The Role of Periostin in Brain Injury Caused by Subarachnoid Hemorrhage

Abstract

Aneurysmal subarachnoid hemorrhage (aSAH) causes serious brain injury, and its mechanisms have not been completely unraveled so far. The causative factors for the brain injury initiated by an aneurysm rupture, which is referred to as the early brain injury (EBI), include elevated intracranial pressure, cerebral hypoperfusion, and blood contents that are directly exposed to the brain surface. At Day 4-14 post aSAH, delayed cerebral ischemia (DCI) often develops, which may worsen the neurological outcomes critically. DCI may be a consequence of EBI. Understanding the complex mechanisms underlying the post-aSAH brain injury (EBI and DCI) is, therefore, important in order to improve the neurological outcomes. In addition, several biomarkers possibly associated with EBI, DCI, and neurological outcome have been investigated, although none of these has been conclusive. A matricellular protein periostin has emerged as an important potential contributor to EBI and DCI, and may serve as the biomarker and a therapeutic molecular target for EBI and DCI. In the present report, the possible role of periostin in aSAH has been reviewed.

Osteopontin in post-subarachnoid hemorrhage pathologies

“…Recently, machine learning analyses have been developed and constructed early prediction models for the occurrence of DCI, angiographic cerebrovascular spasm, and delayed cerebral infarct using admission clinical factors and plasma levels of three types of matricellular proteins (OPN-a, periostin, and galectin-3) at post-SAH days one to three in a clinical setting [35]. Periostin and galectin-3 have been implicated in EBI and DCI or delayed cerebral infarction after SAH [36][37][38][39][40][41][42][43][44]. However, a clinical study demonstrated that plasma OPN-a levels at days one to three were also one of the three most important features in all of the three prediction models with high accuracy and sensitivity [35].…”

Clarithromycin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage via Suppressing Periostin-Related Pathways in Mice

“…Periostin is a 90-kDa matricellular protein which is a kind of non-structural, inducible, and multifunctional extracellular matrix protein [1]. In a normal condition, periostin exists at low levels in adult tissues and is upregulated in an injured or inflamed tissue [1,30]. Our previous studies reported that plasma periostin was increased in an acute phase of aneurysmal SAH in clinical settings [8,9].…”

“…Subarachnoid hemorrhage (SAH) remains a poor-outcome cerebrovascular disorder and is associated with secondary neurological disorders and brain damages that proceed after its onset [1,2]. Early brain injury (EBI) is considered to be the main cause of poor outcomes, and begins to occur immediately after aneurysmal rupture, which triggers elevation of intracranial pressure and thereby global cerebral hypoperfusion and ischemia, as well as spreading of blood components into the subarachnoid space [3].…”