NIBR
POSTDOCTORAL PROGRAM

DavidRowlandsDavid Rowlands, PhD
(Co-Mentor: Mark Dowling, PhD)

Chemical Biology & Therapeutics
Cambridge, Massachusetts, United States


Current therapies for chronic respiratory diseases such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are largely palliative, providing short-term relief of symptoms and improvement in quality of life. With an aging population, increased chronic tobacco use, and a decline in air quality, COPD is projected to become the third leading cause of death by 2030.

Within the Respiratory group at NIBR, our goal is to develop transformative therapies that halt and reverse the underlying disease mechanisms of 1) increased mucus burden resulting in air flow obstruction, and 2) impaired mucociliary clearance leading to increased risk of respiratory infection, and to develop therapies aimed at regenerating the alveolus in emphysema and IPF. Central to these goals, our group draws on complex 3D organoid assays cultured from primary patient cells, novel in vivo models and ex vivo lung preparations, and molecular profiling of patient material to identify and validate key pathways responsible for airway epithelial cell dysfunction. We aim to leverage such approaches to delineate the effect of aging on epithelial cell function in these disease mechanisms.

Selected Publications

MicroRNA-140-5p regulates disease phenotype in experimental pulmonary arterial hypertension and identifies SMURF1 as a novel therapeutic target.
Rothman AM, Arnold ND, Pickworth JA, Ironmonger J, Ciuclan, L, Allen R, Guth-Gundel S, Southwood M, Morrell NW, Thomas M, Francis SE, Rowlands DJ, Lawrie A.
J Clin Invest. 2016, in press.

Mitochondrial transfer from bone-marrow derived stromal cells to pulmonary alveoli protects against acute lung injury.
Islam NM, Das SR, Emin MT, Wei M, Sun L, Westphalen K, Rowlands DJ, Quadri SK, Bhattacharya S, Bhattacharya, J.
Nat Med. 2012 Apr 15; 18(5):759-65. 

Activation of TNFR1 ectodomain shedding by mitochondrial Ca2+ determines the severity of lung inflammation in mouse lung microvessels.
Rowlands DJ, Islam MN, Das S, Huertas A, Quadri SK, Horiuchi K, Inamdar N, Emin MT, Lindert J, Ten VS, Bhattacharya S, Bhattacharya J.
J Clin Invest. 2011 May; 121(5):1986-99.

Click here for additional publications.