Sunad Rangarajan

ORCID: 0000-0001-5313-4828
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About
Contact & Profiles
Research Areas
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Medical Imaging and Pathology Studies
  • Pulmonary Hypertension Research and Treatments
  • Neonatal Respiratory Health Research
  • Metabolism, Diabetes, and Cancer
  • Restless Legs Syndrome Research
  • Autophagy in Disease and Therapy
  • Parkinson's Disease Mechanisms and Treatments
  • Sleep and Wakefulness Research
  • Cancer, Hypoxia, and Metabolism
  • Cell Adhesion Molecules Research
  • Immune Response and Inflammation
  • Oral health in cancer treatment
  • Occupational exposure and asthma
  • Mitochondrial Function and Pathology
  • TGF-β signaling in diseases
  • Inhalation and Respiratory Drug Delivery
  • Glycosylation and Glycoproteins Research
  • Soft tissue tumor case studies
  • Cancer Diagnosis and Treatment
  • Quinazolinone synthesis and applications
  • Fungal Plant Pathogen Control
  • Connective Tissue Growth Factor Research
  • Occupational and environmental lung diseases

University of Colorado Anschutz Medical Campus
2018-2024

University of Colorado Denver
2022-2024

University of Alabama
2020

University of Alabama at Birmingham
2012-2019

Berkeley Public Health Division
2019

University of California, Berkeley
2019

University of California, San Francisco
2019

Pulmonary and Allergy Associates
2015-2017

St.John's Medical College Hospital
2007

Idiopathic pulmonary fibrosis (IPF) is a disease with relentless course and limited therapeutic options. Nintedanib (BIBF-1120) multiple tyrosine kinase inhibitor recently approved by the U.S. Food Drug Administration for treatment of IPF. The precise antifibrotic mechanism(s) action nintedanib, however, not known. Therefore, we studied effects nintedanib on fibroblasts isolated from lungs patients Protein gene expression profibrotic markers were assessed Western immunoblotting real-time...

10.1165/rcmb.2014-0445oc article EN American Journal of Respiratory Cell and Molecular Biology 2015-06-14

Contraction is crucial in maintaining the differentiated phenotype of myofibroblasts. an energy-dependent mechanism that relies on production ATP by mitochondria and/or glycolysis. Although role mitochondrial biogenesis adaptive responses skeletal muscle to exercise well appreciated, mechanisms governing energetic adaptation myofibroblasts are not understood. Our study demonstrates induction and aerobic glycolysis response differentiation-inducing factor transforming growth β1 (TGF-β1). This...

10.1074/jbc.m115.646984 article EN cc-by Journal of Biological Chemistry 2015-09-02

Matricellular proteins mediate pleiotropic effects during tissue injury and repair. CCN1 is a matricellular protein that has been implicated in angiogenesis, inflammation, wound In this study, we identified as gene differentially up-regulated alveolar mesenchymal cells of human subjects with rapidly progressive idiopathic pulmonary fibrosis (IPF). Elevated levels mRNA were confirmed lung tissues IPF undergoing transplantation, was predominantly localized to fibroblastic foci. expression ex...

10.1096/fj.201500173 article EN The FASEB Journal 2016-02-16

Mitochondrial dysfunction has been associated with age-related diseases, including idiopathic pulmonary fibrosis (IPF). We provide evidence that implicates chronic elevation of the mitochondrial anion carrier protein, uncoupling protein-2 (UCP2), in increased generation reactive oxygen species, altered redox state and cellular bioenergetics, impaired fatty acid oxidation, induction myofibroblast senescence. This pro-oxidant senescence reprogramming occurs concert conventional actions UCP2 as...

10.1111/acel.13674 article EN Aging Cell 2022-08-07

Idiopathic pulmonary fibrosis (IPF) is a fatal progressive fibrotic lung disease characterized by the presence of invasive myofibroblasts in lung. Currently, there are only two FDA-approved drugs (pirfenidone and nintedanib) for treatment IPF. There no defined criteria to guide specific drug therapy. New methodologies needed not predict personalized therapy, but also screen novel molecules that on horizon We have developed model system exploits phenotype IPF tissue. This ex vivo 3D uses...

10.1172/jci.insight.91377 article EN JCI Insight 2017-01-25

Abstract Cellular plasticity and de-differentiation are hallmarks of tissue/organ regenerative capacity in diverse species. Despite a more restricted for regeneration, humans with age-related chronic diseases, such as cancer fibrosis, show evidence recapitulation developmental gene programs. We have previously identified resident population mesenchymal stromal cells (MSCs) the terminal airways-alveoli by bronchoalveolar lavage (BAL) human adult lungs. In this study, we characterized MSCs...

10.1038/srep37445 article EN cc-by Scientific Reports 2016-11-21

Transforming growth factor-β (TGF-β) mediates growth-inhibitory effects on most target cells via activation of the canonical SMAD signaling pathway. This activity may be coupled with cellular differentiation. Our studies demonstrate that TGF-β1 inhibits proliferation primary, non-transformed human lung fibroblasts in association induction myofibroblast Differentiated myofibroblasts maintain capacity to proliferate response exogenous mitogenic stimuli and are resistant serum...

10.1371/journal.pone.0116995 article EN cc-by PLoS ONE 2015-02-06

Introduction: Most often, cannulation of the right internal jugular vein (IJV) is preferred over left IJV.However, in situations where IJV cannot be utilized for accessing central circulation, as our case, used.cannulation has additional risks due to anatomical variations.Despite use ultrasound guidance, variations and tortuous course make more prone failure or malposition cannula leading catastrophic complications.case report: A 63-year-old female with multiple comorbidities presented...

10.5348/ijcri-2013-10-381-cr-10 article EN cc-by International Journal of Case Reports and Images 2013-01-01

Abstract Injury to the lungs causes acute inflammation that can lead pathological lung fibrosis. Airspace macrophages (AMs) are critical for repair of injured tissue, but they contribute fibrosis through mechanisms incompletely understood. Siglecs expressed by immune cells. In mice, Siglec-F is chiefly AMs where it considered inflammosuppressive. We hypothesized its deletion would worsen injury and in response intratracheal bleomycin challenge. evaluated expression function mice challenged...

10.1101/2024.10.04.616703 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-10-05
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