Faculty | Research interest/projects | |
---|---|---|
Arteel, Gavin, PhD | gearteel@pitt.edu | Our group is investigating the magnitude and impact of the changes to the hepatic matrisome in the context of the development and recovery from liver disease. As the main detoxifying organ in the body, the liver has tremendous ability to heal and regenerate from injury. The regenerative response in the liver can be perturbed and impacts recovery from injury or damage. The extracellular matrix (ECM) consists of a diverse range of components that work bi-directionally with surrounding cells to create a dynamic microenvironment that regulates cell signaling, recruitment, and tissue function. The basic definition of the ECM comprises fibrillar proteins (e.g., collagens, glycoproteins and proteoglycans). More recently, groups have extended the definition to include ECM affiliated proteins, regulator/modifier proteins and secreted factors (i.e., the ; 'matrisome'). Quantitative and qualitative changes to the ECM structure and superstructure can impact overall health of the organ and organism. Remodeling of the hepatic ECM/matrisome in response to injury is well understood in some contexts. For example, changes to the ECM associated with fibrosis are considered almost synonymous with hepatic ECM changes. Proteomic-based studies in other organs haves demonstrated that the matrisome responses dynamically in composition after insult well before fibrotic changes to the organ. These changes to the ECM may not alter overall ECM architecture and are therefore histologically undetectable. Nevertheless, these changes have potential to alter hepatic phenotype and function. These acute responses can be viewed as an arm of the wound healing response and facilitate recovery from damage, which resolves once the damage is repaired. However, under conditions of chronic injury, these changes likely contribute to activation of a significant remodeling response that leads to scar formation (i.e., fibrosis). It is our goal to better understand this process, as well as to develop minimally-invasive biomarkers to predict interindividual risk. |
Stephen F. Badylak, DVM, PhD, MD | badylaks@upmc.edu | Dr. Badylak's laboratory is a highly interdisciplinary environment that conducts studies that range from basic fundamental molecular mechanistic investigations to human clinical studies. The major focus of the laboratory is the development of regenerative medicine strategies for tissue and organ replacement; especially for clinical problems that presently have no viable therapy or poor therapeutic approaches. See more |
Juliane Beier, PhD | jibeier@pitt.edu | Obesity and its associated liver disease (i.e., MASFLD/MASH) are epidemic in the US population; indeed, it is estimated that up to 30% of US adults have underlying liver disease, most likely predominantly due to obesity. The impact of this new status quo in the risk of liver injury caused by environmental exposures is understudied. Importantly, such an interaction would imply that risk may be underestimated at this time. Vinyl chloride (VC) is a known human hepatotoxicant that causes a spectrum of both benign and malignant diseases, including hepatocellular carcinoma (HCC), hemangiosarcoma and toxicant associated steatohepatitis (TASH). However, these direct effects of VC exposure require high occupational exposures and have limited relevance with existing VC safety regulations. The impact of low environmental exposures, in contrast to high occupational exposures to VC, is unknown. Importantly, the effect of low exposure must consider aspects that may modify hepatotoxicity. In this context, the impact of underlying disorders (i.e., obesity) or lifestyle choices (i.e., diet) that may modify risk is critical. The Beier lab has demonstrated that low doses of VC that are not overtly hepatotoxic, may serve as a contributing factor in the development and progression of liver disease and cancer and is now working on the underlying mechanisms. Current available projects include: 1) What are the mechanisms of the interaction between exposure and liver disease? Elucidating and analyzing mitochondrial dysfunction, organelle miscommunication and epigentetic/epitranscriptomic changes. 2) What are the mechanisms by which low level VC can promote tumor formation and enhance carcinogenesis? 3) Can we prevent/predict/treat this interaction? This would include pharmacologic or genetic interventions in cell culture and animal models. |
Bharat Bhushan, PhD | bhb14@pitt.edu | Our research is focused on understanding the processes of liver injury and compensatory liver regeneration during acute and chronic liver diseases with long-term goal of developing pharmacological therapies for liver diseases. Following liver diseases are the major focus of our lab: (i) acetaminophen overdose induced acute liver failure and (ii) metabolic dysfunction-associated steatotic liver disease (MASLD) |
