MilliporeSigma
  • Genetic background-dependent abnormalities of the enteric nervous system and intestinal function in Kif26a-deficient mice.

Genetic background-dependent abnormalities of the enteric nervous system and intestinal function in Kif26a-deficient mice.

Scientific reports (2021-02-06)
Yukiko Ohara, Lisa Fujimura, Akemi Sakamoto, Youichi Teratake, Shuichi Hiraoka, Haruhiko Koseki, Takeshi Saito, Keita Terui, Tetsuya Mitsunaga, Mitsuyuki Nakata, Hideo Yoshida, Masahiko Hatano
ABSTRACT

The Kif26a protein-coding gene has been identified as a negative regulator of the GDNF-Ret signaling pathway in enteric neurons. The aim of this study was to investigate the influence of genetic background on the phenotype of Kif26a-deficient (KO, -/-) mice. KO mice with both C57BL/6 and BALB/c genetic backgrounds were established. Survival rates and megacolon development were compared between these two strains of KO mice. Functional bowel assessments and enteric neuron histopathology were performed in the deficient mice. KO mice with the BALB/c genetic background survived more than 400 days without evidence of megacolon, while all C57BL/6 KO mice developed megacolon and died within 30 days. Local enteric neuron hyperplasia in the colon and functional bowel abnormalities were observed in BALB/c KO mice. These results indicated that megacolon and enteric neuron hyperplasia in KO mice are influenced by the genetic background. BALB/c KO mice may represent a viable model for functional gastrointestinal diseases such as chronic constipation, facilitating studies on the underlying mechanisms and providing a foundation for the development of treatments.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
β-Nicotinamide adenine dinucleotide 2′-phosphate reduced tetrasodium salt hydrate, ≥97% (HPLC)
Sigma-Aldrich
Nitrotetrazolium Blue chloride, ≥90.0% (HPLC)
Sigma-Aldrich
Acetylthiocholine iodide, ≥98% (TLC), powder or crystals
Sigma-Aldrich
Ethopropazine hydrochloride, ≥98% (HPLC), powder