Evidence map›Paper›PMID 34346167›Full record

ArticleCNS neuroscience & therapeutics2021

Platelet-derived growth factor (PDGF)-BB protects dopaminergic neurons via activation of Akt/ERK/CREB pathways to upregulate tyrosine hydroxylase.

Huan Chen, Yan Teng, Xingmin Chen, Zhihao Liu, Fan Geng, Yanzhuo Liu, Haisong Jiang, Ziyan Wang, Lu Yang

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Roles of PDGF/PDGFR signaling in various organs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
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  12. Observational
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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

9 authors.

Huan ChenInstitute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Yan TengInstitute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.ORCID 0000-0002-2014-0954
Xingmin ChenSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Zhihao LiuSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Fan GengSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Yanzhuo LiuSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Haisong JiangInstitute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Ziyan WangSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Lu YangInstitute of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.ORCID 0000-0001-9144-3234

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe neurotropic growth factor PDGF-BB was shown to have vital neurorestorative functions in various animal models of Parkinson's disease (PD). Previous studies indicated that the regenerative property of PDGF-BB contributes to the increased intensity of tyrosine hydroxylase (TH) fibers in vivo. However, whether PDGF-BB directly modulates the expression of TH, and the underlying mechanism is still unknown. We will carefully examine this in our current study.

methodMPTP-lesion mice received PDGF-BB treatment via intracerebroventricular (i.c.v) administration, and the expression of TH in different brain regions was assessed by RT-PCR, Western blot, and immunohistochemistry staining. The molecular mechanisms of PDGF-BB-mediated TH upregulation were examined by RT-PCR, Western blot, ChIP assay, luciferase reporter assay, and immunocytochemistry.

resultsWe validated a reversal expression of TH in MPTP-lesion mice upon i.c.v administration of PDGF-BB for seven days. Similar effects of PDGF-BB-mediated TH upregulation were also observed in MPP

conclusionOur data demonstrated that PDGF-BB directly regulated the expression of TH via activating the downstream Akt/ERK/CREB signaling pathways. Our finding will further support the therapeutic potential of PDGF-BB in PD, and provide the possibility that targeting PDGF signaling can be harnessed as an adjunctive therapy in PD in the future.

Indexed as

AnimalsBecaplerminCell Line, TumorCyclic AMP Response Element-Binding ProteinDopaminergic NeuronsFemaleHumansImmunohistochemistryInjections, IntraventricularMAP Kinase Signaling SystemMiceMice, Inbred C57BLMPTP PoisoningNeuroprotective AgentsOncogene Protein v-aktParkinson Disease, SecondaryBecaplerminCyclic AMP Response Element-Binding ProteinNeuroprotective AgentsOncogene Protein v-aktTyrosine 3-Monooxygenasedopaminergic neuronParkinson's diseasePDGF-BBtyrosine hydroxylase

Identifiers

PMID34346167
PMCPMC8504523

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Registered trials

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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.