Timothy R. Billiar, MD | billiartr@upmc.edu | Dr. Billiar’s laboratory is funded in a number of areas, with the main research focus on immune response to injury and shock. See more |
Irina Bochkis, PhD | bochkisi@pitt.edu | The Bochkis lab applies experimental and computational methods to identify genetic and epigenetic mechanisms regulating metabolism. We are focusing on understanding how genome-wide chromatin changes, which include chromatin accessibility, nuclear localization and dynamics, and genome organization, lead to physiological dysfunction. Our laboratory utilizes functional genomics, chromatin biology, physiology, and transcriptional regulation in a comprehensive approach to decipher molecular mechanisms in mammalian models of human metabolic disease. |
Timothy Burns, MD, PhD | burnstf@upmc.edu | My research and clinical interests revolve around the development of targeted therapies for KRAS-mutant NSCLC as well as novel strategies to overcome resistance to targeted therapies for EGFR-mutant and MET-altered NSCLC. My three main research themes are 1) novel pre-clinical target validation and drug development (TWIST1 in oncogene driven NSCLC and TKI resistance; targeting metabolism in oncogene driven lung cancer); and 2) elucidating mechanisms of resistance for targeted inhibitors to develop rationale therapeutic combinations that can be tested in the clinic and 3) development of targeted therapy approaches for the treatment of brain metastases. The first line of research in my laboratory focuses on the role of the EMT transcription factor TWIST1 in oncogene-driven NSCLC and therapeutic resistance. The second line of research in my lab focuses on studying the mechanisms of resistance to targeted agents currently in phase 1 and 2 trials to develop rationale therapeutic combinations in the clinic. The third line of research in my lab is focused on lung cancer brain metastases, and we are exploring whether targeting the HGF-MET-TWIST1 pathway or downstream metabolic pathways can be an effective strategy for preventing or treating lung brain metastases. In additional to these preclinical studies, we are using both radiogenomic and cell free DNA approaches to predict molecular phenotypes of brain metastases to identify patients with brain metastases that can benefit from MET targeted therapy in the clinic. Finally, we have undertaken an investigator-initiated trial to test whether we can treat brain metastases with MET TKIs. |
Anne-Ruxandra, Carvunis, PhD | anc201@pitt.edu | www.carvunis.com de novo evolution of genes and microproteins: fundamental mechanisms and relations to immunology, cell biology, genomics. Lab combines computational and experimental approaches, at large and small scale. |
Yuan Chang, MD | yc70@pitt.edu | Viral oncogenesis |
Yu-Chih Chen, PhD | cheny25@upmc.edu | We aim to establish comprehensive high-throughput multi-omics single-cell analysis assisted with deep learning for cancer precision medicine. https://www.ycchenlab.org/ |
Charleen Chu, MD, PhD | ctc4@pitt.edu | We discovered that the mitochondrial kinase PINK1 regulates dendritic branching and spine maturation. Moreover, PINK1 is neuroprotective in several genetic models of neurodegenerative diseases, including mutations in the Alzheimer’s- and frontotemporal dementia-linked protein Tau, valosin-containing protein and mitochondrial polymerase-gamma. We plan to study the underlying signaling and cell biological mechanisms using patient-derived iPSC models, primary neuron cultures and Pink1-/- mice. |
Christopher L. Cunningham, PhD | cunningc@pitt.edu | The Cunningham Lab is interested in understanding the neural and sensory biology of the vertebrate auditory system. See more |
Evan Delgado, PhD | evd7@pitt.edu | Immune-oncology in liver cancers studying both lymphocyte and myeloid cell responses. Tumor metabolomics and the relationship between liver cancer cells and immune microenvironment. Studying inflammatory responses and T-cell recruitment to the liver. Development and generation of humanized liver cancer models. |
Steven Dobrowolski, PhD | dobrowolskis@upmc.edu | We determined osteopenia in the inborn error of metabolism PAH deficient phenylketonuria owes to mesenchymal stem cell developmental defect precipitated by oxidative stress and mitochondrial energy deficit. In the Pahenu2 classical PKU mouse model, we are applying oximetry, respirometry, oxidative stress assessment, and molecular means to characterize pathophysiological mechanisms and design interventions. |
