ArticleJournal of molecular neuroscience : MN2019
Ghrelin Promotes Cortical Neurites Growth in Late Stage After Oxygen-Glucose Deprivation/Reperfusion Injury.
Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- In Vitro Oxygen Glucose Deprivation Model of Ischemic Stroke: A Proteomics-Driven Systems Biological Perspective.Molecular neurobiology · 2022Pooled it
- Hypoxic Preconditioned Neural Stem Cell-Derived Extracellular Vesicles Contain Distinct Protein Cargo from Their Normal Counterparts.Current issues in molecular biology · 2023Article
- Ghrelin Regulates Expression of the Transcription Factor Pax6 in Hypoxic Brain Progenitor Cells and Neurons.Cells · 2022Article
- Effects of Ghrelin on Olfactory Ensheathing Cell Viability and Neural Marker Expression.Journal of molecular neuroscience : MN · 2021Article
- Severe Zinc Deficiency Causes the Loss and Apoptosis of Olfactory Ensheathing Cells (OECs) and Olfactory Deficit.Journal of molecular neuroscience : MN · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Acyl ghrelin, a novel brain-gut peptide, is an endogenous ligand for the growth hormone secretagogue receptor. Accumulated research data have shown that acyl ghrelin exercises a significant neuroprotective effect against cerebral ischemia/reperfusion (I/R) injury in animal models and in cultured neurons during the acute phase, usually, 1 day after cerebral ischemia. The chronic effects of acyl ghrelin 1 week after brain ischemia remain largely unknown. In this study, we explored the effects of acyl ghrelin on cultured organotypic brain slices and cortical neurons which were injured by oxygen-glucose deprivation/reperfusion(OGD/R) for 7 days. The underlying molecular mechanisms were deciphered based on label-free proteomic analysis. Acyl ghrelin treatment promoted neurite (axons and dendrites) growth and alleviated the neuronal damage in both cultured brain slices and neurons. Proteomic analysis showed that cell division control protein 42 (Cdc42) mediates the effects of acyl ghrelin on neurite growth. Acyl ghrelin stimulated the expression of Cdc42 and neurite growth in cultured neurons comparing with OGD/R group. Inhibition of Cdc42 attenuated the effects of acyl ghrelin. These results suggest that acyl ghrelin promotes neurite growth during the later stage after OGD/R injury via Cdc42. Our study suggests that acyl ghrelin may be promising to restore the neuronal structure in the late phase after stroke.
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Registered trials
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.