Our research faculty includes developmental biologists, lung researchers, vascular biologists, and neurobiologists who have NIH-funded laboratories. Our senior investigators (Drs. Reddy, Raj, and Chauhan) are leaders in their field who have more than 36 years of independent NIH and VA funded research. Current research focuses on providing new insights into the complex physiology and pathology of childhood and adult diseases, some of which originate in the fetus and newborn. We use preclinical models to develop new therapies and identify biomarkers for devastating lung diseases such as chronic lung disease of infancy and chronic pulmonary hypertension, Alzheimer’s disease (AD), and traumatic brain injury (TBI). Many ongoing research projects involve collaboration with faculty throughout UIC and beyond.
Meet the team:
Reddy, Sekhar, PhD
Chief, Section of Developmental Biology & Basic Research
Professor of Pediatrics and Pathology
Raj, Usha, MD, MHA
Anjuli S. Nayak Endowed Professor of Pediatrics
Professor, Departments of Physiology & Biophysics, Pharmacology, and Anatomy & Cell Biology
Chauhan, Neelima, PhD
Research Associate Professor
Chen, Tianji, PhD
Research Assistant Professor
Ramasamy, Jagadeesh, PhD
Research Assistant Professor
Tamatam, Chandra Mohan, PhD
Research Assistant Professor
Sekhar Reddy, PhD
Chandra Tamatam, PhD
Oxidant stress in vascular and alveolar remodeling is attributed to chronic lung diseases in neonates and adults. Dr. Reddy uses inflammatory and oxidant stress-induced preclinical neonatal and adult lung injury models to define mechanisms underlying optimal repair and impaired/abnormal repair after injury. His group, including Dr. Tamatam, recently demonstrated that preconditioning the immature lung with increased Nrf2 activity and its target cytoprotective gene expression protects from oxidant-stress-induced alveolar simplification, a significant hallmark of BPD pathogenesis. He also showed that Nrf2-deficiency results in persistent inflammation after injury and enhances susceptibility to infection. Current research explores the therapeutic potential of pharmacologic Nrf2 activation in accelerating lung repair and restoring homeostasis after damage. Additionally, in collaborative studies with Dr. Hamid Rabb (at Johns Hopkins), his lab investigates pathogenic mechanisms of abnormal tissue remodeling after kidney injury using preclinical models and clinical samples.
- Tamatam CM, Reddy MM, Potteti HR, Yamamoto M, Kensler TW, Reddy SP (2020). Preconditioning the Immature Lung with Enhanced Nrf2 Activity Protects Against Oxidant-Induced Hypo-Alveolarization in Mice. Scientific Reports, 10:19034. PMID: 33149211. DOI: 10.1038/s41598-020-75834-8.
- Reddy NM, Tamatam CM, Ankireddy A, Reddy SP. Nrf2 Is Required for Optimal Alveolar-Macrophage-Mediated Apoptotic Neutrophil Clearance after Oxidant Injury. Antioxidants 2022, 11(2), 212. https://doi.org/10.3390/antiox11020212.
- Elangovan I, Vaz M, Tamatam C, Potteti H, Machireddy N, Reddy SP (2018). Fosl1 Promotes Kras-Induced Lung Cancer Through Amphiregulin and Cell Survival Gene Regulation. Am J Respir Cell Mol Biology, 58:625-635. PMID: 29112457. DOI: 10.1165/rcmb.2017-0164OC.
- Potteti HR, Noone P, Tamatam CR, Reddy NM, Ankireddy A, Noel S, Rabb H, Reddy SP (2021). Nrf2 Mediates Hypoxia Inducible HIF1α Activation in Kidney Tubular Epithelial Cells. Am J Physiol Renal Physiol, 320(3):F464-F474. PMID: 33491566. DOI: 1152/ajprenal.00501.2020.