H. Henry Dong, PhD | dongh@pitt.edu | 1)To understand the etiology of gestational diabetes mellitus (GDM). Pancreatic beta-cells compensate for maternal insulin resistance during pregnancy. Failure of beta-cells to compensate for maternal insulin resistance is causative for GDM. Using beta-cell conditional gene knockout approach, we investigate beta-cell compensatory mechanism in mice with GDM. 2) To understand the mechanism of nonalcoholic steatohepatitis (NASH). Using monocyte-conditional gene knockout approach in combination with ex vivo studies in human primary hepatocytes, we characterize key factors in macrophage polarization to gain mechanistic insights into proinflammatory macrophage activation, a predisposing factor that triggers hepatic inflammation and drives the evolution of steatosis to NASH. |
Chris Donnelly, PhD | cjdon25@pitt.edu | The Pathobiology underlying neuronal death in motor neuron disease, ALS and dementia as related to intracellular inclusions. |
Andrew Duncan, PhD | duncana@pitt.edu | Research in the Duncan lab focuses on liver development, homeostasis and regeneration. We are especially interested in the role of hepatic chromosome variations (polyploidy and aneuploidy) and how they influence the liver’s response to acute and chronic injury. See more |
Mo Ebrahimkhani, M.D. | mo.ebr@pitt.edu | 1) Genetically guided multilineage tissue morphogenesis with a focus on self-vascularized human liver organoids; 2) Exploiting developed organoids to study cell fate control in liver and for disease modeling; 3) Engineering hematopoietic niche for human therapeutics |
Yvonne Eisele, PhD | eiseley@pitt.edu | Research in the Eisele laboratory focuses on protein aggregation disorders like Alzheimer’s disease and transthyretin-related amyloidosis. See more |
Delphine Gomez, PhD | gomezd@pitt.edu | The molecular mechanisms controlling vascular smooth muscle cell phenotype and behavior during vascular development and diseases. Current projects include studies to determine: 1) Epigenetic alterations in major cardiovascular diseases including peripheral artery disease and aortic aneurysm and their consequence on smooth muscle cell phenotype, 2) identification of new functional non-coding RNA in SMC, and 3) relationship between mechanotransduction and epigenetic programming. |
Baoli Hu, PhD | baolihu@pitt.edu | The Hu lab’s research aims to understand the cellular and molecular mechanisms of brain tumor evolution, and to develop new therapies for these devastating diseases. With a special interest in the oncobiology of glioma and medulloblastoma, we employ multidisciplinary approaches to understand brain cancer stem cells, cell plasticity within the tumor microenvironment, and neurodevelopment relevant to tumorigenesis, tumor evolutionary trajectories under treatment. The sole aim of these projects is to provide the preclinical basis for translational research in druggable target and predictive biomarker discovery. |
Hun-Way Hwang, MD, PhD | Hunway.Hwang@pitt.edu | We study mRNA processing in different cell types in vivo and its role in human disease. See more |
Brett Kaufman, PhD | bkauf@pitt.edu | Cell-free DNA signaling, Antisense mtDNA therapies, mtDNA and cardioprotection: https://www.kaufmanlab-pitt.org/research |
Samira Kiani, MD | samira.kiani@pitt.edu | We develop controllable CRISPR-based gene therapies for modulation of the immune system. We seek the application of this in a variety of diseases such as infectious diseases and cancer |
Melanie Koenigshoff, MD, PhD | koenigshoffm@upmc.edu | The Königshoff Lab focuses on deciphering mechanisms involved in lung injury, aging and regeneration, with the aim to identify novel therapeutic targets relevant for chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) or idiopathic pulmonary fibrosis. See more |
Julia Kofler, MD | koflerjk@upmc.edu | Research in the Kofler lab focuses on identifying and evaluating genetic modifiers of Alzheimer’s disease and other neurodegenerative pathologies using human postmortem tissue. |
Hang Lin, PhD | hal46@pitt.edu | The Lin lab has recently found that human iPSCs-derived chondrocytes displayed significantly higher capacity in generating hyaline cartilage than those from primary mesenchymal stem cells. We plan to conduct mechanistic study to determine the associated pathways , as well as to examine the utility of iPSCs-derived chondrocyte in repair cartilage injury using animal models. |
Silvia Liu, PhD | shl96@pitt.edu | My research interests focus on developing novel computational models and application into diverse collaborative works. For methodological development, I’m working on both bulk and single-cell long-read RNA-seq data to detect fusion transcripts and mutation isoforms. I have been working on developing novel machine learning algorithms to perform meta- and integrative- genomic data analysis. For application works, I have been collaboration with different labs for bioinformatics and biostatistics genomic data analysis, including DNA-seq, ChIP-seq, Bisulfite-seq, RNA-seq, single-cell and spatial transcriptomics. These collaborative projects promote innovative ideas for the methodology works. |
