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How to ‘deconvolute’ lung evolution - the evolutionary origins of pulmonary physiology

Part 2 of 3
Published on September 29, 2016   25 min

A selection of talks on Cell Biology

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My name is John Torday, I'm a Professor of Evolutionary Medicine at University of California, Los Angeles. This is lecture 14 in the evolutionary physiology course, the evolutionary origins of pulmonary physiology.
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In the late 1960s, it was discovered that the hormone Cortisol could accelerate lung development in preterm lambs in the womb. Primarily, stimulating lung surfactant production by the alveolar type two cell, thus eliminating surfactant deficiency, a major cause of disease or death in preterm infants. This was a breakthrough in the emerging discipline of neonatology and is considered one of the major discoveries of 20th century biomedical research.
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The fact that a simple molecule like cortisol could have such a profound effect on a complex process such as lung development was the impetus for the in-depth study of its mechanism of action. Fifty years later those studies culminated in fundamental understanding of how and why the mammalian lung evolved. By focusing on the cell-cell interactions involved in regulating surfactant production, that were necessary for the progressive decrease in Alveolar diameter to increase the surface area to blood volume ratio. The evolution of a lung is now understood. Briefly, adipocyte differentiation-related protein shown as ADRP actively facilitates the uptake, storage and transfer of surfactant substrate to the alveolar type II cell, mediated by the effects of leptin and PTHrP or Parathyroid hormone-related protein. The stretching of the alveolar wall during breathing stimulates these molecular signaling mechanisms, maintaining homeostasis within the alveolar space for oxygenation.
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How to ‘deconvolute’ lung evolution - the evolutionary origins of pulmonary physiology

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