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ACTH-like Peptides Compensate Rat Brain Gene Expression Profile Disrupted by Ischemia a Day After Experimental Stroke
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This rat study examined gene expression in the penumbra-associated frontal cortex 24 h after transient middle cerebral artery occlusion (tMCAO), comparing ischemia with treatment by two ACTH-derived peptides, ACTH(4-7)PGP (Semax) and ACTH(6-9)PGP, using RNA-Seq. The authors report 3774 differentially expressed genes (DEGs) under ischemia, versus 1539 DEGs under Semax and 2066 DEGs under ACTH(6-9)PGP at 24 h after tMCAO, with both peptides reducing expression distortions caused by ischemia for 1171 genes linked to immune and neurosignaling pathways. There were 32 DEGs between ACTH(6-9)PGP and Semax administration at this time point. The authors state that ACTH(6-9)PGP's effect was more similar to Semax than different from it a day after tMCAO, compensating ischemia-disrupted gene expression profiles.
Abstract
Background: Ischemic stroke results from a disruption of cerebral blood flow. Adrenocorticotropic hormone (ACTH) serves as the basis for the creation of synthetic peptides as neuroprotective agents for stroke therapy. Previously, using RNA-Seq we first revealed differential expressed genes (DEGs) associated with ACTH(4-7)PGP (Semax) and ACTH(6-9)PGP peptides under cerebral ischemia conditions. Analysis was carried out at 4.5 h after transient middle cerebral artery occlusion (tMCAO) model in the ipsilateral frontal cortex of a rat brain. Methods: Here, we analyzed the penumbra-associated frontal cortex of rats and actions under the same peptides at 24 h after tMCAO using RNA-Seq. Results: 3774 DEGs (fold change > 1.5 and Padj < 0.05) were identified under ischemia conditions, whereas 1539 and 2066 DEGs were revealed under Semax and ACTH(6-9)PGP peptides at 24 h after tMCAO. Furthermore, both peptides significantly reduced expression distortions caused by ischemia for 1171 genes associated with immune and neurosignaling pathways. Concomitantly, there were 32 DEGs under ACTH(6-9)PGP versus Semax administration at 24 h after tMCAO. Besides, neurogenesis-, angiogenesis-, protein kinase- and growth factor-related DEGs were revealed under peptides action. Previously, we observed the neuroprotective effect of peptides at the histological level in rat brains at 24 h after tMCAO. Thus, here we demonstrate the transcriptome manifestation of this histological effect. Furthermore, comparison with previous data at the 4.5 h post-tMCAO time point showed that the pattern of peptide action on the transcriptome depends on the time elapsed after tMCAO. Conclusions: We revealed that the effect of ACTH(6-9)PGP was more similar to Semax than different from it a day after tMCAO. At this time point, ACTH-like peptides compensated rat brain gene expression profiles disrupted by ischemia. Thus, our results may be useful for selecting more effective structures for future anti-stroke drugs and appropriate post-stroke time points for their testing.
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