Pamela Moalli, MD, PhD | pmoalli@mail.magee.edu | Translational Research Laboratories in Urogynecology: our lab develops novel solutions to improve outcomes for women with gynecologic conditions. Our technologies include interactive synthetic biomaterials, stem cell technologies, synthetic and biologic scaffolding technologies |
Michael Morowitz, MD | michael.morowitz@chp.edu | Dietary interventions to mitigate immune dysfunction after antibiotic disruption of the gut microbiome |
Benjamin Nacev, PhD | nacevba@upmc.edu | nacevlab.com Our lab is interesting in studying epigenetic dysregulation as a pathologic event in cancer to ultimately develop better therapies. We focus on bone and soft tissue tumors known as sarcomas, in which genetic events in epigenetic regulators are common compared to other solid tumors. We use a variety of biochemical, pharmacological, and genetic approaches together with epigenomic profiling. We have a wide range of potential projects available and would look forward to discussing opportunities. |
Kari N. Nejak-Bowen, MBA, PhD | knnst5@pitt.edu | Our lab, which has funding for several projects, studies the signaling processes and pathways in rare liver diseases, with a focus on cellular reprogramming, autophagy, and cell-cell interactions. |
Steffi Oesterreich, PhD | oesterreichs@upmc.edu | Breast cancer from the approach of genomics and the estrogen receptor |
Andrey A. Parkhitko, PhD | aparkhitko@pitt.edu | The main area of my research is to contribute to understanding of the metabolic mechanisms of aging and age-related diseases. The goal is to understand basic mechanisms of age-dependent metabolic reprogramming and to translate these insights into a mammalian system and ultimately into humans. See more. |
Jeremy N. Rich, MD, MHS, MBA | richjn@upmc.edu | The Rich laboratory studies malignant brain tumors through the prism of stem cell biology. To interrogate molecular pathways that maintain cancer stem cells, numerous approaches are taken, including analyses of epigenetic, epitranscriptomic, metabolic, and transcriptional regulation. Interplay between tumor cells and the tumor microenvironment (e.g., immune responses, vasculature, etc.) are under active investigation. Each project includes the development of novel therapeutic paradigms to serve as preclinical basis for clinical trial design. |
Ivona Vasile Pandrea, MD, PhD | pandrea@pitt.edu | SIV infection is associated with a hypercoagulable status that is closely correlated with inflammation and T cell immune activation; hypercoagulation is even more severe in old nonhuman primates (NHP) infected with SIV. We performed antiretroviral treatments in young and old NHPs infected with SIV to assess whether or not this approach is sufficient to improve coagulation, inflammation and immune activation status and to asses the effect of age. ELISA, immunohistochemistry and flow cytometry will be used to measure numerous biomarkers of immune activation and inflammation in the animals for includion in a publication. |
Julie Philippi, PhD | jap103@pitt.edu | The Phillippi Lab is a team of blood vessel enthusiasts studying how cell-matrix signaling influences microvascular dysfunction to uncover new mechanisms of cardiopulmonary diseases, organ/tissue failure, and preserving donor organ function. A long-term goal is to develop less invasive treatments options for cardiopulmonary diseases such as aortic aneurysm, heart failure and lung failure. Current initiatives include developing ECM biomaterials for vasa vasorum regeneration, establishing a novel animal model for aneurysm, and designing approaches for less invasive surgeries. Learn more at: http://mirmresearch.net/Cardiac-Research-Laboratory/default.asp |
Reben Raeman, MS, PhD | reben.raeman@pitt.edu | The primary focus of our lab is to elucidate host and environmental factors driving hepatic inflammation and fibrosis in non-alcoholic steatohepatitis (NASH). See more |
Melanie Scott, MD, PhD | scottm@upmc.edu | Trauma, infection and sepsis, hemorrhage/hypoxia and coagulopathy - Liver damage and repair - role of extracellular vesicles and also extracellular matrix-bound microvesicles in inflammation, organ damage and protection |
