Staff Profile

I am a member of the Biosciences Institute and work across a number of research themes:

• Reproduction, Development and Child Health
• Ageing and Geroscience
• Cell Signalling

I am also part of the Rare Disease NUCore and the Biomedical Engineering NUCore

Roles & responsibilities

Current

• Lecturer in Musculoskeletal Genetics
• Module Leader: BGM3062 Genetics of Development and its Disorders
• Deputy Module Leader: BGM2057 Medical genomics: from DNA to disease
• Member of the Biochemistry and Genetics Curriculum Committee
• Member of the Newcastle University Public Lectures Committee
• Member of the British Society of Matrix Biology (BSMB) Organising Committee https://bsmb.ac.uk/
• Public Engagement Lead for the Reproduction, Development and Child Health research theme
• Work Package Lead and Public Engagement Lead for the MSCA CHANGE project https://www.change-msca.eu/
• Member of the Animal Welfare and Ethical Review Body (AWERB)

Past

• Public Engagement and Dissemination (WP9) coordinator, EU-FP7 SYBIL project http://www.sybil-fp7.eu/
• Chair of the IGM Public Engagement Committee https://blogs.ncl.ac.uk/igmengagement/
• Deputy Module Leader: GNM8000/1 Introduction to Human Genetics and Genomics

Areas of expertise

• Bone development
• Cartilage biology
• Skeletal dysplasia
• Musculoskeletal ageing
• Tissue engineering

Qualifications:

• Associate Fellow of the Higher Education Academy
• PhD: Wellcome Trust Centre for Cell Matrix Research, Manchester University, UK
• MSc (Hons): Institute of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland (5 year integrated BSc and MSc course)

Google scholar: Click here

SCOPUS: Click here.

ORCID: Click here.

Research interests:

Cartilage biomechanics and musculoskeletal complications of chondrodysplasias and osteoarthritis/ageing

During my PhD project and the subsequent PostDoc career I have developed and analysed several transgenic models of chondrodysplasias, specifically pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED). I have generated and analysed a mouse model of PSACH which recapitulates the patients’ phenotype, including the early onset osteoarthritis. I was also the first to show that the myopathy associated with COMP mutations in PSACH results from an underlying tendinopathy and I presented a novel study describing these complications in detail. I’m currently looking forward to expanding these studies in cellular and animal models to gain more understanding of pathobiology of chondrodysplasias and ageing.

I’m specifically interested in the abnormalities in the extracellular matrix ultrastructure associated with chondrodysplasias and ageing. I’d like to know how the cells sense and react to such changes and how this in turn impacts on the biomechanical properties of tissues. I’m also interested in musculoskeletal complications, such as myopathy and/or tendinopathy, trying to perceive the knee joint as a system of various interconnected tissues and through this approach gain a broader understanding of musculoskeletal conditions and their complications, such as osteoarthritis.

Funding:

EU H2020, Dunhill Medical Trust, NC3Rs, JGW Patterson Foundation

Lecturer:

Current

• BGM3026 Genetics of development and its disorders (Module Leader, Lecturer, and Seminar Lead)
• BGM2057 Medical genomics: from DNA to disease (Deputy Module Leader, Lecturer, and Seminar Lead)
  
• MMB8031 Developmental Genetics (Lecturer)
  
• MEC8023 Biomaterials and Tissue Engineering (Lecturer)

• GNM8000 Introduction to Human Genetics and Genomics (Deputy Module Leader and Lecturer)
  
• GNM8001 Introduction to Human Genetics and Genomics (Deputy Module Leader and Lecturer)
  

