دورية أكاديمية

Effect of hypoxia on lung, heart, and liver insulin-like growth factor-I gene and receptor expression in the newborn rat.

التفاصيل البيبلوغرافية
العنوان: Effect of hypoxia on lung, heart, and liver insulin-like growth factor-I gene and receptor expression in the newborn rat.
المؤلفون: Moromisato DY; Division of Respiratory and Critical Care, Harbor-UCLA Medical Center, Torrance, CA 90509, USA., Moromisato MY, Zanconato S, Roberts CT Jr
المصدر: Critical care medicine [Crit Care Med] 1996 Jun; Vol. 24 (6), pp. 919-24.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
اللغة: English
بيانات الدورية: Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 0355501 Publication Model: Print Cited Medium: Print ISSN: 0090-3493 (Print) Linking ISSN: 00903493 NLM ISO Abbreviation: Crit Care Med Subsets: MEDLINE
أسماء مطبوعة: Publication: Philadelphia, PA : Lippincott Williams & Wilkins
Original Publication: New York, Kolen.
مواضيع طبية MeSH: Heart/*growth & development , Hypoxia/*physiopathology , Insulin-Like Growth Factor I/*genetics , Liver/*growth & development , Lung/*growth & development, Animals ; Animals, Newborn ; Binding, Competitive ; Body Weight ; Eating ; Female ; Gene Expression Regulation, Developmental ; Insulin-Like Growth Factor I/metabolism ; Organ Size ; Prospective Studies ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptor, IGF Type 1/genetics ; Receptor, IGF Type 1/metabolism
مستخلص: Objectives: We examined the effect of 7 days of hypoxia in the newborn rat on: a) body, heart, and lung growth; b) circulating insulin-like growth factor-I (IGF-I); c) lung, heart, and liver IGF-I gene expression; and d) lung IGF-I type 1 receptor gene expression and IGF-I receptor binding. We hypothesize that hypoxic exposure would modify body and organ growth and alter IGF-I gene and receptor expression in an organ specific manner.
Design: Randomized, controlled prospective study.
Setting: University research laboratory.
Subjects: Eleven newborn rat litters (n = 10 per litter) comprised the hypoxia-exposed group and 11 litters comprised the control group (room air).
Interventions: Hypoxia-group rats were placed in a chamber with an FIO2 of 0.12 on postnatal day 1. Control group rats breathed room air. Exposure to hypoxia continued for 7 days.
Measurements and Main Results: Hepatic, lung, and cardiac IGF-I mRNA levels and lung IGF-I type 1 receptor mRNA were analyzed, using the ribonuclease protection assay. Crude membrane extracts were used for competitive binding studies with IGF-I and insulin. Somatic growth in the hypoxic group was reduced by 22% (final weight: hypoxic, 14.8 +/- 1.2 g; control, 17.1 +/- 1.5 g; p < .001). The relative weight (organ weight/body weight [mg/g]) of the heart was increased by 39% (p < .001) in the hypoxic pups compared with the normoxic animals, while the relative weight of the lung was unchanged. With hypoxia, IFG-I mRNA concentrations were significantly increased both in the heart and lung (30% and 33%, respectively, p < .02); but, in contrast, IGF-I mRNA concentrations were not significantly different in the liver. The IGF-I receptor mRNA in the lung was increased by 200% (p < .02) in hypoxia compared with controls. There was no effect of hypoxia on specific or nonspecific binding of IGF-I or insulin in the lung tissue. However, specific binding was 33% greater in the IGF-I compared with the insulin experiments.
Conclusions: a) Hypoxia increased IGF-I mRNA in the heart, and increased both IGF-I mRNA and IGF-I type 1 receptor mRNA in the lung. b) The effects of hypoxia on IFG-I are tissue-specific.
معلومات مُعتمدة: HD26939 United States HD NICHD NIH HHS; HL11907 United States HL NHLBI NIH HHS
المشرفين على المادة: 67763-96-6 (Insulin-Like Growth Factor I)
EC 2.7.10.1 (Receptor, IGF Type 1)
تواريخ الأحداث: Date Created: 19960601 Date Completed: 19960821 Latest Revision: 20190706
رمز التحديث: 20240627
DOI: 10.1097/00003246-199606000-00008
PMID: 8681592
قاعدة البيانات: MEDLINE
الوصف
تدمد:0090-3493
DOI:10.1097/00003246-199606000-00008