GSE162298
Identifying the molecular mechanisms that underlie impaired kidney development due to maternal diabetes.
The prevalence of diabetes has significantly increased among women of childbearing age worldwide, and it is known that infants who are exposed to maternal diabetes in utero are at increased risk of congenital anomalies of the kidney and urinary tract. The primary role of the kidney is to filter blood through the nephrons. These anomalies can result in a reduction in the number of nephrons that are formed during kidney development, or decreased congenital nephron endowment, which is linked to hypertension and chronic kidney disease. It is unknown how exposure to maternal diabetes in utero results in abnormal kidney development and the long-term health consequences of this exposure remain ill-defined. In this study, we profiled gene expression in the developing mouse kidney from C57BL/6J control and maternal diabetes exposed (DM_Exp) mice at single cell resolution. Consistent with previous studies, clusters with distinct transcriptional signatures clearly identify major compartments and cell types of the developing kidney. Overall design: Single cell RNA sequencing pooled cells from 1 kidney from postnatal day 2 (P2) C57BL/6J control and 1 kidney from postnatal day 2 (P2) DM_Exp male mice.