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Study · Not a test of the peptide alone · 2021

1 result

LncRNA AC136007.2 alleviates cerebral ischemic-reperfusion injury by suppressing autophagy.

Liu N, Peng A, Sun H, Zhuang Y, Yu M, Wang Q, Wang J

Aging13 Aug 2021Cited by 23 (Europe PMC)

PMID34419936 (opens in a new tab)PMCIDPMC8386572 (opens in a new tab)DOI10.18632/aging.203369 (opens in a new tab)PepBankPUB-34419936
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Summary

Differential expression and diagnostic significance of the long noncoding RNA (lncRNA) AC136007.2 has been reported in patients with acute ischemic stroke (AIS). However, its role on disease progression and outcome remains unclear. Here, we employed an oxygen-glucose deprivation/reperfusion (OGD/R) model in neuronal SH-SY5Y cells and performed middle cerebral artery occlusion (MCAO) surgery in rats to investigate the function of AC136007.2 in ischemia-reperfusion (I/R) injury. AC136007.2 expression was determined by RT-qPCR and cell viability was examined using CCK-8, Edu, LDH, and apoptosis assays. Pro-inflammatory cytokine expression was assessed using ELISA. OGD/R downregulated AC136007.2 expression in SH-SY5Y cells, decreased viability by inducing apoptosis, and stimulated secretion of TNF-α, IL-6, and IL-1β. In turn, lentivirus-mediated AC136007.2 overexpression significantly reversed these phenomena. LC3 immunofluorescence and western blotting analyses of LC3-I/II and Beclin-1 expression and AMPK/mTOR phosphorylation status showed that AC136007.2 suppressed autophagy in SH-SY5Y cells via inactivation of AMPK/mTOR signaling. Notably, incubation with the AMPK activator AICAR abolished the pro-survival effect of AC136007.2 upon OGD/R treatment. Importantly, intraventricular injection of AC136007.2 significantly reduced cerebral infarction and brain edema in MCAO rats, as shown by TTC staining and water content measurements. We conclude that AC136007.2 alleviates cerebral I/R injury by suppressing AMPK/mTOR-dependent autophagy.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone1

In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).

  1. 01LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In SH-SY5Y cells during OGD/R, AICAR abolished the pro-survival effect of AC136007.2.

    In plain wordsIn cells deprived of oxygen and glucose, AICAR removed the survival benefit compared with AC136007.2 overexpression alone.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAC136007.2-mediated cell survival
    Study

    humann: not reported in source

    SH-SY5Y cells exposed to oxygen-glucose deprivation/reperfusion with AC136007.2 overexpression
    Comparator
    AC136007.2 overexpression without AICAR during OGD/R
    Outcome group
    Neuroprotection · Nervous system and cognition

    Source sentences

    Summary
    Notably, incubation with the AMPK activator AICAR abolished the pro-survival effect of AC136007.2 upon OGD/R treatment.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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