| Faculty | Research interest/projects | |
|---|---|---|
| Christiano Alves, PhD | cra92@pitt.edu | Our research is dedicated to advancing human health through innovative genome editing technologies and molecular therapies. My group focuses on developing optimized treatments for severe neuromuscular and metabolic diseases. In addition, our experience in identifying clinically relevant biomarkers complements our ultimate goal of translating scientific discoveries into impactful clinical solutions. For more details please see: https://alveslab.us Current Projects accepting students: a. Development of Customized Genome Editing Approaches to Combat Sporadic ALS b. Development of Alternative CRISPR-based Strategies for In Vivo Treatment of Severe Neurological Diseases |
| Gavin Arteel, 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. |
| Tullia Bruno, PhD | tbruno@pitt.edu | Immunotherapy, specifically anti-PD1, has improved patient survival in a range of tumor types including head and neck squamous cell carcinoma (HNSCC) and non-small cell lung cancer (NSCLC). Despite the success of anti-PD1 therapy, only 20% of patients produce a durable response to this treatment. Further, there are some solid tumor types i.e. ovarian cancer, which yield very little therapeutic benefit from current standard of care immunotherapies. Thus, a need exists to develop additional therapeutic strategies to treat these patients, which includes evaluation of other tumor infiltrating immune cells that could further augment the CD8+ and CD4+ intratumoral T cell response. B cells represent a possible target for immunotherapy due to their predominance in the tumor microenvironment (TME) and crucial role in the immune response. However, B cell function in cancer and in the context of immunotherapy has been understudied. In fact, conclusions on an anti- or pro- tumor role for B cells in the TME remain incomplete. However, in multiple solid tumors, current evidence suggests an anti-tumor role for B cells. Specifically, detection of B cells within tertiary lymphoid structures (TLS) correlates with increased survival and immunotherapeutic response. While B cells have been identified in multiple tumor types, their complete phenotypic signature and interplay with other components within the TME have been understudied. Further, the complex composition of TLS in patient tumors is severely underappreciated, which is an overt focus of the Bruno laboratory. Specifically, we aim to understand B cell infiltration and TLS development within solid tumors to generate effective B-cell focused immunotherapies to augment the current successes of standard of care immunotherapies such as anti-PD1. To this end, we take a multi-level approach to understanding B cells and TLS composition in human tumors. Specifically, we transcriptionally assess B cells via single cell RNAseq with paired BCR seq, we interrogate B cell subsets within patient tumors using multi-parameter flow cytometry (15-30 parameters), we locationally evaluate B cells within and outside TLS utilizing multispectral imaging (Vectra Polaris) and spatial transcriptomics (Nanostring GeoMax Digital Spatial Profiler), and we evaluate the function of B cells and their interplay with other important immune cells within the TME via micro-scale in vitro functional assays. |
| Sandra Cascio, PhD | sac131@pitt.edu | My laboratory investigates the intercellular communications between stroma, tumor cells and immune cells within the tumor microenvironment. I am particularly focused on gaining a better understanding of how factors, secreted by stromal and tumor cells, modulate the immunosuppressive activities of tumor-associated myeloid cells, driving resistance to immunotherapies. Using mouse models of ovarian cancer and clinical samples, my long-term goal is to identify novel therapeutical approaches to enhance anti-tumor immunity. |
| Divay Chandra, MD, MSc, ATSF | chandrad@upmc.edu | The Chandra Lab conducts Genetic Map-to-Therapeutic studies in airway disease, with a primary focus on identifying and characterizing novel genes that confer susceptibility to chronic obstructive pulmonary disease (COPD). Our research centers on airway epithelial biology, leveraging a multidisciplinary approach that integrates computational and functional genomics, mechanistic studies in primary and immortalized airway epithelial cell lines, transgenic mouse models, and human lung tissue. We aim to uncover the molecular mechanisms by which these genes influence epithelial function and disease progression. This foundational work is highly translational and is designed to enable the development of RNA-based therapeutics. We have generated our first patentable therapeutic and are launching a start-up company to develop these novel therapeutics further. The lab is supported by multiple federal and foundation grants. Lab website: chandralab.pitt.edu |
| Yuan Chang, MD | yc70@pitt.edu | Our laboratory performs basic and applied research on viral oncogenesis with efforts focused in the following three areas: Merkel cell carcinoma and Merkel cell polyomavirus. We recently discovered a new human polyomavirus that we call Merkel cell polyomavirus (MCV). This virus is etiologically associated with a rare, but one of the most clinically aggressive skin cancers in humans. We are currently investigating the transforming properties of this virus and its encoded oncogenes. Kaposi's sarcoma-associated herpesvirus. We are investigating biologic properties of KSHV, the eighth human herpesvirus, also identified in our laboratory. KSHV causes Kaposi's sarcoma, the most common AIDS-associated malignancy, as well as a B-cell lymphoma. Through extensive molecular piracy, the virus has incorporated numerous genes which affect cell proliferation pathways, apoptosis, cell cycle regulation and immune modulation. New Pathogen Discovery. We continue to be interested in the search for new pathogens in human diseases and have developed new methodologies, which utilize information gained from the Human Genome Project, as well as advanced sequencing technologies. |
