Journal
BIOLOGICAL & PHARMACEUTICAL BULLETIN
Volume 41, Issue 5, Pages 786-796Publisher
PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.b18-00041
Keywords
calcineurin; enteric glial cell; small intestine; inflammation; nuclear factor of activated T cells (NFAT)
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Funding
- Japan Society for the Promotion of Science (JSPS KAKENHI) [16K08744, 22500312]
- Grants-in-Aid for Scientific Research [22500312, 16K08744] Funding Source: KAKEN
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Although calcineurin is abundantly expressed in the nervous system and involved in neurite extension and synaptic plasticity in neurons, little is known about its roles in glial cells. To investigate the roles of calcineurin in glial cells, we generated glial calcineurin B1-conditional knockout (CKO) mice and analyzed the abnormalities in the small intestine. The CKO mice were generated by crossing foxed calcineurin B1 mice with glial fibrillary acidic protein (GFAP)-Cre mice. The CKO mice exhibited growth retardation approximately from the third postnatal week and died mostly within the fourth postnatal week. The small intestine of the CKO mice was thin and hemorrhagic. The mucosal layer was degenerated and GFAP expression was reduced in the CKO small intestine. These pathological changes were associated with inflammation and increased intestinal permeability. In contrast, no apparent abnormalities were observed in the large intestine of the CKO mice. Nuclear factor of activated T cells failed to translocate into the nucleus after stimulation in enteric glial cells of the CKO small intestine. In conclusion, the calcineurin B1 deficiency in glial cells impairs the small intestine and leads to malnutrition and eventual death in mice, suggesting that calcineurin plays a novel and important role in enteric glial cells.
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