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Protective monocytes in cerebral ischemia

ABSTRACT: Stroke is a highly prevalent and devastating disease with limited therapeutic options. Most efforts to develop treatments for stroke have thus far met with limited success in large clinical trials. The brain has an enormous capacity for self-preservation, and elucidating how the brain protects itself may provide novel insights into stroke treatment. Ischemic tolerance (IT), a phenomenon in which application of sub-lethal stress [preconditioning (PC) stimulus; PC] induces a state of tolerance to a subsequent ischemic insult, represents an example of endogenous neuroprotection. IT can be induced in brain by systemic administration of the Toll-like receptor-4 ligand lipopolysaccharide (LPS). Different populations of immune cell could potentially play a role in PC induced by LPS. In particular, monocytes, which are the main target of LPS, can exert a powerful protective effect either directly or by modulating the immune system.

ORGANISM(S): Mus musculus

PROVIDER: GSE84327 | GEO | 2016/07/13

SECONDARY ACCESSION(S): PRJNA328868

REPOSITORIES: GEO

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Project description:Genes upregulated in stroke infiltrating stem cells were compared against the parent non-infiltrated mouse stem cell line derived from immortomouseTM. Abstract Background and Purpose- Although the therapeutic potential of bone marrow-derived stem cells (SC) has been addressed in different experimental models of ischemic stroke, it is still unclear how SC induce neuroprotection following stroke. In this study, we describe a novel method for recovering SC infiltrating post-stroke brain tissue allowing the determination of genes which become persistently activated / or depressed (compared to their naïve counterparts) during SC-mediated neuroprotection. Methods- Ischemic stroke was induced in C57BL/6 mice by middle cerebral artery occlusion for 1 h, followed by reperfusion. SC were isolated from H-2Kb-tsA58 (immortomouseTM) mice, and were administered (i.v.) 24 h after reperfusion. At the onset of therapeutic improvement (14 days after ischemia), infarcted brain tissue was isolated and infarct-infiltratng SC cultured at 33°C. Microarray analysis and RT-PCR were performed to compare persistent differential gene expression between naïve and infiltrating SC populations. Results- Z-scoring revealed dramatic changes in extracellular genes of analyzed cells. Pair-wise analysis detected 80 extracellular factor genes that were up-regulated ( 2 fold, P<0.05, Benjamini-Hochberg correction) between naïve and infiltrated SC. Although several conventional neuroregenerative, nerve guidance and angiogenic factors (bFGF, bone morphogenetic protein, angiopoietins, neural growth factors were among the expressed genes detected we identified Cytokine receptor-like factor 1 (Crlf1), Fgf7, family with sequence similarity 19, member A5 (Fam19a5), Glypican 1 (Gpc1), Dickkopf homolog 2 (Dkk2), Endothelial cell-specific molecule 1, Osteopontin (OPN)35, Tissue factor pathway inhibitor 2, Masp3 mRNA for MBL-associated serine protease-3, Glial cell line derived neurotrophic factor (Gdnf), Bone morphogenetic protein 2 (Bmp2), Olfactomedin 1, Sushi-repeat-containing protein, X-linked 2 (Srpx2). Conclusions- SC infiltrating the post-i schemic brain assume a persistently altered pattern of expressed extracellular genes compared to naïve SC that contributes to neuroprotection, regeneration and angiogenesis in infarcts. Keywords: Gene activation / suppression study Comparison of persistent stem cell gene expression induced by stroke-infarct infiltration

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Protective monocytes in cerebral ischemia

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