• Articles

  • Hayman DJ, Modebadze T, Charlton S, Cheung K, Soul J, Lin H, Hao Y, Miles CG, Tsompani D, Jackson RM, Briggs MD, Piróg KA, Clark IM, Barter MJ, Clowry GJ, LeBeau FEN, Young DA. Increased hippocampal excitability in miR-324-null mice. Scientific Reports 2021, 11(1), 10452.
  • Woods S, Charlton S, Cheung K, Hao Y, Soul J, Reynard LN, Crowe N, Swingler TE, Skelton AJ, Piróg KA, Miles CG, Tsompani D, Jackson RM, Dalmay T, Clark IM, Barter MJ, Young DA. microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs. RNA 2020, 26, 1575-1588.
  • Dennis EP, Edwards SM, Jackson RM, Hartley CL, Tsompani D, Capulli M, Teti A, Boot-Handford RP, Young DA, Piróg KA, Briggs MD. CRELD2 is a novel LRP1 chaperone that regulates non-canonical WNT signalling in skeletal development. Journal of Bone and Mineral Research 2020, 35(8), 1452-1469.
  • Piróg KA, Dennis EP, Hartley CL, Jackson RM, Soul J, Schwartz JM, Bateman JF, Boot-Handford RP, Briggs MD. XBP1 signalling is essential for alleviating mutant protein aggregation in ER-stress related skeletal disease. PLoS Genetics 2019, 15(7), e1008215.
  • Paganini C, Monti L, Costantini R, Besio R, Lecci S, Biggiogera M, Tian K, Schwartz JM, Huber C, Cormier-Daire V, Gibson BG, Pirog KA, Forlino A, Rossi A. Calcium activated nucleotidase 1 (CANT1) is critical for glycosaminoglycan biosynthesis in cartilage and endochondral ossification. Matrix Biology 2019, 81, 70-90.
  • Bell PA, Dennis EP, Hartley CL, Jackson RM, Porter A, Boot-Handford RP, Pirog KA, Briggs MD. Mesencephalic astrocyte-derived neurotrophic factor is an important factor in chondrocyte ER homeostasis. Cell Stress and Chaperones 2018, 24(1), 159-173.
  • Briggs MD, Bell PA, Wright MJ, Pirog KA. New therapeutic targets in rare genetic skeletal diseases. Expert Opinion on Orphan Drugs 2015, 3(10), 1137-1154.
  • Cameron TL, Gresshoff IL, Bell KM, Piróg KA, Sampurno L, Hartley CL, Sanford EM, Wilson R, Ermann J, Boot-Handford RP, Glimcher LH, Briggs MD, Bateman JF. Cartilage-Specific Ablation of XBP1 Signaling in Mouse Results in a Chondrodysplasia Characterized by Reduced Chondrocyte Proliferation and Delayed Cartilage Maturation and Mineralization. Osteoarthritis and Cartilage 2015, 23(4), 661-670.
  • Piróg KA, Irman A, Young S, Halai P, Bell PA, Boot-Handford RP, Briggs MD. Abnormal Chondrocyte Apoptosis in the Cartilage Growth Plate is Influenced by Genetic Background and Deletion of CHOP in a Targeted Mouse Model of Pseudoachondroplasia. PLoS One 2014, 9(2), e85145.
  • Piróg KA, Katakura Y, Mironov A, Briggs MD. Mild myopathy is associated with COMP but not MATN3 mutations in mouse models of genetic skeletal diseases. PLoS One 2013, 8(11), e82412.
  • Bell PA, Piróg KA, Fresquet M, Thornton DJ, Boot-Handford RP, Briggs MD. Loss of matrilin 1 does not exacerbate the skeletal phenotype in a mouse model of multiple epiphyseal dysplasia caused by a Matn3 V194D mutation. Arthritis & Rheumatism 2012, 64(5), 1529-1539.
  • Suleman F, Gualeni B, Gregson HJ, Leighton MP, Piróg KA, Edwards S, Holden P, Boot-Handford RP, Briggs MD. A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia. Human Mutation 2012, 33(1), 218-231.
  • Pirog KA, Briggs MD. Skeletal Dysplasias Associated with Mild Myopathy-A Clinical and Molecular Review. Journal of Biomedicine and Biotechnology 2010, Article no. 686457.
  • Piróg KA, Jaka O, Katakura Y, Meadows RS, Kadler KE, Boot-Handford RP, Briggs MD. A mouse model offers novel insights into the myopathy and tendinopathy often associated with pseudoachondroplasia and multiple epiphyseal dysplasia. Human Molecular Genetics 2010, 19(1), 52-64.
  • Pirog-Garcia KA, Meadows RS, Knowles L, Heinegard D, Thornton DJ, Kadler KE, Boot-Handford RP, Briggs MD. Reduced cell proliferation and increased apoptosis are significant pathological mechanisms in a murine model of mild pseudoachondroplasia resulting from a mutation in the C-terminal domain of COMP. Human Molecular Genetics 2007, 16(17), 2072-2088.
  • Piróg KA, Kowalczyk AK, Rokita HB. Changes in Bcl-2 expression in vaccinia virus-infected human peripheral blood monocytes. Viral Immunology 2005, 18(1), 224-231.

