The National Institutes of Health (NIH) recently awarded a Yale University scientist with a $3 million dollar research grant to help fund his work on exploring the molecular networks that underlie the histological features of idiopathic pulmonary fibrosis (IPF). The research project hopes to offer new insights into the disease and lead to the discovery of new paths to developing improved therapeutic interventions.
Pulmonary fibrosis is an aggressive, progressive fatal lung disease in which the alveoli and the lung tissue are damaged, becoming thick and scarred (fibrosis is caused by excessive collagen deposition), leading to severe breathing difficulties and a compromised oxygen transfer between the lungs and the bloodstream. The disorder is characterized by a shortness of breath that gradually worsens, with respiratory failure being the main cause of death. There is no cure for IPF and it is estimated that almost 130,000 individuals in the United States and 5 million worldwide suffer from the disease. IPF has a particularly poor prognosis and around two-thirds of the patients die within five years after being diagnosed.
According to the grant’s recipient, Naftali Kaminski, IPF is known to have a number of histopathological characteristics, including alveolar cell hyperplasia, an excess of myofibroblast foci, and aberrant remodeling. Kaminski’s grant began on August 14 and runs until the end of May 2019.
The researcher’s work has previously identified hallmark patterns of IPF in mRNA and microRNA expression, as well as global alterations in DNA methylation. While these findings contributed to what is known today about IPF, they have yet to be utilized in comparing the characteristics of lung tissue during the disease’s stages.
“Until we start getting into the lung microenvironments and see … whether we can distinguish changes within the IPF lung … we won’t be able to understand its pathogenesis and what we actually need to block to reverse the disease,” Kaminski said.
Thanks to the grant from the NIH, Kaminski and his team can now focus on exploring the genomic and transcriptomic profiles of various histologically defined regions of lungs affected by IPF, obtained from patients who have undergone lung transplants.
According to the grant’s abstract, this research initiative will entail generating mRNA, miRNA, and epigenomic profiles of differentially affected regions of sick lungs using microCT-guided microdissection, next-generation sequencing, and laser capture microdissection-reduced representation bisulfite sequencing.
Kaminski and his team will also aim to establish how certain cells have an impact on genomic and epigenomic changes in IPF by studying distinct cell populations sampled from individuals with and without IPF at baseline and in response to fibrosis-like perturbations.
The researcher also noted that all findings from this research will be made available through a searchable, web-based resource called IPFmap, which he had previously established with University of Pittsburgh scientist Panagiotis Benos.
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