Open AccessIntermittent neonatal hypoxia elicits the upregulation of inflammatory‐related genes in adult male rats through long‐lasting programming effects
Author(s) -
Gehrand Ashley L.,
Kaldunski Mary L.,
Bruder Eric D.,
Jia Shuang,
Hessner Martin J.,
Raff Hershel
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12646
Subject(s) - intermittent hypoxia , hypoxia (environmental) , downregulation and upregulation , medicine , cxcl1 , endocrinology , peripheral blood mononuclear cell , chemokine , population , microarray , inflammation , obstructive sleep apnea , gene expression , andrology , biology , gene , chemistry , biochemistry , environmental health , organic chemistry , oxygen , in vitro
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.