• Authored Book

  • Pirog KA. Terapia genowa (Gene therapy). Wydaw: Jagiellonian University Press, 2002.

• Book Chapters

  • Briggs MD, Bell PA, Piróg KA. Pseudoachondroplasia and Multiple Epiphyseal Dysplasia: Molecular Genetics, Disease Mechanisms and Therapeutic Targets. In: Grässel S; Aszódi A, ed. Cartilage. Springer International Publishing AG, 2017, pp.135-153.
  • de-las-Heras-Ruiz T, Pirog KA. Tissue Engineering Approaches for the Study and Therapeutic Intervention in Osteoarthritis. In: Osteoarthritis. SM Group Open Access eBooks, 2016.

• Conference Proceedings (inc. Abstracts)

  • Dennis EP, Capulli M, Teti A, Pirog KA, Briggs MD. The role of Creld2 in skeletal development and homeostasis. In: 43rd Annual European Calcified Tissue Society Congress. 2016, Rome, Italy: Bone Abstracts.
  • Gibson BG, Sonntag S, Selbert S, Pirog KA, Briggs MD. Transgenic mice with an allelic series of aggrecan mutations model the human phenotypes. In: British Society for Matrix Biology / Bone Research Society Third Joint Meeting. 2015, Edinburgh: Wiley-Blackwell Publishing Ltd.
  • Dennis EP, Edwards SM, Boot-Handford RP, Pirog KA, Briggs MD. The role of CRELD2 in skeletal development and homeostasis. In: British Society for Matrix Biology / Bone Research Society Third Joint Meeting. 2015, Edinburgh: Wiley-Blackwell Publishing Ltd.
  • Bell PA, Gualeni B, Pirog KA. Reverse genetics approach in search for the novel MED locus. In: British Society for Matrix Biology / Bone Research Society Third Joint Meeting. 2015, Edinburgh: Wiley-Blackwell Publishing Ltd.
  • Bell PA, Jackson R, Pirog K. Importance of glycosylation state and aggregation in ER-associated degradation of mutant matrilin proteins and induction of UPR. In: British Society for Matrix Biology / Bone Research Society Third Joint Meeting. 2015, Edinburgh: Wiley-Blackwell Publishing Ltd.
  • Pirog KA, Meadows RS, Boot-Handford RP, Briggs MD. Mutant chondrocytes are characterised by altered cell shape and changes to the organisation of primary cilia in a genetic mouse model of mild pseudoachondroplasia. In: British Society for Matrix Biology Autumn 2013 Meeting. 2013, Cardiff: Wiley-Blackwell.
  • Rajpar MH, Pirog KA, Briggs MD, Boot-Handford RP. Molecular dissection of the unfolded protein response in hypertrophic chondrocytes. In: Spring Meeting of the British Society for Matrix Biology. 2010, Manchester, UK: Wiley-Blackwell Publishing Ltd.
  • Pirog KA, Meadows RS, Thornton DJ, Kadler KE, Boot-Handford RP, Briggs MD. Genetic background influences the severity of chondrodysplasia phenotype. In: Annual General Meeting of the British Society for Matrix Biology. 2009, York, UK: Wiley-Blackwell Publishing Ltd.
  • Pirog-Garcia KA, Meadows RS, Heinegard D, Thornton DJ, Kadler KE, Boot-Handford RP, Briggs MD. Genetic background influences the severity of growth plate dysplasia in a mouse model of pseudoachondroplasia. In: Autumn Meeting of the British Society for Matrix Biology. 2007, Newcastle upon Tyne, UK: Wiley-Blackwell Publishing Ltd.
  • Pirog-Garcia KA, Meadows RS, Wagener R, Heinegard D, Thornton DJ, Kadler KE, Boot-Handford RP, Briggs MD. T583M COMP knockin mouse - a model of mild pseudoachondroplasia resulting from C-terminal COMP mutation. In: Autumn Meeting of the British Society for Matrix Biology. 2006, Manchester, UK: Wiley-Blackwell Publishing Ltd.

• Reviews

  • Briggs MD, Dennis EP, Dietmar H, Pirog KA. New developments in chondrocyte ER-stress and related diseases. F1000Research 2020, 9, 290.
  • Briggs MD, Bell PA, Pirog KA. The utility of mouse models to provide information regarding the pathomolecular mechanisms in human genetic skeletal diseases: The emerging role of endoplasmic reticulum stress (Review). International Journal of Molecular Medicine 2015, 1483-1492.