Journalartikel

Bone status of acetylcholinesterase-knockout mice


AutorenlisteKauschke, Vivien; Kneffel, Mathias; Floel, Wolfgang; Hartmann, Sonja; Kampschulte, Marian; Duerselen, Lutz; Ignatius, Anita; Schnettler, Reinhard; Heiss, Christian; Lips, Katrin Susanne

Jahr der Veröffentlichung2015

Seiten222-230

ZeitschriftInternational Immunopharmacology

Bandnummer29

Heftnummer1

ISSN1567-5769

eISSN1878-1705

DOI Linkhttps://doi.org/10.1016/j.intimp.2015.07.046

VerlagElsevier


Abstract

Acetylcholinesterase (AChE) hydrolyzes acetylcholine (ACh) to acetate and choline and thereby terminates nerve impulse transmission. ACh is also expressed in bone tissue and enhances here proliferation and differentiation of osteoblasts, which makes it interesting to investigate effects of AChE deficiency on bone. To our knowledge, this is the first study that analyzed bone of heterozygous acetylcholinesterase-knockout (AChE-KO) mice.

Tibia, femur, thoracic and lumbar vertebrae of 16-week-old female heterozygous AChE-KO mice and their corresponding wildtypes (WT) were analyzed using real-time RT-PCR, dual-energy X-ray absorptiometry, biomechanics, micro-computed tomography, histology and histomorphometry.

Our data revealed that heterozygous AChE-MO did not cause negative effects upon bone parameters analyzed. In contrast, the number of osteoclasts per perimeter was significantly reduced in lumbar vertebrae. In addition, we found a significant decrease in trabecular perimeter of lumbar vertebrae and cortical area fraction (Ct.Ar/Tt.Ar) in the mid-diaphysis of femurs of AChE-KO mice compared to their WT. Therefore, presumably a local homozygous knockout of AChE or AChE-inhibitor administration might be beneficial for bone formation due to ACh accumulation. However, many other bone parameters analyzed did not differ statistically significantly between AChE-KO and WT mice. That might be reasoned by the compensating effect of butyrylcholinesterase (BChE). (C) 2015 Elsevier B.V. All rights reserved.




Zitierstile

Harvard-ZitierstilKauschke, V., Kneffel, M., Floel, W., Hartmann, S., Kampschulte, M., Duerselen, L., et al. (2015) Bone status of acetylcholinesterase-knockout mice, International Immunopharmacology, 29(1), pp. 222-230. https://doi.org/10.1016/j.intimp.2015.07.046

APA-ZitierstilKauschke, V., Kneffel, M., Floel, W., Hartmann, S., Kampschulte, M., Duerselen, L., Ignatius, A., Schnettler, R., Heiss, C., & Lips, K. (2015). Bone status of acetylcholinesterase-knockout mice. International Immunopharmacology. 29(1), 222-230. https://doi.org/10.1016/j.intimp.2015.07.046



Schlagwörter


ALZHEIMERS-DISEASE PATIENTSHIP FRACTUREOSTEOBLAST DIFFERENTIATIONOSTEOCLASTS


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