| 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/ |
| 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 |
| 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 |
| Xin (Daniel) Gao, PhD | danielgao@pitt.edu | Potential projects involve four research areas: 1. Developing therapeutic base editing end prime editing strategies to treat inherited genetic diseases; 2. Creating precise gene integration technologies to enable mutation-agnostic and gene-agnostic treatments; 3. Investigating preventive and regenerative therapies through comprehensive exploration of genetic and cellular landscapes; 4. Engineering delivery systems to overcome limitations in cargo capability and host immune response.) |
| Subhadip Ghatak, PhD | Ghataks@pitt.edu | Dr. Ghatak’s laboratory focuses on exosome-mediated intercellular crosstalk in tissue regeneration and repair and the role of miRNA in wound healing. Efficient wound healing and the resolution of inflammation relies on successful crosstalk via exosomes between the resident keratinocytes and blood-borne wound-site macrophages. His laboratory is further investigating the intercellular crosstalk between different cell types in cutaneous wound healing. Dr. Ghatak developed specialized genetic tools for the cell-specific labeling of exosomes in order to study the significance of intercellular crosstalk in tissue regeneration and repair. |
| Daniel Kass, MD | kassd2@upmc.edu | Our lab is interested in the biology of pulmonary fibrosis. Idiopathic pulmonary fibrosis, or IPF, is the most common of pulmonary fibrosis. IPF typically results in death within 3 to 4 years from the time of diagnosis. Specifically our lab focuses on the how the fibroblast is activated in IPF and leads to excessive deposition of extracellular matrix including collagen I. We combine molecular biology tools such as cloning with basic cell biology and omics readouts. We also study ex vivo and in vivo models of pulmonary fibrosis. Workers in our lab will have opportunities to meet with patients with pulmonary fibrosis. This provides students with the context for what we do. We believe that this is an important component of the training. Our goal is to design novel therapies for the patients who suffer from pulmonary fibrosis. Projects accepting students: 1. E-Box Accessibility in Myofibroblasts in Pulmonary Fibrosis - This study will examine the role of TWIST1 in the activation of myofibroblasts in pulmonary fibrosis. The student will gain experience in “massively parallel reporter assays” or MPRAs—an omics approach to the classical luciferase assay. The student will clone multiple TWIST1 constructs to determine how TWIST1 dimerization impacts fibrotic gene expression. The student will also gain experience in models of pulmonary fibrosis. 2. CXCL6 drives collagen synthesis in Pulmonary Fibrosis - This study focuses on the biology of collagen translation in pulmonary fibrosis as driven by the chemokine CXCL6. We will investigate CXCL6 signaling in fibroblasts. We will also investigate how the components of the ribosome may be essential for efficient translation of collagen I. |
| Melanie Koenigshoff, MD, PhD | koenigm@pitt.edu | The Königshoff Lab 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. |
| Tatiana Kudryashova, PhD | tvk4@pitt.edu | Dr. Kudryashova's lab research interests are focused on investigation of molecular and cellular mechanisms of pulmonary arterial hypertension (PAH), especially mechanisms of pulmonary vascular remodeling, clinically important and currently irreversible feature of PAH, with specific focus on the contribution of smooth muscle cells. Current research projects in the lab are focused on the studying impact of HIPK2, HIPPO-YAP/TAZ, and mTOR-Akt signaling pathways and their interactions on pathobiology of pulmonary vascular cells from patients with PAH and on identifying novel approaches to attenuate pulmonary vascular remodeling and overall pulmonary hypertension. Our long-standing research interests are also focused on studying the role of cell-cell interactions and extracellular matrix remodeling in development and progression of pulmonary vascular remodeling in PAH. |
| Jing Li, PhD | jil601@pitt.edu | The Li Lab studies the immunoregulatory mechanisms regulating anti-tumor immunity and autoimmune responses, with specific emphasis on regulatory CD8+ T cells and human immunology. |
| 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. |
| Benjamin Nacev, PhD | nacevba@upmc.edu | 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. nacevlab.com |
| Niranjana Natarajan, PhD | NATARAJ1@pitt.edu | My work focuses on macrophage fibroblast paracrine signaling events that mediate cardiac fibrosis in cardiovascular disease. We are also interested in taking a systems approach to understand inter organ crosstalk and inflammatory signaling in the pathology of heart failure with preserved ejection fraction (HFpEF). Possible rotation projects: - Role of medium chain fatty acid GPCRs in macrophage polarization and profibrotic signaling. - Macrophage – fibroblast crosstalk in pathological tissue fibrosis (heart failure with preserved ejection fraction model) - Myeloid trained immunity in heart failure – role of SCFA metabolites butyrate in macrophage trained immunity and HDAC modulation |
| 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 |
