Intermittent neonatal hypoxia elicits the upregulation of inflammatory‐related genes in adult male rats through long‐lasting programming effects

Physiological Reports

Ashley L. Gehrand²  Mary L. Kaldunski¹  Eric D. Bruder²  Shuang Jia¹  Martin J. Hessner¹ 

[1] Max McGee National Research Center for Juvenile Diabetes, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin;Endocrine Research Laboratory, Aurora St. Luke's Medical Center, Aurora Research Institute, Milwaukee, Wisconsin

关键词: Glucose;    inflammation;    insulin;    intermittent hypoxia;    neonatal;    newborn;    programming;   

DOI  :  10.14814/phy2.12646

来源: Wiley

【 摘 要 】

Abstract

The long-term effects of neonatal intermittent hypoxia (IH), an accepted model of apnea-induced hypoxia, are unclear. We have previously shown lasting “programming” effects on the HPA axis in adult rats exposed to neonatal IH. We hypothesized that neonatal rat exposure to IH will subsequently result in a heightened inflammatory state in the adult. Rat pups were exposed to normoxia (control) or six cycles of 5% IH or 10% IH over one hour daily from postnatal day 2–6. Plasma samples from blood obtained at 114 days of age were analyzed by assessing the capacity to induce transcription in a healthy peripheral blood mononuclear cell (PBMC) population and read using a high-density microarray. The analysis of plasma from adult rats previously exposed to neonatal 5% IH versus 10% IH resulted in 2579 significantly regulated genes including increased expression of Cxcl1, Cxcl2, Ccl3, Il1a, and Il1b. We conclude that neonatal exposure to intermittent hypoxia elicits a long-lasting programming effect in the adult resulting in an upregulation of inflammatory-related genes.

【 授权许可】

CC BY   
© 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.