Daniel Shiwarski, PhD | djs87@pitt.edu | The Shiwarski Tissue Engineering Lab conducts research that integrates vascular hematology, developmental and mechanobiology, with cell biology, biomechanics, and tissue engineering. Using a combination of microfluidic systems, 3D bioprinting, biomechanical analyses, fluorescence microscopy, and next-Gen omics our goal is to determine how extra cellular matrix (ECM) composition and 3D structure elicit biomechanical cues that alter receptor signaling to drive tissue maturation and disease progression. Current projects have translational implications for the fields of cardiology, pulmonology, vascular medicine, hematology, cancer invasion, renal disease, and regenerative medicine. |
Ian Sigal, PhD | ias6@pitt.edu | How do neural tissues get hurt? We work to understand how mechanical insult contributes to damage neural tissues, particularly in chronic conditions. Our ultimate goal is the development of tools to prevent the damage and enhance regeneration and recovery. www.OcularBiomechanics.com |
Kanaiya Singh, PhD | singhk@pitt.edu | Regenerative Medicine, Epigenetics, Single cell Multiomics, Diabetes, Wound Healing, Tissue Nanotransfection; https://mirm-pitt.net/staff/kanhaiya-singh-phd/ |
Cynthia St. Hilaire, PhD, FAHA | sthilaire@pitt.edu | www.sthilairelab.pitt.edu, vascular disease, cardiovascular calcification, cellular reprogramming, genetic disease modeling |
Roderick J. Tan, MD, PhD | tanrj@upmc.edu | The Tan Lab has projects evaluating the role of Keap1/Nrf2 pathway in the development of chronic kidney disease. Kidney disease that is accompanied by proteinuria (abnormal spilling of protein into the urine) has a higher risk of progressing to complete kidney failure and the need for dialysis. We are investigating how the Keap1/Nrf2 pathway impacts various proteinuric chronic kidney diseases including FSGS, Alport syndrome, and diabetic nephropathy. We are also investigating neural control of kidney disease progression governed by renal sensory neurons and sympathetic neurons. Projects include rodent experiments and manipulations. |
Sina Tavakoli, MD, PhD | sit23@pitt.edu | Research Interest: 1) Development of novel molecular imaging tracers for in vivo visualization of different aspects of inflammation, particularly leukocyte chemotaxis; 2) Molecular imaging of inflammation in pulmonary (e.g., ARDS and lung fibrosis) and cardiovascular (e.g., atherosclerosis and myocardial infarction) diseases using positron emission tomography (PET) and CT in preclinical models. |
Thanos Tzounopoulos, PhD | thanos@pitt.edu | Our research has been focused on the histological, molecular, synaptic, intrinsic and plasticity properties of cochlear and auditory brain circuits. See more. |
Ivona, Vasile-Pandrea, MD, PhD | pandrea@pitt.edu | Our lab is studying the mechanisms responsible for the development of HIV/SIV-associated comorbidities. We are performing translational studies to test new therapeutic and dietary interventions aimed at reducing chronic inflammation and hypercoagulation and improve the gut function and metabolic status of individuals infected with HIV/SIV. Diverse non-human primate models of progressive, non-progressive and elite controlled SIV infection developed by our laboratory are used for these studies. |
Nam Vo, PhD | nvv1@pitt.edu | Mechanisms of the interplay between cellular senescence and autophagy in driving epigenetic dysregulation in spinal aging and low back pain. https://www.orthoresearch.pitt.edu/people/nam-vo-phd |
Jing Hong Wang, MD, PhD | jhw51@pitt.edu | Cancer Immunology and Immunotherapy with a focus on Head and Neck cancer and B cell lymphoma, lymphomagenesis, antibody gene diversification |
Xiaosong Wang, MD, PhD | xiaosongw@pitt.edu | We are seeking graduate students to join our leading-edge integrative genomics initiatives aimed at identifying pathological genetic aberrations and immunological targets from multi-dimensional cancer genomics datasets. The research project for this rotation will interface the “dark side” of cancer genetics with cancer pathobiology and immunobiology. Specifically, the student will investigate a cryptic class of adjacent gene rearrangements in more aggressive and therapy-resistant forms of breast and/or ovarian cancers, examine their function in cancer progression and immunotherapy resistance, as well as develop novel therapeutics. For more information, please visit: https://www.cagenome.org/lab |
Zhou Wang, PhD | wangz2@upmc.edu | Targeting androgen receptor in prostate cancer; mechanisms of antiandrogen resistance; pre-clinical animal models of prostate cancer; mechanisms of benign prostatic hyperplasia (BPH). |
Alan Wells, MD, DMSc | wellsa@upmc.edu | The Wells lab explores cancer metastasis with ex vivo 'human-on-a-chip' models that dissect the critical stages of cancer cells colonizing the distant organs. These microphysiologic systems are designed to study tumor biology along with the inflammatory and immune responses and to test therapies. |
