VIP Enhances Phagocytosis of Fibrillar Beta-Amyloid by Microglia and Attenuates Amyloid Deposition in the Brain of APP/PS1 Mice | Zendy

Min Song | Zendy; Jiaxiang Xiong | Zendy; Yanyan Wang | Zendy; Jun Tang | Zendy; Bo Zhang | Zendy; Yun Bai | Zendy

Open Access

VIP Enhances Phagocytosis of Fibrillar Beta-Amyloid by Microglia and Attenuates Amyloid Deposition in the Brain of APP/PS1 Mice

Author(s) -

Min Song,

Jiaxiang Xiong,

Yanyan Wang,

Jun Tang,

Bo Zhang,

Yun Bai

Publication year - 2012

Publication title -

plos one

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.99

H-Index - 332

ISSN - 1932-6203

DOI - 10.1371/journal.pone.0029790

Subject(s) - microglia , vasoactive intestinal peptide , neurodegeneration , neuroprotection , phagocytosis , amyloid (mycology) , amyloid beta , tumor necrosis factor alpha , microbiology and biotechnology , chemistry , biology , endocrinology , medicine , inflammation , neuropeptide , immunology , pharmacology , peptide , biochemistry , receptor , inorganic chemistry , disease

Vasoactive intestinal peptide (VIP) is a multifunctional neuropeptide with demonstrated immunosuppressive and neuroprotective activities. It has been shown to inhibit Amyloid beta (Aβ)-induced neurodegeneration by indirectly suppressing the production and release of a variety of inflammatory and neurotoxic factors by activated microglia. We demonstrated that VIP markedly increased microglial phagocytosis of fibrillar Aβ42 and that this enhanced phagocytotic activity depended on activation of the Protein kinase C (PKC) signaling pathway. In addition, VIP suppressed the release of tumor necrosis factor alpha (TNF-α) and nitric oxide(NO) from microglia activated by combined treatment with fibrillar Aβ42 and low dose interferon-γ (IFN-γ). We utilized an adenovirus-mediated gene delivery method to overexpress VIP constitutively in the hippocampus of APPswPS1 transgenic mice. The Aβ load was significantly reduced in the hippocampus of this animal model of Alzheimer's disease, possibly due to the accumulation and activation of cd11b-immunoactive microglial cells. The modulation of microglial activation, phagocytosis, and secretion by VIP is a promising therapeutic option for the treatment of Alzheimer's disease(AD).

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research