Evidence map›Paper›PMID 32565669›Full record

ArticleMolecular vision2020

Tyrosine triple mutated AAV2-BDNF gene therapy in an inner retinal injury model induced by intravitreal injection of

Asaka Lee Shiozawa, Tsutomu Igarashi, Maika Kobayashi, Kenji Nakamoto, Shuhei Kameya, Shigeto Fujishita, Hiroshi Takahashi, Takashi Okada

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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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.

Asaka Lee ShiozawaDepartment of Biochemistry and Molecular Biology, Nippon Medical School, Tokyo, Japan.
Tsutomu IgarashiDepartment of Biochemistry and Molecular Biology, Nippon Medical School, Tokyo, Japan.
Maika KobayashiDepartment of Biochemistry and Molecular Biology, Nippon Medical School, Tokyo, Japan.
Kenji NakamotoDepartment of Ophthalmology, Nippon Medical School, Tokyo, Japan.
Shuhei KameyaDepartment of Ophthalmology, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan.
Shigeto FujishitaDepartment of Drug Discovery Research, Teika Pharmaceutical Co., Ltd., Toyama, Japan.
Hiroshi TakahashiDepartment of Ophthalmology, Nippon Medical School, Tokyo, Japan.
Takashi OkadaDepartment of Biochemistry and Molecular Biology, Nippon Medical School, Tokyo, Japan.
Nippon Medical School · JPChiba Hokusou Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Glaucoma is a group of chronic optic neuropathies characterized by the degeneration of retinal ganglion cells (RGCs) and their axons, and they ultimately cause blindness. Because neuroprotection using neurotrophic factors against RGC loss has been proven a beneficial strategy, extensive attempts have been made to perform gene transfer of neurotrophic proteins. This study used the inner retinal injury mouse model to evaluate the neuroprotective effect of tyrosine triple mutated and self-complementary adeno-associated virus (AAV) encoding brain-derived neurotrophic factor (BDNF; tm-scAAV2-BDNF). Methods: C57BL/6J mice were intravitreally injected with 1 μl of tm-scAAV2-BDNF and its control AAV at a titer of 6.6 E+13 genome copies/ml. Three weeks later, 1 μl of 2 mM Results: The RNA expression of BDNF in retinas treated with tm-scAAV2-BDNF was about 300-fold higher than that of its control AAV. Meanwhile, the expression of recombinant BDNF protein increased in retinas treated with tm-scAAV2-BDNF. In addition, histological analysis revealed that tm-scAAV2-BDNF prevented thinning of the inner retina. Furthermore, b-wave amplitudes of the tm-scAAV2-BDNF group were significantly higher than those of the control vector group. Histopathological and electrophysiological evaluations showed that tm-scAAV2-BDNF treatment offered significant protection against NMDA toxicity. Conclusions: Results showed that tm-scAAV2-BDNF-treated retinas were resistant to NMDA injury, while retinas treated with the control AAV exhibited histopathological and functional changes after the administration of NMDA. These results suggest that tm-scAAV2-BDNF is potentially effective against inner retinal injury, including normal tension glaucoma.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorDependovirusDisease Models, AnimalElectroretinographyGene ExpressionGenetic TherapyGenetic VectorsImmunohistochemistryIntravitreal InjectionsMiceMice, Inbred C57BLN-MethylaspartateRecombinant ProteinsRetinal DiseasesBDNF protein, humanBrain-Derived Neurotrophic FactorN-MethylaspartateRecombinant Proteins

Identifiers

PMID32565669
PMCPMC7300199
OpenAlexW3036532086

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.