Effects of hypoxia on stress proteins in the piglet heart at birth
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A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Pamela Louapre1, Jean F Grongnet, Robert M Tanguay
1AGROCAMPUS de Rennes, INRA UMRVP, 65, rue de Saint-Brieuc-CS 84215-35042 Rennes Cedex, France.
Insights
Hypoxia at birth significantly increases alphaB-crystallin expression in piglets' hearts. This heat shock protein
Area of Science:
- Cardiovascular Physiology
- Neonatal Stress Response
- Molecular Biology
Background:
- Hypoxia at birth can cause lasting heart damage.
- Heat shock proteins (HSPs) offer cellular protection, but their role during birth hypoxia is unclear.
Purpose of the Study:
- To investigate the expression of HSPs and nitric oxide synthases (NOS) in piglets experiencing hypoxia at birth.
- To determine the specific response of alphaB-crystallin to hypoxic stress during the neonatal period.
Main Methods:
- Newborn piglets were exposed to hypoxic conditions (5% oxygen) for 1 or 4 hours.
- Recovery periods varied from 1 to 68 hours.
- Western blot analysis was used to measure levels of alphaB-crystallin, other HSPs, and NOS isoforms.
Main Results:
- AlphaB-crystallin expression was significantly elevated in the left ventricle following hypoxia.
- Hypoxia-inducible factor 1-alpha (HIF1α) and Heme oxygenase 1 were also overexpressed.
- Neuronal NOS showed a moderate increase in the left ventricle.
Conclusions:
- The heat shock protein alphaB-crystallin is strongly upregulated in the neonatal heart during hypoxia.
- This response distinguishes alphaB-crystallin from other HSPs like Hsp27 under low oxygen conditions.
- Heme oxygenase is not the sole HSP exhibiting oxygen-dependent gene expression.
Abstract:
Hypoxia at birth represents a very stressful event that can result in severe lifelong consequences in different tissues, including those of the heart. Heat shock and other associated stress proteins are involved in cellular protection, but their roles are not clearly defined at the time of birth. Newborn piglets were subjected to 5% oxygen and 95% nitrogen for either 1 or 4 hours. They were allowed to recover over periods of 1 to 68 hours. The relative levels of alphaB-crystallin, HspB8, Hsp20, Hsp27, Hsp60, and Hsp70 as well as nitric oxide synthases (NOS) (endothelial NOS, inducible NOS, neuronal NOS) were examined by Western blot analysis. Surprisingly, alphaB-crystallin expression was drastically increased in animals submitted to hypoxia. The hypoxia-associated factor HIFlalpha was also strongly and rapidly overexpressed. Heme oxygenase 1 was also increased. To a lesser extent, neuronal NOS was also increased in the left ventricle of animals submitted to hypoxia. This work clearly shows that the Hsp chaperone alphaB-crystallin is strongly overexpressed in the left ventricle of animals submitted to hypoxia. This observation dissociates the response to low oxygenation of alphaB-crystallin and other stress-associated proteins including Hsp27, and it indicates that heme oxygenase is not alone among HSPs in its oxygen-related gene expression.
