Preterm birth increases susceptibility to hyperglycemia-induced glomerular alterations in the kidneys of male mice [scRNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1180529 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR31181542_1.fastq.gz | Fastqsanger.gz | |||
| SRR31181542_2.fastq.gz | Fastqsanger.gz | |||
| SRR31181544_1.fastq.gz | Fastqsanger.gz | |||
| SRR31181544_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 5 |
Similar Datasets
Project description:Diabetic kidney disease (DKD) is the leading cause of progressive chronic kidney disease in adults in the United States. However, the impact of preterm birth on the progression of DKD has not been studied. The goal of this project is to determine the effect of preterm birth on kidney health in a diabetic mouse model. CD-1 pups born preterm (19 days post conception (dpc)) and term (20 dpc) were studied, and outcomes of the male mice were reported, all compared to term mice. Preterm and term mice were treated with streptozotocin at six weeks to induce hyperglycemia. Body weight and blood sugar were monitored. Histologic, molecular, and imaging techniques were used to characterize the mice at 18 weeks. The preterm mice with diabetes had a lower podocyte density, lower proximal tubular fraction, and more atubular glomeruli compared to the term mice without diabetes. They also had a lower podocyte density and lower renin expression compared to term mice with diabetes. Based on single-cell RNA sequencing, preterm mice with diabetes had increased expression of genes related to the angiogenesis migration pathway-related in endothelial cells and increased expression of genes in the actin adhesion pathway in podocytes compared to term mice with diabetes. Furthermore, the preterm mice with diabetes exhibited a weaker endothelial cell-podocyte interaction compared to term mice with diabetes. These data suggest that preterm birth increases susceptibility to glomerular and tubular damage after a brief “second hit” of hyperglycemia. In conclusion, preterm birth disrupts endothelial-podocyte crosstalk and increases susceptibility to kidney injury induced by hyperglycemia.
2025-06-04 | GSE280780 | GEO
Project description:Diabetic kidney disease (DKD) is the leading cause of progressive chronic kidney disease in adults in the United States. However, the impact of preterm birth on the progression of DKD has not been studied. The goal of this project is to determine the effect of preterm birth on kidney health in a diabetic mouse model. CD-1 pups born preterm (19 days post conception (dpc)) and term (20 dpc) were studied, and outcomes of the male mice were reported, all compared to term mice. Preterm and term mice were treated with streptozotocin at six weeks to induce hyperglycemia. Body weight and blood sugar were monitored. Histologic, molecular, and imaging techniques were used to characterize the mice at 18 weeks. The preterm mice with diabetes had a lower podocyte density, lower proximal tubular fraction, and more atubular glomeruli compared to the term mice without diabetes. They also had a lower podocyte density and lower renin expression compared to term mice with diabetes. Based on single-cell RNA sequencing, preterm mice with diabetes had increased expression of genes related to the angiogenesis migration pathway-related in endothelial cells and increased expression of genes in the actin adhesion pathway in podocytes compared to term mice with diabetes. Furthermore, the preterm mice with diabetes exhibited a weaker endothelial cell-podocyte interaction compared to term mice with diabetes. These data suggest that preterm birth increases susceptibility to glomerular and tubular damage after a brief “second hit” of hyperglycemia. In conclusion, preterm birth disrupts endothelial-podocyte crosstalk and increases susceptibility to kidney injury induced by hyperglycemia.
2025-06-04 | GSE280781 | GEO
Project description:Preterm birth increases susceptibility to hyperglycemia-induced glomerular alterations in the kidneys of male mice
| PRJNA1180526 | ENA
Project description:Preterm birth increases susceptibility to hyperglycemia-induced glomerular alterations in the kidneys of male mice [bulk RNA-seq]
| PRJNA1180530 | ENA
Project description:Background: Preterm birth increases the long-term risk of diabetes and chronic kidney disease (CKD), yet its impact on diabetic kidney disease (DKD) is unclear. We previously showed that male preterm mice with diabetes develop early features of DKD, including reduced podocyte density, decreased renin expression, activation of angiogenesis pathways, and impaired endothelial–podocyte signaling. Here, we examine whether preterm birth similarly accelerates DKD progression in female mice and compare structural and transcriptomic outcomes in the females to the prior male cohort to assess sex-specific differences. Methods: Preterm mice were delivered by Cesarean section at 19 days post conception (dpc) and term mice at 20 dpc. Hyperglycemia was induced at 6 weeks with streptozotocin to generate term-diabetic (T-D) and preterm-diabetic (PT-D) groups; controls were term-nondiabetic (T-ND) and preterm-nondiabetic (PT-ND). Body weight and glucose were monitored, and kidneys were analyzed at 18 weeks using histologic, stereologic, imaging, and transcriptomic methods. Results: Compared with T-ND females, PT-D females showed higher albuminuria, more atubular glomeruli, reduced proximal tubule (PT) fraction, and pro-fibrotic gene activation. Compared to T-D females, PT-D females had higher blood urea nitrogen (BUN) levels and reduced PT fraction. This was associated with activation of pathways associated with the vasculature and suppression of mitochondrial metabolism gene pathways, along with Notch signaling alterations. Sex differences included a lower PT fraction in preterm females than males and fewer atubular glomeruli in PT-D females than PT-D males. Renin expression was lower in PT-D than T-D in males only. When comparing PT-D to T-D across sexes, 582 differentially expressed genes were unique to females. Notch signaling was upregulated in both male and female PT-D mice compared to T-D. Conclusion: Preterm birth increases susceptibility to kidney injury in females after exposure to hyperglycemia. However, preterm females with hyperglycemia are more resistant to kidney damage than males.
