Photo of Peter F. Maye, Ph.D.

Peter F. Maye, Ph.D.

Assistant Professor, Reconstructive Sciences
Associate Director, Skeletal Biology and Regeneration Graduate Program
Academic Office Location:
Reconstructive Sciences
UConn Health
263 Farmington Avenue
Farmington, CT 06030-3705
Phone: 860-679-7347
Fax: 860-679-2910
Email: pmaye@uchc.edu
Website(s):

Skeletal Biology and Regeneration Graduate Program

Skeletal Development & Regeneration

Research in my lab has a great interest in understanding signaling mechanisms that influence the fate of skeletal progenitors during the development, maintenance, and regeneration of bone tissues.  Ongoing work includes the use of mouse and human embryonic stem cells and induced pluripotent stem (iPS) cells and learning how to direct their differentiation into cells of the axial skeleton.  We also investigate adult bone marrow mesenchymal stem cells (MSCs) and the signaling pathways that influence their fate and function.

Rare Skeletal Diseases

Research in my lab is also interested in different skeletal dysplasia that impact bone tissues. We have become very interested in a rare craniofacial disorder known as cherubism.  Currently, this work is focused on understanding how the Transforming Growth Factor Beta signaling pathway contributes to the pathology of this disease. 

Differentiation of embyronic stem cells and iPS cells into mature skeletal cell types


Understanding how to generate skeletal progenitors from pluripotent stem cells has potentially great value for understanding the molecular basis of skeletal diseases and for the field of regenerative medicine.  Currently, the field is beginning to make real progress in understanding how to differentiate pluripotent stem cells in a very defined way into skeletal progenitors.  However, the cell types generated in vitro are very heterogeneous and their functional validation remains poorly tested. With this in mind, part of our strategy involves genetically engineering mouse and human ES and iPS cells with fluorescent reporters that enable us to visualize and study the biology of distinct skeletal progenitors generated in vitro.  In conjunction with different reporter stem cell lines, we are investigating how different signaling pathways influence the differentiation of pluripotent stem cells into paraxial mesoderm.  We are very interested in how to make paraxial mesoderm cells because they have the potential to give rise to wide breadth of mature skeletal cell types including, osteoblast, chondrocyte, tenocyte, myoblast, and dermal fibroblast.


 Cherubism and Transforming Growth Factor (TGF) Beta Signaling 


Cherubism is a rare autosomal dominant craniofacial disorder affecting pre-pubertal children, which is characterized by multilocular lesions in the mandible and/or maxilla consisting of numerous giant osteoclasts and extensive fibrous-osseous tissue hyperplasia.  Currently, there is no accepted treatment for this disease.  Based on certain characteristics of the cherubism phenotype, we suspected that increased TGFβ signaling may have a key role in the presentation of this disease and have used a mouse model of Cherubism to investigate this possibility.  Our ongoing studies are very encouraging and provide evidence that reducing TGFbeta signaling may be an effective therapuetic approach to treat patients.  


 


 


  


 


 


  

Not accepting students for Lab Rotations at this time

Journal Articles

Title or AbstractTypeSponsor/EventDate/YearLocation
Murine Animal Models to Interrogate the Function and Commitment of Skeletal ProgenitorsTalkNew England Musculoskeletal Institute Research Day2016Farmington, CT
Understanding the Coordinated Development of Bone Tissue and the Bone MarrowLectureUniversity of Hartford2016West Hartford, CT
Cherubism and Transforming Growth Factor Beta SignalingTalkDental Dean's Lecture Series2016Farmington, CT
Development of Genetic Models to Study Cartilage BiologyTalkNew England Musculoskeletal Institute Research Day2014Farmington, CT
Genetic Approaches to Study Adult Bone Marrow Skeletal ProgenitorsTalkConnecticut Science Festival Stem Cell Panelist2014Farmington, CT
Mouse Transgenesis: Approaches to Genetically Engineer MiceLectureUniversity of Hartford2014West Hartford, CT
Fate Mapping with Osterix Cre Mice Reveals the Origin and Contribution of Bone Marrow Mesenchymal Stem CellsTalkAmerican Society for Bone and Mineral Research Meeting2012Minneapolis, MN
Differentiating Embryonic Stem Cells Down the Axial Skeletal LineageLectureCentral Connecticut State University2012New Britain, CT
Differentiating Embryonic Stem Cells Down the Axial Skeletal LineageTalkStem Cells and Regenerative Biology Symposium, UCONN Health2011Farmington, CT
New Fluorescent Protein Reporter Animal Models to Study Skeletal BiologyPosterASBMR2010Toronto, Canada
The Application of Transgenic Reporter Mice to Study Skeletal Cell TypesTalkDental Dean's Seminar Series2010Farmington, CT
Characterizing the Osteogenic Potential of Mesenchymal Stem Cells and Their Immediate Cellular DerivativesPosterAmerican Society for Bone and Mineral Research2009Denver, CO
The Next Generation of Fluorescent Protein Reporter Animal Models to Mark Skeletal Cell TypesTalkRegenerative Engineering Workshop2009Farmington, CT
Dermo1 Lineage Tracing Identifies Early Osteoprogenitor Cells in Adult Murine Bone Marrow Mesenchymal Stem Cell CulturesPosterASBMR2008Montreal, Canada
Engineering Mice with Multiple BAC Fluorescent Protein Reporter Gene ElementsPosterAmerican Society for Bone and Mineral Research2008Montreal, Canada
Engineering Mice with Multiple Reporter Gene ElementsTalkNew England Musculoskeletal Institute Research Day2008Farmington, CT
Engineering Mice with Multiple BAC Fluorescent Protein Reporter Gene ElementsPosterEndocrine Society /Endocrine Fellows Forum2007Honolulu, Hawaii
A Bacterial Recombination Strategy to Generate Linked Multiple Gene Reporter ConstructsPosterIADR2007New Orleans, LA
A Bacterial Recombination Strategy to Link Multiple Gene Reporter ConstructsPosterStemConn2007Hartford, CT
Characterization of LRP5 Mutant Osteoblast Cultures using Collagen 1a1 GFP Reporter MicePosterASBMR2006Philadelphia, PA
Haploinsufficiency of Beta-Catenin Results in Reduced Bone MassPosterASBMR2005Nashville, Tennessee