Evidence map›Paper›PMID 28396435›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Intranasal MSC-derived A1-exosomes ease inflammation, and prevent abnormal neurogenesis and memory dysfunction after status epilepticus.

Qianfa Long, Dinesh Upadhya, Bharathi Hattiangady, Dong-Ki Kim, Su Yeon An, Bing Shuai, Darwin J Prockop, Ashok K Shetty

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 252 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
252citing papers in PubMed, 3 pooled it
12.3field-weighted citation impact, top 1% 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

252 citing papers in PubMed, 3 syntheses or guidelines pooled it, 399 citations in OpenAlex.

  1. Pooled it
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  8. Clinical Applications of Extracellular Vesicles: Promises and Pitfalls.International journal of molecular sciences · 2026
    Review
  9. Current trends in exosomes as therapeutic drug delivery systems.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
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192 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Qianfa LongInstitute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine, Temple, TX 76502.
Dinesh UpadhyaInstitute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine, Temple, TX 76502.
Bharathi HattiangadyInstitute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine, Temple, TX 76502.
Dong-Ki KimInstitute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine, Temple, TX 76502.
Su Yeon AnInstitute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine, Temple, TX 76502.
Bing ShuaiInstitute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine, Temple, TX 76502.
Darwin J ProckopInstitute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine, Temple, TX 76502; prockop@medicine.tamhsc.edu shetty@medicine.tamhsc.edu.
Ashok K ShettyInstitute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine, Temple, TX 76502; prockop@medicine.tamhsc.edu shetty@medicine.tamhsc.edu.
Temple College · USCentral Texas Veterans Health Care System · US

Funding

Preparation and Distribution of Adult Stem CellsP40OD011050 · OD · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI PROCKOP, DARWIN JOHNSON · 2012 to 2017
$6.0M
Combined NSC Grafting and Neurogenic Drug Therapy for Temporal Lobe EpilepsyI01BX002351 · VA · OLIN TEAGUE VETERANS CENTER · PI SHETTY, ASHOK K · 2015 to 2018
–
BLR&D Research Career Scientist AwardIK6BX003612 · VA · OLIN TEAGUE VETERANS CENTER · PI SHETTY, ASHOK K · 2017 to 2019
–
BLRD VA I01 BX002351BLRD VA IK6 BX003612NIH HHS P40 OD011050
6 · The paper itself

Abstract

Status epilepticus (SE), a medical emergency that is typically terminated through antiepileptic drug treatment, leads to hippocampus dysfunction typified by neurodegeneration, inflammation, altered neurogenesis, as well as cognitive and memory deficits. Here, we examined the effects of intranasal (IN) administration of extracellular vesicles (EVs) secreted from human bone marrow-derived mesenchymal stem cells (MSCs) on SE-induced adverse changes. The EVs used in this study are referred to as A1-exosomes because of their robust antiinflammatory properties. We subjected young mice to pilocarpine-induced SE for 2 h and then administered A1-exosomes or vehicle IN twice over 24 h. The A1-exosomes reached the hippocampus within 6 h of administration, and animals receiving them exhibited diminished loss of glutamatergic and GABAergic neurons and greatly reduced inflammation in the hippocampus. Moreover, the neuroprotective and antiinflammatory effects of A1-exosomes were coupled with long-term preservation of normal hippocampal neurogenesis and cognitive and memory function, in contrast to waned and abnormal neurogenesis, persistent inflammation, and functional deficits in animals receiving vehicle. These results provide evidence that IN administration of A1-exosomes is efficient for minimizing the adverse effects of SE in the hippocampus and preventing SE-induced cognitive and memory impairments.

Indexed as

NeurogenesisAdministration, IntranasalAnimalsCell LineExosomesHumansMaleMemory DisordersMesenchymal Stem CellsMiceStatus Epilepticusadult neurogenesisexosomesmemory dysfunctionneuroinflammationstatus epilepticus

Identifiers

PMID28396435
PMCPMC5410779
OpenAlexW2606603228

What OpenQuestion holds

Textmetadata
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.