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Induction and Characterization of Pulmonary Hypertension in Mice using the Hypoxia/SU5416 Model

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Abnormal sympathoadrenal development and systemic hypotension in PHD3-/- mice.

Tammie Bishop¹, Denis Gallagher, Alberto Pascual

¹The Henry Wellcome Building for Molecular Physiology, University of Oxford, Headington Campus, Roosevelt Drive, Oxford OX3 7BN, United Kingdom.

Molecular and Cellular Biology

|March 12, 2008

Summary

The hypoxia-inducible factor (HIF) prolyl hydroxylase PHD3 is crucial for normal development of the sympathoadrenal system. Loss of PHD3 leads to increased cell numbers but impaired function and lower blood pressure.

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Area of Science:

Neuroscience
Developmental Biology
Molecular Biology

Background:

Cell culture studies suggest PHD3 regulates neuronal apoptosis.
Hypoxia-inducible factors (HIFs) are key regulators of cellular response to oxygen levels.

Purpose of the Study:

To investigate the in vivo role of PHD3 in neuronal development and function.
To elucidate the interaction between PHD3 and HIFs in the sympathoadrenal system.

Main Methods:

Generation and analysis of PHD3 knockout (PHD3(-/-)) mice.
Genetic crosses with HIF-1alpha and HIF-2alpha heterozygous mice.
Assessment of neuronal apoptosis, cell numbers, and sympathoadrenal system function.

Main Results:

PHD3(-/-) mice exhibit reduced apoptosis and increased cell numbers in the superior cervical ganglion (SCG), adrenal medulla, and carotid body.
A functional interaction between PHD3 and HIF-2alpha, but not HIF-1alpha, was observed.
Despite increased cell mass, the sympathoadrenal system in PHD3(-/-) mice was hypofunctional, showing reduced innervation, secretory capacity, and blood pressure.

Conclusions:

PHD3 is essential for the proper anatomical and physiological development of the sympathoadrenal system, beyond just controlling cell survival.
A PHD3-HIF-2alpha pathway regulates sympathoadrenal development.
Dysregulation of PHD3 can impact critical functions like blood pressure regulation.