Evidence map›Paper›PMID 25675001›Full record

ArticleMarine drugs2015

Involvement of JNK and caspase activation in hoiamide A-induced neurotoxicity in neocortical neurons.

Zhengyu Cao, Xichun Li, Xiaohan Zou, Michael Greenwood, William H Gerwick, Thomas F Murray

Open access · goldAbstract read
In one paragraph

Article in Marine drugs, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Natural Cyclopeptides as Anticancer Agents in the Last 20 Years.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Zhengyu CaoState Key Laboratory of Natural Medicines and Jiangsu Provincial Key Laboratory for TCM Evaluation and Translational Development, School of TCM, China Pharmaceutical University, Nanjing 211198, China. zycao1999@hotmail.com.
Xichun LiState Key Laboratory of Natural Medicines and Jiangsu Provincial Key Laboratory for TCM Evaluation and Translational Development, School of TCM, China Pharmaceutical University, Nanjing 211198, China. Xichun_li@163.com.
Xiaohan ZouState Key Laboratory of Natural Medicines and Jiangsu Provincial Key Laboratory for TCM Evaluation and Translational Development, School of TCM, China Pharmaceutical University, Nanjing 211198, China. imzouxiaohan@163.com.
Michael GreenwoodDepartment of Pharmacology, School of Medicine, Creighton University, Omaha, NE 68178, USA. michael.greenwood@unmc.edu.
William H GerwickCenter for Marine Biotechnology and Biomedicine, Scripps Institution of Oceanography and Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA 92093, USA. wgerwick@ucsd.edu.
Thomas F MurrayDepartment of Pharmacology, School of Medicine, Creighton University, Omaha, NE 68178, USA. tfmurray@creighton.edu.
Creighton University · USChina Pharmaceutical University · CNScripps Institution of Oceanography · US

Funding

Neurotoxins from Marine Algae and CyanobacteriaR01NS053398 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GERWICK, WILLIAM HENRY, MURRAY, THOMAS F · 2005 to 2015
$4.3M
NINDS NIH HHS NS053398NINDS NIH HHS R01 NS053398
6 · The paper itself

Abstract

The frequent occurrence of Moorea producens (formerly Lyngbya majuscula) blooms has been associated with adverse effects on human health. Hoiamide A is a structurally unique cyclic depsipeptide isolated from an assemblage of the marine cyanobacteria M. producens and Phormidium gracile. We examined the influence of hoiamide A on neurite outgrowth in neocortical neurons and found that it suppressed neurite outgrowth with an IC50 value of 4.89 nM. Further study demonstrated that hoiamide A stimulated lactic acid dehydrogenase (LDH) efflux, nuclear condensation and caspase-3 activity with EC50 values of 3.66, 2.55 and 4.33 nM, respectively. These data indicated that hoiamide A triggered a unique neuronal death profile that involves both necrotic and apoptotic mechanisms. The similar potencies and similar time-response relationships between LDH efflux and caspase-3 activation/nuclear condensation suggested that both necrosis and apoptosis may derive from interaction with a common molecular target. The broad-spectrum caspase inhibitor, Z-VAD-FMK completely inhibited hoiamide A-induced neurotoxicity. Additionally, hoiamide A stimulated JNK phosphorylation, and a JNK inhibitor attenuated hoiamide A-induced neurotoxicity. Collectively, these data demonstrate that hoiamide A-induced neuronal death requires both JNK and caspase signaling pathways. The potent neurotoxicity and unique neuronal cell death profile of hoiamide A represents a novel neurotoxic chemotype from marine cyanobacteria.

Indexed as

AnimalsApoptosisCaspase InhibitorsCaspasesCell DeathCyanobacteriaDepsipeptidesEnzyme ActivationEnzyme InhibitorsEutrophicationMAP Kinase Kinase 4MiceNecrosisNeocortexNeuronsNeurotoxicity SyndromesCaspase InhibitorsCaspasesDepsipeptidesEnzyme Inhibitorshoiamide AMAP Kinase Kinase 4NeurotoxinsProtein Kinase Inhibitors

Identifiers

PMID25675001
PMCPMC4344608
OpenAlexW1976045837

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.