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RNA-seq of mice islets from wt and miR-29a/b-1 pancreatic beta cell specific overexpression transgenic mice

ABSTRACT: We investigated the mechanism associated with miR-29 effects by comparing gene expression of whole primary islets isolated from miR-29a/b-1 pancreatic beta cell specific overexpression transgenic mice (βTG mice) and their control littermates by RNA sequencing. Ten-week-old mice were chosen to avoid secondarily affected genes. We identified 346 genes that showed significant differences (p-value < 0.05 and >2-fold change) between the two groups. We then used gene ontology (GO) algorithms to perform functional annotations of these differential genes. The top enriched pathways were linked primarily to inflammatory response, secretory vesicle, and ion channel activity. Islets from the βTG mice showed an enhanced inflammatory response based on an assessment of both the upregulated and the downregulated genes , which suggested a likely positive regulation of phagocytosis (Ahsg), regulation of blood vessel diameter (P2rx1/Kng1/Nos2), and monocyte chemotaxis (Cxcl10/Cxcl17).

ORGANISM(S): Mus musculus

PROVIDER: GSE151844 | GEO | 2020/06/05

REPOSITORIES: GEO

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Project description:The miR-29 family is an important player in the molecular pathophysiology of distinct types of cancer, with roles that seems to depend on cellular context. Reduced miR-29 levels are associated with more aggressive disease and its overexpression in cancer and leukemic cell lines inhibits proliferation. In contrast, its overexpression in hematopoietic progenitors, promotes leukemogenesis. We explored the potential roles of miR-29a in the molecular pathophysiology of T-cell acute lymphoblastic leukemia (T-ALL). As compared to normal T-cells, miR-29a levels are extremely reduced in T-ALL and in the Jurkat cell line. Microarrays analysis in Jurkat cells, following the introduction of synthetic miR-29a mimics, revealed the down-regulation of several predicted targets, including previously described targets (DNMT3a/b, CDK6, PXDN, MCL1, PIK3R1 and CXXC6), and novel targets with roles in active DNA demethylation, such as members of the ten-eleven-translocation (TET) family and TDG. Reduced miR-29a levels contribute to altered epigenetics, as its introduction in Jurkat cells, promotes the demethylation of the AHR gene (commonly methylated in T-ALL). In T-ALL patients, miR-29a levels are significantly associated with blast counts and disease free survival. Our results highlight the relevance of miR-29 in T-ALL physiopathology, and may help to clarify some contrasting findings reported in the literature. In order to identify potential miR-29a targets in T-cell lymphoblastic leukemia, Jurkat cells were electroporated with synthetic RNA molecules corresponding to miR-29a mimics (pre-miR) or inhibitors (anti-miR); and microarray profiles were compared to the profiles of Jurkat cells eletroporated with the corresponding negative controls. Transcripts with levels reduced following the introduction of the pre-miR-29a (as compared to pre-miR-Control), or transcripts acumulated folowing introduction of the anti-miR-29a inhibitor (as compared to anti-miR-Control), were considered potential targets; and were further compared to microRNA target prediction databases. Two paired samples were used for this analysis.

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RNA-seq of mice islets from wt and miR-29a/b-1 pancreatic beta cell specific overexpression transgenic mice

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