Hematopoietic α7 nicotinic acetylcholine receptor deficiency increases inflammation and platelet activation status, but does not aggravate atherosclerosis

J Thromb Haemost. 2015 Jan;13(1):126-35. doi: 10.1111/jth.12765. Epub 2014 Nov 13.

Abstract

Background: The autonomic nervous system attenuates inflammation through activation of the α7 nicotinic acetylcholine receptor (α7nAChR), a pathway termed the cholinergic anti-inflammatory reflex. Interestingly, α7nAChR is expressed on immune cells and platelets, both of which play a crucial role in the development of atherosclerosis.

Objective: To investigate the role of hematopoietic α7nAChR in inflammation and platelet function in atherosclerotic ldlr(-/-) mice and to identify its consequences for atherosclerotic lesion development.

Methods: Bone marrow from α7nAChR(-/-) mice or wild-type littermates was transplanted into irradiated ldlr(-/-) mice. After a recovery period of 8 weeks, the mice were fed an atherogenic Western-type diet for 7 weeks.

Results: Hematopoietic α7nAChR deficiency clearly increased the number of leukocytes in the peritoneum (2.6-fold, P < 0.001), blood (2.9-fold; P < 0.01), mesenteric lymph nodes (2.0-fold; P < 0.001) and spleen (2.2-fold; P < 0.01), indicative of an increased inflammatory status. Additionally, expression of inflammatory mediators was increased in peritoneal leukocytes (TNFα, 1.6-fold, P < 0.01; CRP, 1.8-fold, P < 0.01) as well as in the spleen (TNFα, 1.6-fold, P < 0.01). The lack of α7nAChR on platelets from these mice increased the expression of active integrin αIIb β3 upon stimulation by ADP (1.9-fold, P < 0.01), indicating increased activation status, while incubation of human platelets with an α7nAChR agonist decreased aggregation (-35%, P < 0.05). Despite the large effects of hematopoietic α7nAChR deficiency on inflammatory status and platelet function, it did not affect atherosclerosis development or composition of lesions.

Conclusions: Hematopoietic α7nAChR is important for attenuation of inflammatory responses and maintaining normal platelet reactivity, but loss of hematopoietic α7nAChR does not aggravate development of atherosclerosis.

Keywords: alpha7 nicotinic acetylcholine receptor; atherosclerosis; bone marrow transplantation; inflammation; platelets.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta / metabolism
  • Aorta / pathology
  • Aortic Diseases / blood
  • Aortic Diseases / etiology*
  • Aortic Diseases / genetics
  • Aortic Diseases / pathology
  • Atherosclerosis / blood
  • Atherosclerosis / etiology*
  • Atherosclerosis / genetics
  • Atherosclerosis / pathology
  • Blood Platelets / metabolism*
  • Bone Marrow Transplantation
  • Diet, Western
  • Disease Models, Animal
  • Female
  • Genotype
  • Hematopoietic Stem Cell Transplantation
  • Hematopoietic Stem Cells / metabolism*
  • Inflammation / blood
  • Inflammation / etiology*
  • Inflammation / genetics
  • Inflammation Mediators / blood
  • Leukocytes / metabolism
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Phenotype
  • Plaque, Atherosclerotic
  • Platelet Activating Factor*
  • Receptors, LDL / deficiency
  • Receptors, LDL / genetics
  • Time Factors
  • alpha7 Nicotinic Acetylcholine Receptor / deficiency*
  • alpha7 Nicotinic Acetylcholine Receptor / genetics

Substances

  • Chrna7 protein, mouse
  • Inflammation Mediators
  • Platelet Activating Factor
  • Receptors, LDL
  • alpha7 Nicotinic Acetylcholine Receptor