Related Experiment Video
Updated: Aug 23, 2026
Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
Published on: November 21, 2025
Sequential induction of Hsp25 and proliferating cell nuclear antigen in the kidney after burn
Jayoung Jeong1, David G Greenhalgh, Kiho Cho
1Burn Research, Shriners Hospitals for Children Northern California and Department of Surgery, University of California at Davis, Sacramento, CA 95817, USA.
Abstract:
Burn injury elicits a wide range of intracellular signaling events leading to alterations in phenotypes of distant organs. Renal dysfunction is one of several serious postburn complications. To better understand the underlying mechanisms of renal dysfunction among burn patients, we investigated alterations in the expression of heat shock proteins (Hsps) and cell cycle-associated proteins in the kidney after burn. Following an approximately 18% total body surface area burn, blood and kidney samples were harvested from mice at several time points. Serum levels of blood urea nitrogen increased significantly at 3 h and returned to basal levels at Day 1 implying a transient dysfunction of glomerular filtration. The expression of Hsp25 was increased at Day 1, whereas no changes in Hsp70 expression were observed. An increase in proliferating cell nuclear antigen (PCNA), a marker of cell proliferation, peaked at Day 3, and its expression was predominantly limited to cells appearing to be tubular epithelial cells in the cortex. In contrast, no significant alterations in the p21 mitosis inhibitor were noted. Furthermore, increases in histones H1 and H2A at Day 3 paralleled the PCNA induction suggesting a burn-mediated alteration in cell cycle activities. The results from this study suggest that a sizeable burn may trigger sequential activation of signaling events involved in the early pathogenesis and subsequent recovery of the kidney after burn.
Insights
A significant burn injury temporarily impairs kidney function, evidenced by increased blood urea nitrogen. This study reveals burn-induced changes in kidney heat shock proteins and cell cycle proteins, suggesting a role in post-burn renal recovery.
Area of Science:
- Renal pathophysiology
- Burn injury mechanisms
- Cellular signaling
Background:
- Burn injuries trigger systemic intracellular signaling, leading to distant organ dysfunction.
- Renal dysfunction is a critical complication following severe burns.
- Understanding kidney response to burns is crucial for patient outcomes.
Purpose of the Study:
- To investigate alterations in heat shock proteins (Hsps) and cell cycle proteins in the kidney post-burn.
- To elucidate the molecular mechanisms underlying burn-induced renal dysfunction.
- To identify potential pathways involved in kidney recovery after thermal injury.
Main Methods:
- Induction of an ~18% total body surface area burn in mice.
- Collection of blood and kidney samples at multiple time points post-burn.
- Analysis of serum blood urea nitrogen levels, Hsp25, Hsp70, proliferating cell nuclear antigen (PCNA), p21, and histone expression.
Main Results:
- Transient increase in serum blood urea nitrogen at 3 hours post-burn, indicating glomerular filtration impairment.
- Increased expression of Hsp25 at Day 1; Hsp70 expression remained unchanged.
- Proliferating cell nuclear antigen (PCNA) expression peaked at Day 3, primarily in cortical tubular epithelial cells.
- Histone H1 and H2A levels increased at Day 3, correlating with PCNA induction, suggesting altered cell cycle activity.
Conclusions:
- Significant burn injury initiates a cascade of signaling events impacting kidney function.
- Burn-mediated changes in Hsps and cell cycle proteins are implicated in early kidney pathogenesis and recovery.
- The kidney exhibits adaptive responses to burn injury, involving cell proliferation and altered cell cycle regulation.
Related Concept Videos
01:29Acute Kidney Injury III: Clinical Manifestations
01:26Kidney Transplant II: Surgical Procedure