Evidence map›Paper›PMID 29804319›Full record

ArticleCNS neuroscience & therapeutics2019

MicroRNA-219 decreases hippocampal long-term potentiation inhibition and hippocampal neuronal cell apoptosis in type 2 diabetes mellitus mice by suppressing the NMDAR signaling pathway.

Ling Zhang, Zheng-Wen Chen, Shu-Fen Yang, Muyasi Shaer, Ying Wang, Jun-Jie Dong, Beili Jiapaer

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  13. Functional Analysis of the 3' Untranslated Region of the HumanNeuropsychiatric disease and treatment · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Ling ZhangDepartment of Cadre Health Care, the Xinjiang Uygur Autonomous Region People's Hospital, Urumchi, China.
Zheng-Wen ChenDepartment of Anesthesiology, the Second Affiliated Hospital of Xinjiang Medical University, Urumchi, China.
Shu-Fen YangDepartment of Nephrology, the Xinjiang Uygur Autonomous Region People's Hospital, Urumchi, China.
Muyasi ShaerDepartment of Cadre Health Care, the Xinjiang Uygur Autonomous Region People's Hospital, Urumchi, China.
Ying WangDepartment of Cadre Health Care, the Xinjiang Uygur Autonomous Region People's Hospital, Urumchi, China.
Jun-Jie DongDepartment of Cadre Health Care, the Xinjiang Uygur Autonomous Region People's Hospital, Urumchi, China.
Beili JiapaerDepartment of Cadre Health Care, the Xinjiang Uygur Autonomous Region People's Hospital, Urumchi, China.ORCID 0000-0001-8862-1482
People's Hospital of Xinjiang Uygur Autonomous Region · CNXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveType 2 diabetes mellitus (T2DM) is a complex polygenic disease that causes hyperglycemia and accounts for 90%-95% of all diabetes mellitus cases. Hence, this study aimed to examine the effects of microRNA-219 (miR-219) on inhibition of long-term potentiation (LTP) and apoptosis of hippocampal neuronal cells in T2DM mice through the N-methyl-d-aspartate receptor (NMDAR) signaling pathway regulation.

methodsThe T2DM mouse models were established, after which LTP in vivo was recorded by means of electrical biology, and the fasting blood glucose of mice was measured. Next, the density of pyramidal neurons in each group was calculated. Additionally, the expression levels of miR-219, the NMDAR signaling pathway [NMDAR1 (NR) 1, NR2A, and NR2B), downstream target proteins [calmodulin-dependent protein kinase-II (CaMK-II) and cAMP response element binding protein (CREB)], and apoptosis-related factors [Bcl2-associated X protein (Bax), c-caspase-9 and c-caspase-3] in the hippocampal tissues were determined. Finally, immunohistochemistry was applied to detect and measure the positive expression of Bax, caspase-9, and caspase-3 proteins.

resultsThe results showed that upregulation of miR-219 increases LTP and density of pyramidal neurons in the hippocampal tissues of mice, while it decreases blood glucose of db/db mice. In addition, miR-219 upregulation also leads to decreased mRNA levels of NR1, NR2A, NR2B, CaMK-II, and CREB and protein levels of NR1, NR2A, NR2B, CaMK-II, CREB, p-CREB, Bax, c-caspase-9, and c-caspase-3. Furthermore, upregulation of miR-219 inhibits positive expression of Bax, caspase-9, and caspase-3 proteins, leading to the suppression of hippocampal neuronal cell apoptosis.

conclusionThe findings from this study indicated that the upregulation of miR-219 decreases LTP inhibition and hippocampal neuronal cell apoptosis in T2DM mice by downregulating the NMDAR signaling pathway, therefore suggesting that MiR-219 might be a future therapeutic strategy for T2DM.

Indexed as

AnimalsApoptosisBlood GlucoseDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Excitatory Postsynaptic PotentialsHippocampusLong-Term PotentiationMicroRNAsNeuronsReceptors, N-Methyl-D-AspartateRNA, MessengerSignal TransductionSpecific Pathogen-Free OrganismsBlood GlucoseMicroRNAsMIRN219 microRNA, mouseReceptors, N-Methyl-D-AspartateRNA, Messengerapoptosishippocampal neuronal cellslong-term potentiationMicroRNA-219NMDAR signaling pathwaytype 2 diabetes mellitus

Identifiers

PMID29804319
PMCPMC6436581
OpenAlexW2803796029

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.