The lungs' blood arteries differ from those of the rest of the body. This distinction is obvious in pulmonary hypertension, in which only the lungs' blood arteries harden gradually, resulting in chronic lung disease, heart failure, and death.
The fundamental causes
of this organ-specific channel stiffening remained unknown until University of
Pittsburgh researcher Stephen Chan and colleagues uncovered an unexpected
revelation regarding these blood vessel cells in pulmonary hypertension
patients: they're hungry.
Chan, Vitalant Chair in
Vascular Medicine and Professor of Medicine in the Division of Cardiology at
the University of Pittsburgh, and his colleagues worked with Thomas Bertero's
team at the Universite Cote d'Azur in France. They discovered that hypertensive
pulmonary blood vessel cells have an insatiable desire for two amino acids.
The findings were
published in the journal Cell Metabolism.
Amino acids are the
building blocks of proteins, which help build cellular structures, carry out
biological functions, and regulate tissue and organ function. As hypertensive
pulmonary blood vessels metabolize glutamine and serine, they create two new
amino acids, called proline and glycine. Proline and glycine are the primary
building blocks of collagen protein, which makes up 30 per cent of our body's
total protein and provides a structural framework for our skin, muscles, bones
and connective tissues. The appetite for glutamine and serine and the resulting
elevated levels of proline and glycine in hypertensive pulmonary blood vessel
cells drive the overproduction of collagen, which leads to vessel stiffening
and impaired function--the hallmark feature of pulmonary hypertension.
Using rodent models for
the disease, the researchers saw that drugs that limit cellular uptake of
glutamine and serine deprived hypertensive pulmonary blood vessels of their
craving. In turn, the lack of cellular glutamine and serine metabolism halted
the excess production of collagen building blocks and collagen production.
Knowing amino acids are most often absorbed through our diets, the team also
discovered that reducing the dietary intake of glutamine- and serine-rich foods
helped reduce collagen overproduction.
"For the first
time, we have a dietary maneuver that may serve as an effective therapy for the
disease," said Chan, who also directs the Vascular Medicine Institute and
Center for Pulmonary Vascular Biology and Medicine at the University of Pittsburgh
School of Medicine and UPMC.
For patients with
pulmonary hypertension, avoiding foods rich in serine and glutamine, or eating
foods with these amino acids depleted, might bolster the effectiveness of
current medications. "It opens up a new way that we could treat this
disease, because now--instead of just relying on medications and
transplantation--there are possibly effective lifestyle interventions,"
said Chan.
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