| Babak Razani, MD, PhD | brazani@pitt.edu | We have a particular interest in atherosclerotic macrophages, macrophage polarization, foam cell formation, adipose tissue metabolism, adipose tissue macrophages, liver metabolism, the autophagy-lysosome system, lysosomal biogenesis, lysosomal acidification, lysosomal acid lipase and lysosomal lipolysis, selective autophagy (particularly p62/SQSTM1), lipophagy, aggrephagy, mitophagy, mTOR signaling, differing roles of mTORC1 and mTORC2, nanoparticle delivery systems, and iPSC (induced pluripotent stem cells). |
| Amrita Sahu, PhD | ams519@pitt.edu | The Sahu Lab is dedicated to uncovering the signaling capacity of skeletal muscle and its role as a central regulator of whole-body health. We investigate how skeletal muscle communicates with other organs to maintain homeostasis—and how this communication is disrupted in disease states and during aging. Recognizing skeletal muscle as a potent endocrine organ, our work seeks to understand how early-life and environmental factors shape trajectories of healthy aging. At a mechanistic level, we study how intrinsic and extrinsic cues drive skeletal muscle aging and dysfunction. From a translational standpoint, our team develops targeted interventions to restore skeletal muscle architecture, with a particular focus on pelvic floor muscle remodeling following childbirth injury and menopause. Clinically, we examine how skeletal muscle responds to environmental stressors, including metal exposures and depression, to better understand muscle vulnerability across the lifespan.. |
| Kanhaiya 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 |
Research in the St. Hilaire Lab focuses on identifying and characterizing the mechanisms underlying the development of vascular and valvular calcification pathologies and bioprosthetic valve failure, with specific interest in defining the mechanisms by which genetic mutations, inflammation, and mechanical stress drive the transformation of a healthy cells into calcifying cells. For these investigations the St. Hilaire Lab obtains human tissues from patients with various cardiovascular diseases, utilizes murine models and primary human patient cells and tissues to create in vitro and ex vivo disease models, and performs biochemical, biomechanical, molecular biology, and next generation sequencing techniques. |
| 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. |
| Hēth R. Turnquist, PhD | het5@pitt.edu | Research Interests: 1. IL-33/ST2 axis & tissue repair: Define how a single receptor on regulatory T cells switches between healing and harm. We are using cutting-edge mouse models and clinical samples to map ST2⁺ Treg biology in cardiac transplantation, chronic rejection, and graft fibrosis. 2. Treg immunotherapy for lung injury: Turn regulatory T cells into a medicine. Our adoptive Treg cell therapy programs are assessing engineered Treg-based therapies for acute lung injury and inflammation, transplantation, and trauma. 3. Whole eye transplantation: Help restore vision for the first time in history. These studies pair surgical innovation with deep immune profiling to understand and prevent rejection of one of the body's most complex organs. 4. Mechanisms of transplant inflammation: Unravel mechanisms sustaining chronic inflammation after transplantation with a particular focus on identifying targetable pathways in memory T cells. |
| 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. |
| Dario Vignali, PhD | dvignali@pitt.edu | Dr. Vignali’s research focuses on gaining a better understanding of the inhibitory mechanisms, including inhibitory receptors and regulatory T cells, that limit anti-tumor immunity in cancer patients. He has discovery-based programs aimed at identifying novel targets for therapeutic intervention, and is also working with UPCI scientists and clinicians to facilitate the translation of novel therapeutic modalities with a focus on immunologically impacted solid tumors (primarily head and neck, melanoma, lung, pancreatic cancer). His UPCI leadership efforts are directed toward providing a bridge between basic and transitional cancer immunology. Lastly, he also works extensively with large and start-up biopharmaceutical companies to bring novel therapeutics to the clinic. |
| 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 |
| Haodi Wu,PhD | haodi@pitt.edu | Human induced pluripotent stem cells (iPSCs) have provided us an exceptional research platform for the mechanistic studies of cardiac diseases in human originated cardiac cells. The researches at Wu lab take advantage of modern stem cell, physiology, genome-editing, and omics technologies to 1) Dissect the molecular mechanisms of inherited dilated and hypertrophic cardiomyopathies; 2) Understand the molecular mechanism of aging in heart cells; 3) Study how environmental risk factors contribute to the remodeling of cardiomyocyte. The long-term goal of our research is to gain a deep mechanistic understanding of the pathogenesis in diseased cardiac cells, and to develop novel molecular tools and compounds to rectify the regulation during the process. |
| Vijay Yechoor, MD | yechoorv@pitt.edu | Dr. Yechoor’s research focuses on developing targeted therapies that target beta cell mass and function in the pathogenesis of diabetes. He has a long record of external funding from the National Institutes of Health, the Veterans Administration, Juvenile Diabetes Research Foundation, and the American Diabetes Association. His currently funded projects include 1) the role of the circadian clock in beta cell stress adaptation, and 2) the role of Tead1 in the transcriptional regulation of quiescence and proliferation of beta cells. More recently, he has extended his research into adipose tissue and cardiac muscle biology. |
[updated: ongoing]