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Gap Junctions01:27

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The cytoplasm of adjacent animal cells can exchange small molecules, ions, and secondary messengers via the communication channels which form the gap junctions. These junctions comprise a few hundred to thousands of molecular channels, each made of two halves, called the connexon hemichannel. A connexon is a hexamer of six transmembrane connexin proteins, which assemble radially, thus forming a pore or channel in the center. One connexon hemichannel docks with a corresponding connexon on the...
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Multicellular organisms employ a variety of ways for cells to communicate with each other. Gap junctions are specialized proteins that form pores between neighboring cells in animals, connecting the cytoplasm between the two, and allowing for the exchange of molecules and ions. They are found in a wide range of invertebrate and vertebrate species, mediate numerous functions including cell differentiation and development, and are associated with numerous human diseases, including cardiac and...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption
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Low Level Pro-inflammatory Cytokines Decrease Connexin36 Gap Junction Coupling in Mouse and Human Islets through

Nikki L Farnsworth1, Rachelle L Walter2, Alireza Hemmati2

  • 1From the Barbara Davis Center for Childhood Diabetes, Department of Bioengineering, University of Colorado, Anschutz Medical Campus, Aurora, Colorado 80045.

The Journal of Biological Chemistry
|December 16, 2015
PubMed
Summary
This summary is machine-generated.

Pro-inflammatory cytokines impair islet function by disrupting connexin36 gap junctions. This study reveals nitric oxide-regulated PKCδ mediates these changes, offering targets to protect against diabetes development.

Keywords:
PKC-δconnexin36cytokinediabetesgap junctionisletnitric oxide

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Area of Science:

  • Endocrinology and Metabolism
  • Cell Biology
  • Diabetes Research

Background:

  • Pro-inflammatory cytokines are implicated in the decline of pancreatic islet function during diabetes development.
  • Cytokine-induced disruption of insulin secretion and calcium dynamics is poorly understood.
  • Connexin36 gap junctions are crucial for glucose-induced calcium oscillations and insulin secretion, and their loss mirrors diabetes progression.

Purpose of the Study:

  • To investigate the mechanisms by which pro-inflammatory cytokines disrupt gap junction coupling in pancreatic islets.
  • To elucidate the role of protein kinase C delta (PKCδ) and nitric oxide (NO) in cytokine-mediated gap junction modulation.

Main Methods:

  • Isolated mouse and human islets were treated with a cytokine mixture (TNF-α, IL-1β, IFN-γ).
  • Measurements included insulin secretion, calcium dynamics, and gap junction coupling.
  • Modulators of PKCδ and NO were used to assess their involvement in cytokine-induced effects.

Main Results:

  • High cytokine levels induced islet cell death and reduced insulin secretion.
  • Low cytokine levels disrupted calcium dynamics and decreased gap junction coupling without affecting insulin secretion.
  • Reduced gap junction coupling was dependent on NO-regulated PKCδ and altered connexin36 membrane organization.

Conclusions:

  • Pro-inflammatory cytokines disrupt islet gap junction coupling through NO-regulated PKCδ and altered connexin36 organization.
  • These findings clarify mechanisms of islet dysfunction in diabetes.
  • The identified pathways offer potential therapeutic targets for ameliorating diabetes-associated islet dysfunction.