Evidence map›Paper›PMID 33652595›Full record

ArticleInternational journal of molecular sciences2021

Neural-Induced Human Adipose Tissue-Derived Stem Cells Conditioned Medium Ameliorates Rotenone-Induced Toxicity in SH-SY5Y Cells.

Mahesh Ramalingam, Sujeong Jang, Han-Seong Jeong

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

3 authors at 1 institution in 1 country.

Mahesh RamalingamDepartment of Physiology, Chonnam National University Medical School, Hwasun 58128, Jeollanam-do, Korea.ORCID 0000-0002-8831-4375
Sujeong JangDepartment of Physiology, Chonnam National University Medical School, Hwasun 58128, Jeollanam-do, Korea.ORCID 0000-0001-8673-7887
Han-Seong JeongDepartment of Physiology, Chonnam National University Medical School, Hwasun 58128, Jeollanam-do, Korea.ORCID 0000-0001-6921-6625
Chonnam National University Hwasun Hospital · KR

Funding

Chonnam National University Hospital Biomedical Research Institute CRI18034-1National Research Foundation of Korea NRF-2018R1D1A1B07050883National Research Foundation of Korea NRF-2020R1F1A1076616National Research Foundation of Korea NRF-2020R1I1A3070388the Jeollanam-do Science and Technology R&D Project Development of Stem Cell-Derived New Drug
6 · The paper itself

Abstract

Parkinson's disease (PD) is an age-related neurodegenerative disease (NDD) characterized by the degenerative loss of dopaminergic neurons in the substantia nigra along with aggregation of α-synuclein (α-syn). Neurogenic differentiation of human adipose-derived stem cells (NI-hADSCs) by supplementary factors for 14 days activates different biological signaling pathways. In this study, we evaluated the therapeutic role of NI-hADSC-conditioned medium (NI-hADSC-CM) in rotenone (ROT)-induced toxicity in SH-SY5Y cells. Increasing concentrations of ROT led to decreased cell survival at 24 and 48 h in a dose- and time-dependent manner. Treatment of NI-hADSC-CM (50% dilution in DMEM) against ROT (0.5 μM) significantly increased the cell survival. ROT toxicity decreased the expression of tyrosine hydroxylase (TH). Western blot analysis of the Triton X-100-soluble fraction revealed that ROT significantly decreased the oligomeric, dimeric, and monomeric phosphorylated Serine129 (p-S129) α-syn, as well as the total monomeric α-syn expression levels. ROT toxicity increased the oligomeric, but decreased the dimeric and monomeric p-S129 α-syn expression levels. Total α-syn expression (in all forms) was increased in the Triton X-100-insoluble fraction, compared to the control. NI-hADSC-CM treatment enhanced the TH expression, stabilized α-syn monomers, reduced the levels of toxic insoluble p-S129 α-syn, improved the expression of neuronal functional proteins, regulated the Bax/Bcl-2 ratio, and upregulated the expression of pro-caspases, along with PARP-1 inactivation. Moreover, hADSC-CM treatment decreased the cell numbers and have no effect against ROT toxicity on SH-SY5Y cells. The therapeutic effects of NI-hADSC-CM was higher than the beneficial effects of hADSC-CM on cellular signaling. From these results, we conclude that NI-hADSC-CM exerts neuroregenerative effects on ROT-induced PD-like impairments in SH-SY5Y cells.

Indexed as

Signal TransductionAdipose Tissuealpha-Synucleinbcl-2-Associated X ProteinCulture Media, ConditionedHumansNeurodegenerative DiseasesNeuronsPoly (ADP-Ribose) Polymerase-1Proto-Oncogene Proteins c-bcl-2RotenoneStem Cellsalpha-SynucleinBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanCulture Media, ConditionedPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Proto-Oncogene Proteins c-bcl-2RotenoneSNCA protein, humanmesenchymal stem cellsParkinson’s diseaseregenerationrotenoneα-synuclein

Identifiers

PMID33652595
PMCPMC7956615
OpenAlexW3129289862

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.