Amyloidosis-inducing activity of blood cells in mouse AApoAII amyloidosis

Xin Ding1, Yingye Liu1, Mu Yang1

  • 1Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan.

Experimental Animals
|October 31, 2017
PubMed

Insights

Mouse senile amyloidosis, caused by apolipoprotein A-II (APOA2) deposits, can spread through blood cells. White blood cells and red blood cells from affected mice transmit the amyloidosis, highlighting blood

Area of Science:

  • Biochemistry
  • Immunology
  • Pathology

Background:

  • Mouse senile amyloidosis involves apolipoprotein A-II (APOA2) depositing as amyloid fibrils (AApoAII) in organs.
  • Previous studies showed AApoAII amyloidosis transmission via feces, milk, saliva, and muscle.

Purpose of the Study:

  • To investigate the transmission of AApoAII amyloidosis through blood components in a mouse model.
  • To identify specific blood fractions responsible for transmitting amyloidosis.

Main Methods:

  • Blood samples from amyloid-laden and amyloidosis-negative mice were fractionated into plasma, white blood cells (WBC), and red blood cells (RBC).
  • Fractions were further separated into soluble and insoluble components.
  • Fractions were injected into recipient mice to assess amyloidosis-induction activities (AIA).

Main Results:

  • WBC and RBC fractions from amyloid-laden mice induced AApoAII amyloid deposition in recipients.
  • Amyloid fibril-like materials and APOA2-reactive proteins were found in the insoluble fraction of blood cells, confirming WBC transmission.
  • Plasma from both amyloid-laden and amyloidosis-negative mice showed AIA, suggesting non-AApoAII factors induce deposition.

Conclusions:

  • AApoAII amyloidosis can be transmitted through blood cells (WBC and RBC).
  • The study identified blood cells as a transmission route for AApoAII amyloidosis.
  • Plasma contains additional factors that may contribute to amyloid deposition, independent of AApoAII fibrils.

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