptosis; Blood-brain barrier; Caspase; Matrix metalloproteinase; Traumatic brain injury