Caspase-1-independent Maturation of IL-1β in Ischemic Brain Injury: is there a Role for Gelatinases?

Diana Amantea, Rossella Russo, Michelangelo Certo, Laura Rombolà, Annagrazia Adornetto, Luigi A Morrone, Maria Tiziana Corasaniti, Giacinto Bagetta

Research output: Contribution to journalReview articlepeer-review

8 Citations (Scopus)


Ischemic stroke is a devastating condition primarily caused by reduced blood supply to the brain. Interleukin (IL)-1β is a pro-inflammatory cytokine that plays a pivotal role in the detrimental inflammatory processes that participate to cerebral ischemic damage. After injury, it is produced by distinct cells of the neurovascular unit as an inactive precursor, pro-IL-1β. Although previous studies have suggested that caspase-1 is the main enzyme implicated in the cleavage of pro-IL-1β into the biologically active cytokine, recent work has demonstrated that, under ischemia-reperfusion conditions, other mechanisms may be involved in cytokine maturation. Indeed, we have shown that in rats subjected to transient middle cerebral artery occlusion (MCAo), elevation of IL-1β levels is paralleled by an elevation of gelatinolytic, but not caspase-1 activity in the injured hemisphere and pharmacological inhibition of gelatinases, i.e. matrix metalloproteases (MMP)-2 and MMP-9 prevents cytokine maturation. These findings further support the hypothesis that, under ischemia-reperfusion injury, cerebral elevation of IL-1β occurs via mechanisms other than caspase-1, likely involving gelatinases.

Original languageEnglish
Pages (from-to)729-37
Number of pages9
JournalMini - Reviews in Medicinal Chemistry
Issue number9
Publication statusPublished - 2016


  • Brain Injuries/metabolism
  • Brain Ischemia/metabolism
  • Caspase 1
  • Gelatinases/metabolism
  • Humans
  • Interleukin-1beta/metabolism


Dive into the research topics of 'Caspase-1-independent Maturation of IL-1β in Ischemic Brain Injury: is there a Role for Gelatinases?'. Together they form a unique fingerprint.

Cite this