Evidence map›Paper›PMID 34400297›Full record

ArticleFree radical biology & medicine2021

Pituitary adenylate cyclase-activating polypeptide attenuates mitochondria-mediated oxidative stress and neuronal apoptosis after subarachnoid hemorrhage in rats.

Yuanjian Fang, Hui Shi, Lei Huang, Reng Ren, Cameron Lenahan, Jie Xiao, Yu Liu, Rui Liu, Rajvee Sanghavi, Chenguang Li and 5 more

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Yuanjian FangDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Hui ShiDepartment of Neurosurgery, Yongchuan Hospital, Chongqing Medical University, Chongqing, China.
Lei HuangDepartment of Neurosurgery, Loma Linda University, Loma Linda, CA, USA; Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, USA.
Reng RenDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Cameron LenahanDepartment of Neurosurgery, Loma Linda University, Loma Linda, CA, USA; Burrell College of Osteopathic Medicine, Las Cruces, NM, USA.
Jie XiaoDepartment of Neurosurgery, Loma Linda University, Loma Linda, CA, USA.
Yu LiuDepartment of Neurosurgery, Loma Linda University, Loma Linda, CA, USA.
Rui LiuDepartment of Neurosurgery, Loma Linda University, Loma Linda, CA, USA.
Rajvee SanghaviBurrell College of Osteopathic Medicine, Las Cruces, NM, USA.
Chenguang LiDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Sheng ChenDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Jiping TangDepartment of Neurosurgery, Loma Linda University, Loma Linda, CA, USA; Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, USA; Department of Anesthesiology, Loma Linda University, Loma Linda, CA, USA.
Jun YuDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Electronic address: 2505020@zju.edu.cn.
John H ZhangDepartment of Neurosurgery, Loma Linda University, Loma Linda, CA, USA; Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, USA; Department of Anesthesiology, Loma Linda University, Loma Linda, CA, USA. Electronic address: zjm135@zju.edu.cn.
Jianmin ZhangDepartment of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Electronic address: johnzhang3910@yahoo.com.
Loma Linda University · USSecond Affiliated Hospital of Zhejiang University · CNChongqing Medical University · CN

Funding

Vascular Biology Core FacilityP01NS082184 · NINDS · LOMA LINDA UNIVERSITY · PI PEARCE, WILLIAM J. · 2014 to 2018
$6.1M
Neurovascular Protection for Early Brain Injury after SAHR01NS081740 · NINDS · LOMA LINDA UNIVERSITY · PI ZHANG, JOHN H · 2013 to 2017
$1.6M
NINDS NIH HHS P01 NS082184NINDS NIH HHS R01 NS081740
6 · The paper itself

Abstract

Mitochondria-mediated oxidative stress and neuronal apoptosis play an important role in early brain injury following subarachnoid hemorrhage (SAH). Pituitary adenylate cyclase-activating polypeptide (PACAP) has been shown to reduce oxidative stress and cellular apoptosis by maintaining mitochondrial function under stress. The objective of this study is to investigate the effects of PACAP on mitochondria dysfunction - induced oxidative stress and neuronal apoptosis in both vivo and vitro models of SAH. PACAP Knockout CRISPR and exogenous PACAP38 were used to verify the neuroprotective effects of PACAP in rats after endovascular perforation - induced SAH as well as in primary neuron culture after hemoglobin stimulation. The results showed that endogenous PACAP knockout aggravated mitochondria dysfunction - mediated ATP reduction, reactive oxygen species accumulation and neuronal apoptosis in ipsilateral hemisphere at 24 h after SAH in rats. The exogenous PACAP38 treatment provided both short- and long-term neurological benefits by attenuating mitochondria - mediated oxidative stress and neuronal apoptosis after SAH in rats. Consistently, the exogenous PACAP38 treatment presented similar neuroprotection in the primary neuron culture after hemoglobin stimulation. Pharmacological inhibition of adenylyl cyclase (AC) or extracellular signal-regulated kinase (ERK) partly abolished the anti-oxidative stress and anti-apoptotic effects provided by PACAP38 treatment after the experimental SAH both in vivo and in vitro, suggesting the involvement of the AC-cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) and ERK pathway. Collectively, PACAP38 may serve as a promising treatment strategy for alleviating early brain injury after SAH.

Indexed as

Pituitary Adenylate Cyclase-Activating PolypeptideSubarachnoid HemorrhageAnimalsApoptosisMitochondriaOxidative StressRatsPituitary Adenylate Cyclase-Activating PolypeptideApoptosisMitochondriaOxidative stressPituitary adenylate cyclase-activating polypeptideSubarachnoid hemorrhage

Identifiers

PMID34400297
PMCPMC8985554
OpenAlexW3193880747

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.