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Related Concept Videos

Overview of Exosomes01:36

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Exosomes are stable, lipid bilayer-enclosed vesicles capable of crossing biological barriers. They can carry a wide range of molecules required for intercellular communication. Once exosomes are released from the cell where they originated, they enter a recipient cell through various pathways such as fusion, receptor-mediated endocytosis, macropinocytosis, and phagocytosis.
Stahl et al. discovered exosomes in 1983, but the exosomes were initially considered waste products released from the...
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RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...
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Adrenergic Receptors: β Subtype01:26

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β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
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Spare Receptors01:30

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Some receptors remain unoccupied even when an agonist produces a maximal response. Such empty ones are called spare receptors. In presence of spare receptors the maximum effect of an agonist drug is achieved with fewer than 100% of the receptors being occupied. To determine the presence of spare receptors, scientists often compare the concentration of the drug needed to produce 50% of the maximum effect (EC50) with the concentration of the drug needed to occupy 50% of the receptors (Kd). If the...
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Adrenergic Receptors: ɑ Subtype01:31

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Transducer Mechanism: Enzyme-Linked Receptors01:27

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Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
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Related Experiment Video

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HPLC-based Assay to Monitor Extracellular Nucleotide/Nucleoside Metabolism in Human Chronic Lymphocytic Leukemia Cells
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Adenosine receptors regulate exosome production.

Nils Ludwig1,2, Juliana H Azambuja1,2,3, Aparna Rao2,4

  • 1Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15213, USA.

Purinergic Signalling
|May 23, 2020
PubMed
Summary

Adenosine receptors regulate exosome production. A2A receptors suppress exosome release across cell types, while A1 and A2B receptor effects vary. Targeting cancer with A2A antagonists may increase tumor exosome release.

Keywords:
AdenosineAdenosine receptorsExosomesExtracellular vesicles

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Preparation of Exosomes for siRNA Delivery to Cancer Cells
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Area of Science:

  • Cell Biology
  • Extracellular Vesicles
  • Purinergic Signaling

Background:

  • Exosomes, crucial extracellular vesicles, carry purinergic pathway components.
  • Cellular mechanisms governing exosome production, particularly those involving adenosine receptors, are not fully understood.

Purpose of the Study:

  • To investigate the role of adenosine receptors (A1R, A2AR, A2BR) in regulating exosome production.
  • To determine how these receptors influence exosome release under normal and stress conditions in different cell types.

Main Methods:

  • Isolated preglomerular vascular smooth muscle cells (PGVSMCs) from wildtype and knockout rats for A1R, A2AR, and A2BR.
  • Quantified exosome production in PGVSMCs and cancer cells under normal, metabolic stress, or cisplatin treatment.
  • Utilized pharmacologic agonists and antagonists for adenosine receptors.
  • Assessed exosome functional activity via Jurkat cell apoptosis assays.

Main Results:

  • A1R and A2AR constrained exosome production in PGVSMCs under normal conditions.
  • A1R, A2AR, and A2BR constrained exosome production under metabolic stress.
  • A2A receptor activation reduced exosome production in cancer cells, enhancing Jurkat cell apoptosis.
  • A2A receptor antagonism increased exosome production under stress or cisplatin treatment.

Conclusions:

  • A2A receptors consistently suppress exosome release in all examined cell types.
  • The influence of A1R and A2BR on exosome production is cell-type and condition-dependent.
  • Targeting cancer with A2A receptor antagonists might unintentionally increase tumor exosome production.