Emidio Pistilli, PhD

Associate Professor

Organization:

West Virginia University School of Medicine

Department:

Human Performance - Exercise Physiology

Classification:

Faculty

Associate Professor

Organization:

West Virginia University School of Medicine

Department:

Microbiology, Immunology & Cell Biology

Classification:

Faculty

Member

Organization:

West Virginia University WVU Cancer Institute

Department:

WVU Cancer Institute Research Programs

Classification:

Faculty

Director of Admissions, Office of Research and Graduate Education

Organization:

West Virginia University Health Sciences Center

Department:

Research & Graduate Education

Classification:

Admin

• BS, Health and Physical Education, The College of New Jersey, 1997
• MS, Exercise Science, Appalachian State University, 2001
• PhD, Exercise Physiology, West Virginia University, 2006

Ten most recent:

Wilson HE, Stanton DA, and Pistilli EE.  Breast cancer-associated skeletal muscle mitochondrial dysfunction and lipid accumulation is reversed by PPARG.  bioRxiv: doi: https://doi.org/10.1101/2020.04.05.026617

Wilson HE, Stanton DA, Montgomery C, Infante AM, Taylor M, Hazard-Jenkins H, Pugacheva EN, Pistilli EE.  Skeletal muscle reprogramming by breast cancer regardless of treatment history or tumor molecular subtype.  NPJ Breast Cancer, 2020; 6 (18): doi 10.1038/s41523-020-0162-2.

Wilson HE, Rhodes KK, Rodriguez D, Chahal I, Stanton DS, Bohlen J, Davis M, Infante AM, Hazard-Jenkins H, Klinke DJ, Pugacheva EN, Pistilli EE. Human breast cancer xenograft model implicates PPAR signaling as a driver of cancer-induced muscle fatigue. Clin Cancer Res. 2019;25 (7):2336-2347.

Bohlen J, McLaughlin SL, Hazard-Jenkins H, Infante AM, Montgomery C, David M, Pistilli EE. Dysregulation of metabolic-associated pathways in muscle of breast cancer patients: preclinical evaluation of interleukin-15 targeting fatigue. J Cachexia Sarcopenia Muscle. 2018;9 (4):701-714.

IL-15Ralpha deficiency in skeletal muscle alters respiratory function and the proteome of mitochondrial subpopulations independent of changes to the mitochondrial genome.
O'Connell GC, Nichols C, Guo G, Croston TL, Thapa D, Hollander JM, Pistilli EE.
Mitochondrion. 2015;25:87-97.

Interleukin-15 directly stimulates pro-oxidative gene expression in skeletal muscle in-vitro via a mechanism that requires interleukin-15 receptor alpha.
O'Connell GC, Pistilli EE.
Biochem Biophys Res Commun. 2015;458(3):614-619.

Muscle-specific deletion of exons 2 and 3 of the IL15RA gene in mice: effects on contractile properties of fast and slow muscles.
O'Connell GC, Guo G, Stricker J, Quinn LS, Ma A, Pistilli EE.
J Appl Physiol (1985). 2015;118(4):437-448.

Resistance exercise training modulates acute gene expression during human skeletal muscle hypertrophy.
Nader GA, von WF, Liu C, Lindvall J, Gutmann L, Pistilli EE, Gordon PM.
J Appl Physiol (1985). 2014;116(6):693-702.

Aging alters contractile properties and fiber morphology in pigeon skeletal muscle.
Pistilli EE, Alway SE, Hollander JM, Wimsatt JH.
J Comp Physiol B. 2014;184(8):1031-1039.

Non-invasive serial casting to treat persistent toe walking in an 18 month old toddler.
Pistilli EE, Rice T, Pergami P, Mandich MB.
NeuroRehabilitation. 2014;34(2):215-220.

Non-invasive serial casting to treat idiopathic toe walking in an 18-month old child.
Pistilli EE, Rice T, Pergami P, Mandich MB.
NeuroRehabilitation. 2014;34(2):215-220.
 

Fall 2020 Classes:

EXPH369: Strength & Conditioning Methods (Course Coordinator)
EXPH386: Advanced Exercise Physiology I (Neuromuscular Physiology section)
EXPH460: Pathophysiology (Neuromuscular Pathophysiology section)
EXPH567: Advanced Exercise Physiology II (Neuromuscular Physiology section)
EXPH 793A: Human Performance and Rehabilitation Engineering (Muscle Function section)

Breast Cancer

Research in this laboratory is focused on breast cancer-induced cachexia, defined as the loss of skeletal muscle mass and greater muscle dysfunction that occurs during tumor growth and in response to traditional therapies.  There is a specific emphasis on the therapeutic implications for the cytokine interleukin-15.  In addition to the effects of IL-15 on lymphocytes, my laboratory has established a direct role of IL-15 in stimulating mitochondrial biogenesis in skeletal muscle.  Therefore, experiments in the lab are focused on these dual roles of IL-15 during cancer and include: 1) mechanisms of IL-15 in altering the tumor microenvironment by promoting infiltration of NK cells and CD 8 T cells into mammary tumors; and 2) mechanisms of IL-15 in promoting mitochondrial biogenesis within skeletal muscle as a way to attenuate the muscle fatigue typically experienced in cancer patients.  We have established a mouse model of mammary tumor growth, evaluated the lymphocyte populations in the mammary tumor microenvironment, and characterized the alterations in muscle contractile properties.  Currently, the lab is evaluating the therapeutic effects of IL-15 in our tumor model using transgenic mice that over-express IL-15 within skeletal muscle and transgenic mice that have muscle-specific knockout of IL15Ralpha.  The lab also has established a collaboration with breast surgeons in the WVU Cancer Institute to acquire muscle biopsy samples from breast cancer patients.  These biopsy samples will be used for NextGen RNASeq to determine the unique genetic signature of muscle in response to breast cancer.  Biopsy samples are being collected from multiple breast tumor subtypes which will allow for identification of molecular markers unique to ER/PR+, Her2+, and triple negative tumors as well as markers common among breast tumors.  The long-term goals of the lab are to acquire data on the therapeutic efficacy of IL-15-based therapies that can be translated to human breast cancer patients as well as to identify novel molecular markers in muscle in response to breast cancer.

 

Recent grants

P20 GM121322   Lockman (PI)   Pistilli (Project lead)  08/01/18-06/30/23

NIH/NIGMS  

Tumor Microenvironment CoBRE

The purpose of this CoBRE application is to develop a Center of Excellence within the West Virginia University Health Sciences Center (WVU HSC) that will focus on studies of the tumor microenvironment (TME), designated the TME CoBRE.  My project is focused on the role of IL-15 in altering the tumor-infiltrating lymphocytes in the microenvironment as well as the role of IL-15 in stimulating mitochondrial biogenesis in skeletal muscle during breast tumor growth.

Current Research:

The research focus of the laboratory is the identification and therapeutic targeting of underlying mechanisms that contribute to cancer-associated muscle fatigue, with a specific focus on breast cancer.  We utilize cell-based models, mouse models of breast cancer, and human tissue biopsies in our experiments.  The goal of this research is to develop a supportive therapy that can alleviate the significant muscle fatigue that is common during tumor growth.