The present data imply that Memo1 in osteoblasts is dispensable for bone structure and expression of Fgf23. However, renal injury marker expression, circulating FGF23, and parathyroid hormone revealed a sex difference with more severely affected females than males of either genotype. During AKI, Fgf23 expression in calvaria, and renal transcriptional changes were comparable between genotypes. Micro-CT revealed no differences between genotypes in bone structure of vertebrae, femur, and tibia. Memo1 expression was blunted in bones of Memo obKO, whereas it remained unchanged in other organs. Memo obKO were viable without changes in gross anatomy, serum electrolytes, or circulating FGF23 concentrations compared to controls. We challenged mice with folic acid for acute kidney injury (AKI) and analyzed organs. We studied organs by micro-computed tomography, qPCR, and western blot. We deleted Memo1 in the osteoblast–osteocyte lineage in Memo fl/fl mice using a Cre under Col1a1 promotor to obtain osteoblast-specific knockout (obKO) mice. Here, we investigated whether Memo1 expression in osteoblasts is required for normal bone structure and FGF23 expression. Loss of the mediator Of cell motility 1 ( Memo1) in mice caused kidney disease and a bone disease with diminished osteoblast and osteoclast biomarkers in serum, resembling alterations occurring in adynamic bone disease in humans with chronic kidney disease or in Klotho-deficient mice.

Microsynth standard primers