An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics

Ilias Angelidis, Lukas M. Simon, Isis E. Fernandez, Maximilian Strunz, Christoph H. Mayr, Flavia R. Greiffo, George Tsitsiridis, Elisabeth Graf, Tim‐Matthias Strom, Oliver Eickelberg, Matthias Mann, Fabian J. Theis, and Herbert B. Schiller

Go to the profile of Nature Communications
Jul 25, 2018
Like 0

Received: 23rd June 18

Aging promotes lung function decline and susceptibility to chronic lung diseases, which are the third leading cause of death worldwide. We used single cell transcriptomics and mass spectrometry to quantify changes in cellular activity states of 30 cell types and the tissue proteome from lungs of young and old mice. Aging led to increased transcriptional noise, indicating deregulated epigenetic control. We observed highly distinct effects of aging on cell type level, uncovering increased cholesterol biosynthesis in type-2 pneumocytes and lipofibroblasts as a novel hallmark of lung aging. Proteomic profiling revealed extracellular matrix remodeling in old mice, including increased collagen IV and XVI and decreased Fraser syndrome complex proteins and Collagen XIV. Computational integration of the aging proteome and single cell transcriptomes predicted the cellular source of regulated proteins and created a first unbiased reference of the aging lung. The lung aging atlas can be accessed via an interactive user-friendly webtool at:

Read in full at bioRxiv.

This is an abstract of a preprint hosted on an independent third party site. It has not been peer reviewed but is currently under consideration at Nature Communications.

Go to the profile of Nature Communications

Nature Communications

Nature Research, Springer Nature

Comments are disabled