Li Gang, PhD | lig@pitt.edu | Post-GWAS functional studies to understand the mechanism of Atherosclerosis and Alzheimer's disease for drug development. |
Vo Nam | nvv1@pitt.edu | Interdependence of autophagy and cellular senescence in intervertebral disc aging and low back pain. |
Sina Tavakoli | sit23@pitt.edu | 1) Development of novel molecular imaging tracers for in vivo visualization of inflammation, particularly leukocyte chemotaxis; 2) Molecular imaging of inflammation in pulmonary (e.g., ARDS and lung fibrosis) and cardiovascular (e.g., atherosclerosis and myocardial infarction) diseases using positron emission tomography (PET) and CT in preclinical models. |
Ben Nacev, MD,Phd | ben46@pitt.edu | The scientific goal of the Nacev Lab is to understand how cancer-associated genetic alterations in chromatin regulators promote cancer and to leverage this understanding to advance new therapeutic approaches in the clinic. Specifically, we model these events and study how the epigenome is dysregulated to alter transcriptional and developmental programs important for cancer growth and oncogenic behavior. To do so, we employ diverse tools including genetic, chemical, and epigenomic approaches. https://nacevlab.com/ |
Shou-Jiang (SJ) Gao,PhD | gaos8@upmc.edu | The Gao lab is part of the Cancer Virology Program (CVP) in the UPMC Hillman Cancer Center. The lab primarily studies the mechanism of infection and oncogenesis of cancer viruses. The student will be exposed to molecular virology, cancer biology, cancer metabolism, epigenetics, epitranscriptomics, interactions of cancer cells with tumor microenvironment and immune cells, inflammation, microbiome and cancer therapy. The lab closely collaborates with computational biologists, particularly Dr Yufei Huang, who is also in CVP, allowing the development of novel systems approaches for dissecting complex biological questions, including the recent development of novel analytic tools for spatially-resolved single cell transcriptomics. Recent works have identified novel tumor suppressive functions of an arginine sensor CASTOR1, which regulates both tumor and immune cells. Ongoing works are examining the functions of CASTOR1 in other types of cancer including lung cancer and HPV-associated head and neck squamous cell carcinoma, and innate and adaptive immunity in models of colitis and colon cancer. |
Robert Lafyatis, MD | lafyatis@pitt.edu | Epigenetic changes and transcriptional regulation of fibroblasts and macrophages in skin and lung fibrosis in systemic sclerosis |
Corrine Kliment, MD, PhD | ckliment@pitt.edu | The Kliment Lab focuses on the role of mitochondrial function in cell fate decisions in the context of lung injury, repair and regeneration We hope to identify novel therapeutic targets relevant for chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) or idiopathic pulmonary fibrosis. |
Melanie Koenigshoff, MD, PhD | koenigm@pitt.edu | The Königshoff Lan focuses on deciphering mechanisms involved in lung aging and regeneration, with the aim to identify novel therapeutic targets relevant for age-related chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) or idiopathic pulmonary fibrosis (IPF) and. Our translational research program focuses on the comprehensive characterization of human lung biospecimen and primary cell and tissue models from patients with chronic lung disease. We aim to identify and investigate target signaling pathways, such as WNT signaling, that impact cellular aging mechanisms that can be tested as potential novel therapies. |
Mo Ebrahimkhani, MD | mo.ebr@pitt.edu | please visit www.ebrahimkhanilab.bio |
Lianghui (Lucy) Zhang, MD, PhD | lhzhang@pitt.edu | Dr. Zhang’s laboratory studies immuno-pathogenesis of viral lung injury and develops novel treatments to reduce its mortality. The lab research focuses on the mechanisms of respiratory viruses-induced lung vascular injury and signals network between endothelial cells and immune cells during the innate and adaptive immune response. Rotation projects: 1) To explore lung vascular endothelial cells as antigen presented cells to signal immune cells to proliferate following influenza virus infection. 2) To identify the coronavirus (COVID 19) proteins to induce human lung vascular endothelial cell death. 3) To characterize the immune profile of endothelial-specific interferon alpha receptor knock out mice following influenza virus infection. The lab website: zhanglab.pitt.edu |
Erin Kershaw, MD | kershawe@pitt.edu | The Kershaw Lab focuses on disorders of "fat" (obesity, dyslipidemia, diabetes, and cardiometbolic disease) through translational research spanning preclinical models (cells, mice) to human; We functionally characterize novel metabolic risk variants by GWAS; https://kershawlab.pitt.edu/ |
[updated: 5/22/2024]