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MiR-765 induces angiogenesis by inhibiting dipeptidyl peptidase 4 and increasing fibroblast growth factor 2

ABSTRACT: miR-765 induces angiogenesis by inhibiting dipeptidyl peptidase 4 and increasing fibroblast growth factor 2

PROVIDER: PRJNA971178 | ENA |

REPOSITORIES: ENA

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miR-765 induces angiogenesis by inhibiting dipeptidyl peptidase 4 and increasing fibroblast growth factor 2

Project description:Given that extracellular vesicles (EVs) secreted from stem cells contain angiogenic microRNAs (miRNAs), these EVs show equivalent angiogenic therapeutic effect to cell transplantation. This study aimed to identify the angiogenic miRNAs from several miRNAs involved in EVs secreted from stem cells. In human dental pulp stem cells (hDPSCs) under hypoxic culture, vascular endothelial growth factor (VEGF) involved in EVs increased. We hypothesized that angiogenic miRNAs increase in EVs that are secreted from hDPSCs under hypoxic culture compared with those under normoxic culture. In the first screening, the expression levels of miRNAs involved in EVs that were secreted from hDPSCs cultured under hypoxic and normoxic conditions were analyzed using miRNA array. In the second screening, 12 miRNAs were individually involved in EVs, and the growth of human aortic endothelial cells was assayed. In the third screening, miRNA-encapsulated EVs were injected in BALB/c mouse hindlimb ischemia model, followed by angiogenesis evaluation by blood flow analysis. Results showed that miR-765 is an angiogenic miRNA, targeting the 3′ untranslated region of dipeptidyl peptidase 4 (DPP4) and upregulating fibroblast growth factor 2 (FGF2) in vitro and in vivo. In conclusion, as an angiogenesis mechanism, miR-765 increased FGF2 expression levels by inhibiting DPP4.

2024-05-08 | GSE232178 | GEO

Dipeptidyl peptidase-IV is associated with decreased glioma growth

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Gene expression of cardiac tissues in dietary obese mice administered with a dipeptidyl peptidase-4 inhibitor

Project description:Dipeptidyl peptidase-4 (Dpp4) inhibitors are used worldwide to combat diabetes, however, their roles in cardiovascular disorders are yet to be defined. Here we show that a DPP4 inhibitor, linagliptin, contributes for the suppression of capillary rarefaction in cardiac tissues of dietary obese mice model. Imposing a high fat diet into mice induced capillary rarefaction and cardiac dysfunction. These pathologies associated with high DPP4 level in circulation, and the administration of linagliptin into dietary obese mice suppressed the development of capillary rarefaction and ameliorated cardiac dysfunction. Early growth response protein 1 (EGR1), known as an angiogenic transcription factor, is significantly reduced in the cardiac tissue upon metabolic stress, and this suppression was inhibited by the administration of linagliptin.

2017-04-27 | GSE98226 | GEO

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Melissococcus plutonius strain:765-6B

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Transcriptional profiling of rats treated with VX-765 and Anakinra

Project description:Various studies showed a significant production/release of IL-1 beta following status epilepticus (SE) and during epileptogenesis. We studied the role of this cytokine in the epileptogenic process by blocking its production and downstream effects in vivo in a model of acquired epilepsy following SE induction. We used a pharmacological strategy consisting of the administration of two drugs, namely VX-765 and Anakinra, which selectively block the biosynthesis and the receptor type 1 of this cytokine, respectively.

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Mesorhizobium loti strain:UFLA 01-765

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Project description:Veterinary trypanocidal benzoxaboroles are peptidase-activated prodrugs

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