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Itsaso Garcia-Arcos, PhD

Itsaso Garcia-Arcos, PhD

Research Assistant Professor
Pulmonary

    Dr Garcia-Arcos earned a degree in Biochemistry and then completed postgraduate and PhD training at the Department of Physiology of the University of the Basque Country (Spain). Her early research focused on liver lipid metabolism; she defined different subpopulations of intracellular lipid droplets in NASH, and analyzed the dynamic shuttling of SND1 protein between the endoplasmic reticulum and the lipid droplets during different nutritional conditions. During her training, she also obtained visiting scientist grants to study the peroxisomal proteomic fingerprint of aging at Uppsala University (Sweden), and intracellular protein interactions and trafficking in pancreatic cells at the University of Bordeaux (France).

    After defending her PhD, with European Doctor Recognition of the doctoral thesis, she joined the lab of Dr Goldberg in Columbia University in 2010. She was awarded a postdoctoral grant from the American Heart Association to study adipose lipoprotein lipase (LpL) in hypertriglyceridemia and adiposity. She found that LpL in brown but not in white adipose tissue was essential for blood triglyceride clearance and that lung LpL had a significant role in plasma triglyceride clearance. Later, Dr Garcia-Arcos joined the lab of Dr Foronjy at Mount Sinai Roosevelt, where she learnt the biology of lung disease.

    Since 2015, Dr Garcia-Arcos is a faculty member in SUNY Downstate Health Sciences University. Besides her research, Dr Garcia-Arcos is also interested in continuing education and mentoring activities, often mentoring students and fellows in research.

    Research Interests:

    My research interests involve lung lipid metabolism and surfactant homeostasis. The lung is a biologically complex organ and its molecular physiopathology involve multiple cell types and different mechanisms of disease. I lead the following lines of research with the general aim of elucidating determinant pathways in the development of pulmonary disease and identifying potential therapeutic targets.

    1) Lung lipid metabolism and surfactant homeostasis

    Pulmonary surfactant is essential for lung function and impaired surfactant function manifests clinically as respiratory distress syndrome. Environmental and genetic factors can reduce the amount of surfactant available in the alveoli, or alter its composition and function. Preterm infants born with immature type 2 cells (T2C) secrete insufficient surfactant and require external surfactant therapy for survival. In adults, surfactant insufficiency is associated with impaired lung function in diseases like chronic obstructive pulmonary disease (COPD) and can cause exacerbations. Smoke exposure damages T2C and causes alterations on surfactant secretion and composition in multiple animal models, and COPD patients have both decreased surfactant amount and altered composition, making it less effective at reducing the surface tension.

    This line of research is focused on pulmonary lipid metabolism. The lung is not usually considered as a highly metabolic organ, but T2C actually do maintain intense lipid metabolic activity to synthesize surfactant, which is mainly composed of phospholipids and minor amounts of cholesterol and specific proteins.

    In the lab, we use cell culture and in vivo models to study the regulation of surfactant homeostasis and its dysregulation during disease. Our experimental approaches include a wide variety of techniques in the areas of molecular biology, biochemistry, histology and physiology.

    2) Low density lipoprotein receptor related protein1 (LRP1) in smoke-induced inflammation

    This research is focused on the small airway epithelial cells. The airway epithelium is the first line of defense against external aggressions and plays a central role in the development of COPD. Patients with COPD suffer a progressive destruction of the small airways and a subsequent loss of pulmonary function. LRP1 is a multifunctional protein that has been recently associated with pulmonary function during COPD in a GWAS study. In fibroblasts and neurons, LRP1 has anti-inflammatory properties.

    We study the function and signaling mechanisms of LRP1 in airway epithelial cells to decipher the signaling mechanism of epithelial LRP1 in smoke-induced inflammation. We use cell cultures and in vivo models of smoke exposure to induce COPD and study the inflammation associated with its progression.

    A complete list of research contributions can be found HERE.

    Department Links

    Pulmonary