Expression of HoxB5, SPC and AQP5 in neonatal rats with hyperoxia-induced chronic lung disease.
- Author:
Wei XU
1
;
Jian-Hua FU
;
Xin-Dong XUE
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Aquaporin 5; analysis; genetics; Chronic Disease; Female; Homeodomain Proteins; analysis; genetics; Hyperoxia; complications; Immunohistochemistry; Lung; pathology; Lung Diseases; etiology; metabolism; Male; Pulmonary Surfactant-Associated Protein C; analysis; genetics; RNA, Messenger; analysis; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction
- From: Chinese Journal of Contemporary Pediatrics 2009;11(1):51-55
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEAlveolar epithelium impairment is one of pathological changes associated with chronic lung disease (CLD). Hoxb5 is one of the few homeobox genes strongly expressed in the developing lung. This study investigated the expression of HoxB5, SPC and AQP5 in rats with CLD in order to explore the role of Hoxb-5 in impairment and reparation of alveolar epithelium.
METHODSEighty neonatal rats were randomly exposed to hyperoxia (model group) or to room air (control group) (n=40 each). The CLD model was induced by hyperoxia exposure. The expression of HoxB5, SPC and AQP5 protein and mRNA in the lung tissue was detected by immunohistochemistry and RT-PCR 1, 3, 7, 14 and 21 days after exposure.
RESULTSIn the model group HoxB5 expression significantly decreased 7, 14 and 21 days after hyperoxia exposure. SPC expression decreased 3 days after hyperoxia exposure but increased significantly 7, 14 and 21 days after hyperoxia exposure as compared to the control group. AQP5 expression was progressively reduced with prolonged hyperoxia exposure.
CONCLUSIONSHyperoxia exposure may lead to alveolar epithelial cell (AEC) damage in neonatal rats. The increased SPC expression and decreased AQP5 expression suggested that the ability of differentiation and transformation of AECII into AECI decreased in neonatal rats with CLD. The decreased HoxB5 expression following hyperoxia exposure might contribute to a decreased ability of differentiation of AECII.