Researchers prevent lung injury in mice by inducing cellular autophagy

Recently, researchers from Drexel University and Yale University found in autophagy research that in the process of autophagy, lung injury caused by exposure to high-concentration oxygen in mice can be reduced. The study has been published American Journal of respiratory and molecular biology in this month, also providing a new way of thinking and methods for the prevention of lung injury in premature children. There are many recombinant proteins used to conduct related research.

Dr. Vineet Bhandari, the head of neonatology at Children's Hospital in St Christopher, said, "When the cells are in extreme stress, autophagy is a process that the cells sacrifice unnecessary organelles to protect themselves. Through research, we believe that if we can enhance the cellular autophagy of lung to effectively reduce cell death, finally protecting the lungs of newborns."

Bhandari is specialized in the study of bronchopulmonary dysplasia (BPD), which is the most common chronic lung disease in preterm children. When the babies are born a few weeks or months before the expected date of birth, their lungs are not fully formed or are not able to make enough surfactant or liquid coating. In order to save their life, doctors often have to manage supplemental oxygen. However, prolonged exposure to excess oxygen can increase lung injury, resulting in lifelong lung problems, which can’t treated easily by recombinant human proteins.

Dr. Vineet Bhandari said, "For some preterm children with a genetic predisposition to lung disease, excessive supplemental oxygen can cause inflammation, leading to cell death. And cell death will cause permanent changes of lung structure. Currently, there are up to 15,000 infants having this problem in United States each year. So the present situation is that babies need supplemental oxygen to save their life, and their lungs should be protected from injury on the other hand.

Autophagy allows cells to survive at ambient pressure. In this process, some unnecessary organelles such as the endoplasmic reticulum or mitochondria disintegrate and fuse into an autophagosome and are swallowed by lysosomes to recycle the contents. "It constitutes the digestion of cellular vacuole and the cells themselves," Bhandari said.

In order to find out whether increasing autophagy in lungs may reduce cell death and ultimately prevent lung injury, Bhandari and his team conducted further studies on a regulatory protein called RPTOR. The research results show that cellular autophagy plays a crucial role on the prevention of lung injury. Flarebio also provides you with excellent recombinant proteins including recombinant INSRR for your research.