Shampa Chatterjee, PhD

Research Associate Professor

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1 John Morgan

3620 Hamilton Walk

Philadelphia, PA 19104

215-898-9101

Fax: 215-898-0868

shampac@pennmedicine.upenn.edu

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Quantum Dots (QDs) as tools to detect VCAM expression (yellow) in vivo. Orndorff et al. American Journal of Physiol. Lung Cell and Mol Physiol. 306 :L260-8, 2014.


The proposed Endothelial Mechanosome. Chatterjee, S: Mechanotransduction: Forces, Sensors and Redox Signaling. Antioxidants and Redox Signaling 20:868-71, 2014.


Endothelial lining of blood vessels (green) shows the dense vascular bed in the lungs.


Revascularization with hind limb ischemia (Browning et al. Antioxidants and Redox Signaling 20:872-86, 2014.


Mechanotransduction induced Signaling in the Stored Lung. Pulmonary Ischemia induced redox signaling drives Danger associated molecular patterns (DAMPs) such as HMGB-1 and its receptor RAGE, cellular adhesion molecules (CAMs) and the transcription factor HIF-1 α. This potentially predisposes the donor lung toward recruitment and adherence of immune cells from the recipient.

Shampa Chatterjee, PhD


Research Associate Professor of Physiology

Degrees & Education

  • PhD (Biochemistry) Indian Institute of Technology, Bombay, India, 1997

  • Fellow ITP, GBF, Gelleschaft fuer Biotechnologische Forschung, Braunschweig, Germany, 1996-1997

  • Fellow, Institut Fuer Medizinische Neurobiologie Otto von Guericke Universitaet Magdeburg, Germany, 1997-1999

  • Postdoctoral Fellow, Institute for Environmental Medicine, University of Pennsylvania Perelman School of Medicine, 1999-2002

  • Research Associate, Institute for Environmental Medicine, University of Pennsylvania Perelman School of Medicine, 2002-2006


Awards & Honors

  • 2015 Hermann Rahn Award

  • 2014 APS select for distinction in scholarship in Am J Physiol Lung Cell Mol Physiol (306 :L260-8, 2014)

  • 2002 Julius Comroe, Jr. Award, American Physiological Society

  • 2000 Caroline tum Suden Professional Excellence Award, American Physiology Society

  • 1997 UNESCO International Training Program Fellowship -97, Braunschweig, Germany

  • 1991 CSIR Research Fellowship Award, Ministry of Human Resources, New Delhi, India

  • 1985 National Talent Search Scholarship, National Council Education, Research & Training, Govt. of India


Research Description

The vascular system is a conduit and connector of blood flow across organs. It serves as a network that integrates biochemical and biophysical signals via transport of blood, nutrients and inflammatory, pathogenic moieties across the body. The lining of the blood vessels, i.e. the endothelium is thus an extensive interface where chemical and mechanical stimuli in blood interact directly with a cellular layer and “convey” signals into tissues. In addition, the endothelium is well recognized as the converging site of inflammation whereby innate and adaptive immune cells adhere to the endothelial layer and transmigrate into tissue. In an adult human, the surface area of the entire endothelium is 3000 m2 which is equivalent to at least six tennis courts. Comprising of one trillion endothelial cells, which weigh more than 100 g, the endothelium can be considered to an extensive and dynamic organ that pervades the entire body. Besides regulating blood vessel tone, the endothelium controls cellular and nutrient trafficking from the blood into the tissue, maintains homeostasis (i.e. a balance between pro- and anti-coagulant activity of blood and pro-and anti-inflammatory environment in tissues). To enable its functions, the endothelium must be able to receive “cues” from the local environment in the form of chemotransduction and mechanotransduction.

My lab is focused on understanding the endothelial machinery with mechanotransduction (sensing alteration in blood flow) and chemotransduction (sensing chemical cues such as inflammatory moieties, oxidants, endotoxins). In this direction, we discovered that the endothelium “senses” stop of blood flow and triggers a signaling cascade that leads to the generation of reactive oxygen species (ROS) via the deactivation of an ATP sensitive potassium (KATP) channel and activation of the enzyme NADPH oxidase 2 (NOX2). We reported extensively on the mechanosensing machinery (comprising of platelet endothelial cell adhesion molecule or PECAM-1 and caveolin-1) or mechanosome that is pivotal in ischemia induced signaling. The pulmonary “endothelial mechanosignaling or mechanotransduction” paradigm can be translated in the clinical setting of lung transplantation, where perfusion is halted (ischemia) during donor lung storage but lung tissue remains oxygenated as the lung is inflated (under 2/3 inflated conditions prior to transplant) air in the alveoli. Currently we are engaged in understanding this cascade, namely the endothelial mechanosignaling-KATP channel-NOX2-ROS –inflammation link so as to “treat” donor lung endothelium during the storage by inhibitors (of the mechanosignaling cascade) or by devices (perfusion circuits that maintain flow during the entire storage period). This focus on the donor organ ahead of transplant could change the current clinical paradigms in pulmonary transplant medicine.

We also observed that endothelial chemotransduction occurs via a signaling pathway involving the production of oxidants and inflammatory moieties (cellular adhesion molecules, C-reactive protein etc.) by the endothelium. In response to inhaled aerosols, endothelial chemotransduction led to increase in the inflammatory burden of the circulating blood leading to further endothelial activation. Continuous activation and oxidant generation can, in the long term, alter endothelial phenotype leading to the onset of various vascular pathologies.


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(searches the National Library of Medicine's PubMed database.)


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