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Ecto-5’-Nucleotidase (Nt5e/CD73)-Mediated Adenosine Signaling Attenuates TGFβ-2 Induced Elastin and Cellular Contraction

ABSTRACT: Ecto-5’-Nucleotidase (Nt5e/CD73)-Mediated Adenosine Signaling Attenuates TGFβ-2 Induced Elastin and Cellular Contraction

PROVIDER: PRJNA895057 | ENA |

REPOSITORIES: ENA

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Ecto-5’-Nucleotidase (Nt5e/CD73)-Mediated Adenosine Signaling Attenuates TGFβ-2 Induced Elastin and Cellular Contraction

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Project description:The understanding of heterogeneity of human memory T cells will help to know the function, development and maintenance of memory population, then to improve the recall response or effective immunotherapy. Ecto-5’-nucleotidase CD73 expression in four subsets of memory T cells decreases with aging. The resistance to apoptosis and high expression of IL7R entitle CD73+ memory T cells to be long-lived population. We found antigen-specific memory T cells have overwhelming CD73 expression. The transcriptional and chromatin accessibility profiles indicate the elevated effector functions in CD73+ memory CD4 T cells comparing to CD73- counterparts. Homer analysis and Transcriptional factor (TF)-regulatory element-target gene triplet network clearly show the crucial role of RUNT and NR family TFs in CD73+ cells. Furthermore, CD73+ memory CD4 T cells were prone to differentiate into TRM-like cells under in-vitro sequential TCR and TGF/IL-15 signaling. The decreased percentage of CD73+ memory T cells with age leads to the less replenishment of TRM cells from peripheral blood.

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Ecto-5'-nucleotidase (CD73) inhibits nociception by hydrolyzing AMP to adenosine in nociceptive circuits.

Project description:Ecto-5'-nucleotidase (NT5E, CD73) is a membrane-anchored protein that hydrolyzes extracellular adenosine 5'-monophosphate (AMP) to adenosine in diverse tissues but has not been directly studied in nociceptive neurons. We found that NT5E was located on peptidergic and nonpeptidergic nociceptive neurons in dorsal root ganglia (DRG) and on axon terminals in lamina II (the substantia gelatinosa) of spinal cord. NT5E was also located on epidermal keratinocytes, cells of the dermis, and on nociceptive axon terminals in the epidermis. Following nerve injury, NT5E protein and AMP histochemical staining were coordinately reduced in lamina II. In addition, AMP hydrolytic activity was reduced in DRG neurons and spinal cord of Nt5e(-/-) mice. The antinociceptive effects of AMP, when combined with the adenosine kinase inhibitor 5-iodotubericidin, were reduced by approximately 50% in Nt5e(-/-) mice and were eliminated in Adenosine A(1) receptor (A(1)R, Adora1) knock-out mice. Additionally, Nt5e(-/-) mice displayed enhanced sensitivity in the tail immersion assay, in the complete Freund's adjuvant model of inflammatory pain and in the spared nerve injury model of neuropathic pain. Collectively, our data indicate that the ectonucleotidase NT5E regulates nociception by hydrolyzing AMP to adenosine in nociceptive circuits and represents a new molecular target for the treatment of chronic pain. Moreover, our data suggest NT5E is well localized to regulate nucleotide signaling between skin cells and sensory axons.

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