Evaluation of serum pannexin-1 as a prognostic biomarker for traumatic brain injury

Ni, Bukao; Cai, Jianping; Lin, Qun; Zheng, Kaihui; Lin, Li; Wu, Jianhua

doi:10.1016/j.cca.2018.11.015

Cited by 3 publications

(3 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The cleaved peptide segments may be released into the serum for detection, and the serum PANX1 concentration is proportional to the activated PANX protein. Relevant studies have shown that serum PANX1 concentration has predictive value for the prognosis of acute supratentorial intracerebral hemorrhage and traumatic brain injury 30 , 31 . Mitophagy served as critical component of mitochondrial quality control by removing damaged/dysfunctional mitochondria from the cell to ensure normal cellular homeostasis and to support cell viability.…”

Section: Discussionmentioning

confidence: 99%

Pannexin 1 targets mitophagy to mediate renal ischemia/reperfusion injury

Su,

Zhang,

Wang

et al. 2023

Commun Biol

View full text Add to dashboard Cite

Renal ischemia/reperfusion (I/R) injury contributes to the development of acute kidney injury (AKI). Kidney is the second organ rich in mitochondrial content next to the heart. Mitochondrial damage substantially contributes for AKI development. Mitophagy eliminates damaged mitochondria from the cells to maintain a healthy mitochondrial population, which plays an important role in AKI. Pannexin 1 (PANX1) channel transmembrane proteins are known to drive inflammation and release of adenosine triphosphate (ATP) during I/R injury. However, the specific role of PANX1 on mitophagy regulation in renal I/R injury remains elusive. In this study, we find that serum level of PANX1 is elevated in patients who developed AKI after cardiac surgery, and the level of PANX1 is positively correlated with serum creatinine and urea nitrogen levels. Using the mouse model of renal I/R injury in vivo and cell-based hypoxia/reoxygenation (H/R) model in vitro, we prove that genetic deletion of PANX1 mitigate the kidney tubular cell death, oxidative stress and mitochondrial damage after I/R injury through enhanced mitophagy. Mechanistically, PANX1 disrupts mitophagy by influencing ATP-P2Y-mTOR signal pathway. These observations provide evidence that PANX1 could be a potential biomarker for AKI and a therapeutic target to alleviate AKI caused by I/R injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Pannexin 1 targets mitophagy to mediate renal ischemia/reperfusion injury

Su,

Zhang,

Wang

et al. 2023

Commun Biol

View full text Add to dashboard Cite

show abstract

“…Overall, these data indicated that myeloid Panx1 channel activation play detrimental roles in brain trauma. Intriguingly, it has been recently proposed that serum Panx1 levels can serve as biomarker outcome for TBI patients [ 147 ]. Panx1 protein levels in the serum of TBI patients were significantly higher when compared to control individuals.…”

Section: Pannexin-1 Channels In Neuroinflammationmentioning

confidence: 99%

“…Panx1 protein levels in the serum of TBI patients were significantly higher when compared to control individuals. Moreover, a negative correlation between Panx1 levels in the serum and favorable outcomes in the patients was found [ 147 ]. A concern with these findings is that Panx1 serum levels were almost as high as normal plasma levels of albumin.…”

Section: Pannexin-1 Channels In Neuroinflammationmentioning

confidence: 99%

Pannexin-1 Channels as Mediators of Neuroinflammation

Seo

Dalal

Contreras

2021

IJMS

View full text Add to dashboard Cite

Neuroinflammation is a major component of central nervous system (CNS) injuries and neurological diseases, including Alzheimer’s disease, multiple sclerosis, neuropathic pain, and brain trauma. The activation of innate immune cells at the damage site causes the release of pro-inflammatory cytokines and chemokines, which alter the functionality of nearby tissues and might mediate the recruitment of leukocytes to the injury site. If this process persists or is exacerbated, it prevents the adequate resolution of the inflammation, and ultimately enhances secondary damage. Adenosine 5′ triphosphate (ATP) is among the molecules released that trigger an inflammatory response, and it serves as a chemotactic and endogenous danger signal. Extracellular ATP activates multiple purinergic receptors (P2X and P2Y) that have been shown to promote neuroinflammation in a variety of CNS diseases. Recent studies have shown that Pannexin-1 (Panx1) channels are the principal conduits of ATP release from dying cells and innate immune cells in the brain. Herein, we review the emerging evidence that directly implicates Panx-1 channels in the neuroinflammatory response in the CNS.

show abstract