Pierce Colpman

Mohammed Family PH Research Scholarship 

Department of Medicine, Queens University, Kingston, ON, Dr. Archer’s Research Group.

Under the supervision of: Dr. Stephen Archer 

About Pierce Colpman

Pierce Colpman is an outgoing and adventurous student, born and raised in Victoria, British Columbia. Pierce moved from Victoria to Kingston to begin his undergraduate career in 2017 and completed a specialized bachelor’s degree in Life Sciences. In Fall 2021, Pierce was accepted into the highly competitive Translational Medicine master’s program at Queen’s University, where he began the next chapter of his career. Pierce volunteered in a clinical setting as an emergency department volunteer at the Royal Jubilee Hospital, in Victoria, B.C., and with the Campus Observation Room in consultation with toxicologists from Hotel Dieu Hospital, in Kingston. These experiences provided Pierce with insight into health sciences, and he is excited to positively impact the people involved.

Colpman’s research looked at the role of dynamin 2 as a mediator of the final step in mitochondrial fission and in the pathogenesis of PAH. This research also explored an entirely new way of inhibiting mitochondrial fission through inhibition of dynamin 2 in the hopes of discovering new potential therapeutic targets for PAH.

Project:

Epigenetic upregulation of Dynamin 2, a regulator of mitochondrial fission, promotes human and experimental pulmonary arterial hypertension

Many key features of pulmonary arterial hypertension (PAH), such as rapid cell growth of pulmonary smooth muscle cells and lack of programmed cell death (apoptosis), result from abnormal mitochondrial function. Mitochondria continuously join (fusion) and divide (fission) in coordination with division of the cell’s nucleus through mitotic fission, a very rapid process in PAH. We discovered that blocking mitochondrial division slows the growth of rapidly dividing PAH pulmonary arterial smooth muscle cells (PASMC) and can even kill them in experimental animal models of PAH. Mitochondrial fission is controlled by a protein named dynamin related protein 1 (Drp1); however, the final step in mitochondrial fission requires assistance from another protein: dynamin 2 (DNM2). DNM2 are expressed in excess in PAH patients and therefore, we can block mitochondrial fission and slow down the growth of the cells by inhibiting DNM2.

Colpman’s project tested the idea that increased DNM2 drives rapid cell division and that inhibiting DNM2 is a potential new form of PAH therapy. They studied how excess DNM2 in PAH cells occurs, by evaluating the microRNA that regulate the level of DNM2, as a potential diagnostic and prognostic biomarker to reveal new ways of treating and diagnosing PAH.

Subsequent work:

Since receiving the PHA Canada Research Scholarship, Colpman continued to explore the molecular mechanisms underlying pulmonary arterial hypertension, publishing an abstract in Circulation titled “The Role of Mitochondrial Fission Factor (MFF) and Increased Midzone Mitochondrial Fission in Pulmonary Arterial Hypertension: Implications for Proliferation, Mitophagy, and Apoptosis” 

(https://www.ahajournals.org/doi/abs/10.1161/circ.148.suppl_1.15168).

This work, developed in collaboration with the Archer Lab, investigates the role of mitochondrial dynamics in pulmonary vascular remodeling and provides new insight into the pathogenesis of PAH.

In parallel, Colpman has been working with Aarogya Technologies to increase accessibility to chronic disease management tools, including for conditions like PH. They are testing a remote monitoring device capable of tracking vitals such as EKG, blood pressure, heart rate, respiratory rate, and oxygen saturation while offering unparalleled connectivity with providers. They see great potential for its use in remote PH care, particularly for patients in rural or underserved communities who face barriers to regular monitoring.