Usha Raj, MD, MHA
Tianji Chen, PhD
Drs. Raj and Chen closely collaborate on the study of the pathobiology of pulmonary hypertension in both newborns and adults. Their work has focused on the specific genetic pathways that modulate pulmonary vascular smooth muscle function. In recent years they have focused on the role of microRNAs and extracellular vesicles in the initiation and maintenance of pulmonary vascular disease. They recently identified a novel new microRNA, miR-212, induced in pulmonary endothelial cells in PH, which acts as a protective molecule. Loss of this miRNA results in devastating disease. They are engineering extracellular vesicles to deliver miR-212 to treat severe PH. Additionally, in collaborative studies with Dr. Jeffrey Hubbell (at the University of Chicago), they are developing methods to engineer the vesicles to target them specifically to pulmonary vessels for more directed therapy to the diseased blood vessels.
Chen T, Sun MR, Zhou Q, Guzman AM, Ramchandran R, Chen J, Ganesh B, Raj JU. Endothelium-Derived Extracellular Vesicles Contribute to the Hypoxia-Induced PASMC Proliferation In-Vitro and Pulmonary Hypertension in Mice. Pulmonary Circulation, December, 2021.
Chen T, Zhou G, Zhou Q, Tang H, Ibe JC, Cheng H, Gou D, Chen J, Yuan JX, Raj JU. Loss of miR-17~92 in Smooth Muscle Cells Attenuates Experimental Pulmonary Hypertension Via Induction of PDLIM5. Am J Resp Crit Care, 191:678-92, 2015. PMID: 25647182.
Neelima Chauhan, PhD
Dr. Chauhan’s research aims to promote the repair of degenerated neurons under such pathological conditions as traumatic brain injury (TBI) and Alzheimer’s disease (AD). Her research team uses candidate, dietary, and pharmacologic, interventional strategies, as well as preclinical models. Additionally, she focuses on testing North Indian Classical Music (NICM) to alleviate cognitive disability in the cognitively compromised aged population.
Gatto R, Chauhan M, Chauhan N (2015). Anti-Edema Effects of Rhepo in Experimental Traumatic Brain Injury. Restor Neurol Neurosci, 33(6): 927-941.
Chauhan MB, Chauhan NB (2015). Brain Uptake of Neurotherapeutics after Intranasal versus Intraperitoneal Delivery in Mice. J Neurol Neurosurg, 2(1): 1-9. PMID: 26366437
Xiao C, Chauhan NB (2020). Ameliorative effects of intranasal antagomir-125b in AD, Alzheimer’s Disease and Dementia, 4 (1): 105-112.
Chauhan NB (2020). MicroRNA Silencing: A Promising Therapy for Alzheimer’s Disease. Neurosci Chron; 1(1):11-15.
Chauhan NB, Mahesh K, Purva G (2020), Alzheimer’s Sound Health, MedDocs eBooks: Alzheimer’s Disease & Treatment, pp 1-9, MedDocs Publishers.
Jagadeesh Ramasamy, PhD.
Dr. Ramasamy’s research focuses on the impact of erythrocyte’s mitochondrial retention in sickle cell disease (SCD) pathophysiology. His group first discovered an abnormal mitochondria number in erythrocytes of SCD patients and its potential contribution to elevated levels of ROS and hemolysis. In another area of translational research, his group is actively involved in developing epigenetic drugs, micronutrients, and siRNA-based therapeutic approaches to reduce the need for opioid medications to prevent pain and improve vascular health in pediatric and adult SCD patients.
Jagadeeswaran R, Rivers A. Evolving Treatment Paradigms in Sickle Cell Disease. Hematology Am Soc Hematolol Educ Program. 2017 (1):440-446; PubMed PMID: 29222291.
Jagadeeswaran R, Vazquez BA, Thiruppathi M, Ganesh BB, Ibanez V, Cui S, Engel JD, Diamond AM, Molokie RE, DeSimone J, et al. Pharmacological Inhibition of LSD1 and Mtor Reduces Mitochondrial Retention and Associated ROS Levels in the Red Blood Cells of Sickle Cell Disease. Exp Hematol. 2017 Jun;50:46-52. PMID: 28238805.
“Exploring the body’s complex processes and translating the research findings to the bedside is a constant source of satisfaction. We’re never done asking questions and discovering why dysfunctions occur and how we can stop them and find ways to repair the process.”
–Sekhar Reddy, PhD
Professor and Chief of the Section of Developmental Biology & Basic Research