2026-05-05 | GSE319377 | GEO
Project description:Preterm birth, defined as birth <37 weeks of gestation, is a leading cause of infant morbidity and mortality. In the United States, approximately 12% of all births are preterm.1 Despite decades of research, there has been little progress in developing effective interventions to prevent preterm birth. In fact, the rate of preterm birth has increased slightly over the last several decades.2 The ultimate goal of the Genomic and Proteomic Network for Preterm Birth Research (GPN-PBR) is to identify possible biomarkers that could predict the susceptibility to spontaneous preterm birth (SPTB) as well as to shed light on the molecular mechanisms involved in its etiologies. Understanding those mechanisms will help us predict SPTB and may facilitate the introduction of more effective prevention and treatment strategies.
2014-08-28 | PXD001268 | Pride
Project description:Preterm birth is often predisposed by chorioamnionitis (CA) and CA affects the fetal gut and lungs via intra-amniotic (IA) inflammation, thus accentuating the proinflammatory effects of preterm birth. It is not known if IA inflammation also affects other perfusion-sensitive organs (e.g., kidneys) before and after preterm birth. Using preterm pigs as model for preterm infants, we hypothesized that CA induces fetal and neonatal renal dysfunctions that can intially be detected via plasma proteome, partly explaining the frequent renal dysfunction in preterm infants. Fetal pigs (88% gestation) were given an IA dose of lipopolysaccharide (LPS, 1 mg/kg, n=28), delivered preterm by cesarean section three days later, and compared with controls (CON, n=26) at birth and postnatal day five. Plasma proteome and protein markers of inflammatory pathways were evaluated.
2021-03-25 | PXD014619 | Pride
Project description:Preterm birth-affecting ~10% of live births globally-is associated with a markedly increased lifetime risk of chronic kidney disease (CKD), reportedly up to fivefold higher than in term births. Yet, the mechanisms linking prematurity to impaired renal development remain incompletely understood. Here, we investigated how preterm birth influences nephron endowment, kidney function, and the trajectory of kidney injury in a mifepristone-induced mouse model. We compared renal structure and function between preterm and term-born mice at postnatal day (P) 30 and P180, quantifying nephron number, glomerular morphology, and injury markers. We also performed bulk RNA sequencing on sorted nephron progenitor cells (NPCs) and non-NPC fractions from post-conception (PC) days 19.5–21.5, spanning the final window of nephrogenesis. Preterm mice exhibited up to 17% fewer nephrons at P30 (p < 0.01) and a ~25% lower kidney-to-body-weight ratio at P30 and P180 (both p < 0.05), despite a ~40% increase in body weight by P180. Injury biomarkers were elevated at P30 and P180, with serum creatinine increased by ~50%, NGAL by ~35%, urinary albumin excretion approximately doubled (p < 0.001), and KIM-1 elevated in preterm versus term controls. Glomerular density at P180 was reduced by ~30% in preterm mice; glomeruli were disproportionately localized in the medulla, and increased Bowman’s space area and capsule ratios suggested filtration defects. Transcriptomic profiling around the time of preterm birth revealed acute induction of cellular stress pathways and transiently impaired NPC differentiation that resolved within 24 hours. Concomitantly, we observed a short-lived increase in NPC proliferation and an approximate 24-hour extension of nephrogenesis, consistent with a compensatory response to bolster nephron formation and indicating a potential therapeutic window. In summary, preterm birth perturbs NPC developmental timing and stress responses, leading to reduced nephron endowment and persistent susceptibility to kidney injury.
2026-04-17 | GSE316576 | GEO
Project description:In this study, the molecular signature of placenta membrane from preterm birth placenta was assessed and compared to full-term placenta by proteomic profiling with the aim to identify molecules relevant to preterm birth.
2020-04-17 | MSV000085301 | MassIVE
Project description:Preterm birth is the leading cause of infant mortality resulting in over one million neonatal deaths annually. Maternal urinary tract infection (UTI) during pregnancy increases risk for preterm birth; however, biological processes mediating UTI-associated preterm birth are not well-described. We established a murine maternal UTI model in which challenge with uropathogenic E. coli resulted in preterm birth in about half of dams. Dams experiencing preterm birth displayed excessive bladder inflammation and altered uteroplacental T cell polarization compared to non-laboring infected dams, with no differences in bacterial burdens. Additional factors associated with preterm birth included higher proportions of male fetuses and lower maternal serum IL-10. Furthermore, exogenous maternal IL-10 treatment absolved UTI-associated preterm birth but contributed to fetal growth restriction in this model.
2025-10-23 | GSE280297 | GEO