Regulation of gap junction channels by infectious agents and inflammation in the CNS

Paul Castellano, Eliseo Eugenin

Research output: Contribution to journalReview article

24 Citations (Scopus)

Abstract

Gap junctions (GJs) are conglomerates of intercellular channels that connect the cytoplasm of two or more cells, and facilitate the transfer of ions and small molecules, including second messengers, resulting in metabolic and electrical coordination. In general, loss of gap junctional communication (GJC) has been associated with cellular damage and inflammation resulting in compromise of physiological functions. Recently, it has become evident that GJ channels also play a critical role in the pathogenesis of infectious diseases and associated inflammation. Several pathogens use the transfer of intracellular signals through GJ channels to spread infection and toxic signals that amplify inflammation to neighboring cells. Thus, identification of the mechanisms by which several infectious agents alter GJC could result in new potential therapeutic approaches to reduce inflammation and their pathogenesis.

Original languageEnglish (US)
Article number122
JournalFrontiers in Cellular Neuroscience
Volume8
Issue numberMAY
DOIs
StatePublished - May 9 2014
Externally publishedYes

Fingerprint

Gap Junctions
Inflammation
Poisons
Second Messenger Systems
Communicable Diseases
Cytoplasm
Ions
Infection
Therapeutics

Keywords

  • Astrocytes
  • Hemichannel
  • HIV
  • Microglia
  • Oligodendrocytes

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

Regulation of gap junction channels by infectious agents and inflammation in the CNS. / Castellano, Paul; Eugenin, Eliseo.

In: Frontiers in Cellular Neuroscience, Vol. 8, No. MAY, 122, 09.05.2014.

Research output: Contribution to journalReview article

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