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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
Published on: August 2, 2018
Osteopontin expression in normal and hypobaric hypoxia-exposed rats.
M Uenoyama1, S Ogata, K Nakanishi
1Division of Environmental Medicine, National Defense Medical College Research Institute, Tokorozawa, Japan.
Acta Physiologica (Oxford, England)
|February 21, 2008
Summary
Hypobaric hypoxia exposure in rats showed decreased osteopontin (OPN) in plasma and adrenal glands, with transient increases in heart and lung. This suggests pulmonary hypertension may not significantly induce OPN without severe pressure overload.
Area of Science:
- Cardiovascular Physiology
- Altitude Medicine
- Molecular Biology
Background:
- Experimental pulmonary hypertension (PH) involves heart and pulmonary artery remodeling.
- Osteopontin (OPN) is a key factor in cardiovascular remodeling due to pressure or volume overload.
- The impact of hypobaric hypoxic environments (HHE) on OPN synthesis requires investigation.
Purpose of the Study:
- To investigate the effects of HHE on the OPN synthesis system.
- To determine OPN expression changes in response to simulated high altitude.
Main Methods:
- 148 male Wistar rats were exposed to simulated 5500 m altitude for up to 21 days.
- Plasma and tissue OPN levels were measured using various techniques.
- Immunohistochemistry was used to assess OPN protein distribution.
Main Results:
- Plasma and adrenal gland OPN levels decreased significantly by day 0.5 of HHE.
- Right ventricle OPN mRNA and lung OPN protein increased transiently on days 1 and 5, respectively.
- Changes in OPN synthesis did not correlate with the moderate increase in pulmonary arterial pressure (PAP).
Conclusions:
- PH induced by HHE at 5500 m may cause minimal OPN induction in the heart and lungs.
- Sustained OPN induction likely requires a more severe pulmonary arterial pressure overload.
- OPN regulation in response to hypoxic PH is complex and depends on pressure severity.
