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Caveolin regulation of microglial activation and proliferation
Author(s) -
Niesman Ingrid R,
Patton Miranda,
Zemke Nathan,
Levy Karen,
Ali Sameh S,
Head Brian P,
Patel Hemal H
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1007.1
Subject(s) - microglia , microbiology and biotechnology , biology , neuroinflammation , gene isoform , knockout mouse , inflammation , receptor , immunology , gene , biochemistry
Microglia are ramified cells serving as central nervous system (CNS) guardians. Following CNS injury or infection, microglia contract and cells adopts an amoeboid morphology capable of proliferation and migration. Though extracellular factors may be involved in this transformation, the control point for microglia activation or repression is unknown. Caveolin (Cav), a cholesterol binding protein, is expressed in inflammatory cells, yet the role of Cav in macrophage physiology is debatable. We propose that Cavs provide critical signaling regulatory points for injury‐induced microglial function. Global Cav‐1 knockout mice show increased hippocampal microglia compared to age matched littermates. Using a mouse microglia cell line (BV2) we investigated the role for Cavs in microglia function. We detected mRNA and protein for all three Cav isoforms (Cav‐1, ‐2, and ‐3) in BV2 cells. Cav‐1 protein was significantly reduced in inactive cells and localized to plasmalemmaand cytoplasmic vesicles (PM/CV). In activated cells, Cav‐1 appeared cytosolic or associated with PM/CV. In contrast, Cav‐3 was highly expressed in inactive cells and localized with processes and perinuclear. In the activated state, Cav‐3 expression decreased and localization was predominantly detected in PM/CV. The present findings suggest distinct regulation of microglial function is Cav isoform specific in CNS and Cav may be an effective inflammatory target in the setting of CNS injury

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