NDLI: Endogenous nitric oxide attenuates erythropoietin gene expression in vivo

Content Provider	Springer Nature Link
Author	Todorov, V. Gess, B. Gödecke, A. Wagner, C. Schräder, J. Kurtz, A.
Copyright Year	2000
Abstract	This study aimed to investigate the role of endogenous nitric oxide (NO) in erythropoietin (EPO) gene expression in mice in vivo. For this purpose EPO mRNA was semiquantitated by ribonuclease protection assay in livers and kidneys of three groups of mice: wild-type (wt), endothelial NO-synthase (NOS) knockout mice (eNOS–/–), and wt treated with the NOS inhibitor N G-nitro-l-arginine methyl ester (50 mg.kg–1.day–1) for 4 days (wt+l-NAME). EPO gene expression was stimulated by normobaric hypoxia (8% O2) or by 0.1% carbon monoxide (CO) inhalation for 4 h each, or by intraperitoneal injection of 60 mg/kg cobaltous chloride (CoCl2) for 6 h. Renal EPO mRNA in wt increased 12-, 40-, and 13-fold over normoxic levels in response to hypoxia, CO and CoCl2 respectively. EPO mRNA was detectable in the livers only after CO exposure. Renal and hepatic EPO gene expression in wt+l-NAME appeared moderately increased relative to wt with a maximal 2.5-fold enhancement after CO exposure. EPO mRNA levels in eNOS–/– mirrored those of wt+l-NAME, but the effects were less prominent. Our data suggest that endogenous NO attenuates EPO gene expression in mice. This effect is dependent on the rate of EPO gene induction.
Starting Page	445
Ending Page	448
Page Count	4
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	439
Issue Number	4
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2014-04-27
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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