The discovery of a vital molecule that regulates breathing could lead to better targeting and treatment of respiratory conditions.
Connexin26 (Cx26) is a key molecule that reacts to CO2 in our bodies and activates breathing, reports Professor Nicholas Dale at the University of Warwick’s School of Life Sciences.
“Important molecules with universal physiological functions are shaped by evolution,” says Dale. “We have exploited this simple fact to show that the CO2-binding characteristics of Cx26 are important in our bodies, too. This is likely to open up new ways to identify and treat people at risk of sleep apneas.”
Cx26 molecules detect levels of CO2 in the blood-stream, and when levels reach a certain point, they tell our bodies to excrete the CO2 and take in oxygen—the vital life-preserving process that allows us to breathe, and creates blood flow to the brain.
Without this essential molecular function, harmful levels of CO2 would remain in the bloodstream, making breathing difficult or impossible.
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Mutations in Cx26 are directly connected to a number of serious conditions—ranging from congenital deafness, to respiratory conditions, and serious syndromes that affect skin, vision, and hearing. As Cx26 is vital to breathing well, people carrying these mutations may be at risk of sleep apnea.
Identifying these mutations and working out how to restore the molecule to its normal function could lead to effective, targeted, personalized treatments to mitigate these risks and improve quality of life.
Different animals have varying levels of sensitivity to CO2. Dale’s group exploited this idea to see whether the properties of Cx26 matched the physiological requirements of: birds, which fly at high-altitude and can tolerate low levels of CO2; humans and rats which are broadly similar at an intermediate level; and mole rats, which live exclusively underground and tolerate very high levels of CO2.
The researchers found that the CO2-binding properties matched the sensitivities of these different animals. Natural selection has thus modified the CO2-binding properties of Cx26, which shows that this molecule is a universally important sensor of CO2 in warm-blooded animals.
The research appears in the Proceedings of the Royal Society B.
Source: University of Warwick
