Henry Tung
Position: PhD candidate
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Ischemic heart disease (IHD) is the leading cause of mortality globally. It is characterized by
reduced blood perfusion to the cardiac tissue, which leads to irreversible myocardial cell death
and the development of non-functional scars. In Canada, about one in twelve individuals over the
age of twenty live with a diagnosed heart condition. Although current therapeutics can control
symptoms and improve the quality of life, restoration of normal cardiac function remains an
unmet need for many cardiomyopathies, including myocardial infarction. One of the reasons for
the lack of a cure is our limited understanding of the cellular environment throughout disease
progression. In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that
orchestrate tissue repair upon injury, is largely unknown. In my proposed research work, we aim
to examine MSCs using cutting-edge technologies that provide a much higher resolution than in
the past. In addition to MSCs, we will capture the behaviours of various other cell types and how
they communicate with each other in response to disease. By understanding the behaviour of
cells in proximity to areas which the disease is progressing or improving, we can identify the cell
types and specific mechanisms responsible for causing damage and facilitating recovery. From
these findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of cardiomyopathies and translate into the
development of potential therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Kajabadi, N., Low, M., Jacques, E., Lad, H., Tung, L. W., Babaeijandaghi, F., Gamu, D.,
Zelada, D., Wong, C. K., Chang, C., Yi, L., Wosczyna, M. N., Rando, T. A., Henríquez,
J. P., Gibson, W. T., Gilbert, P. M., & Rossi, F. M. V. (2023). Activation of β-catenin in
mesenchymal progenitors leads to muscle mass loss. Developmental cell, S1534-
5807(23)00051-5. https://doi.org/10.1016/j.devcel.2023.02.009
2. Groppa, E., Martini, P., Derakhshan, N., Theret, M., Ritso, M., Tung, L. W., Wang, Y.
X., Soliman, H., Hamer, M. S., Stankiewicz, L., Eisner, C., Erwan, L. N., Chang, C., Yi,
L., Yuan, J. H., Kong, S., Weng, C., Adams, J., Chang, L., Peng, A., ... Rossi, F. M. V.
(2023). Spatial compartmentalization of signaling imparts source-specific functions on
secreted factors. Cell reports, 42(2), 112051.
https://doi.org/10.1016/j.celrep.2023.112051
3. Messing, M., Sekhon, M. S., Hughes, M. R., Stukas, S., Hoiland, R. L., Cooper, J.,
Ahmed, N., Hamer, M. S., Li, Y., Shin, S. B., Tung, L. W., Wellington, C. L., Sin, D.
D., Leslie, K. B., & McNagny, K. M. (2022). Prognostic peripheral blood biomarkers at
ICU admission predict COVID-19 clinical outcomes. Frontiers in immunology, 13,
1010216. https://doi.org/10.3389/fimmu.2022.1010216
4. Babaeijandaghi F., Paiero A*., Long R.*, Tung L.W., Smith S.P., Cheng R., Smandych
J., Kajabadi N., Chang C.K., Ghassemi A., Kennedy W., Soliman H., Schutz P., & Rossi,
F. (2022). TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of
macrophages during muscle regeneration. PNAS, 119(44), e2209976119.
https://doi.org/10.1073/pnas.2209976119
5. Babaeijandaghi, F., Cheng, R., Kajabadi, N., Soliman, H., Chang, C. K., Smandych, J.,
Tung, L. W., Long, R., Ghassemi, A., & Rossi, F. (2022). Metabolic reprogramming of
skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular
dystrophy therapeutics. Science translational medicine, 14(651), eabg7504.
https://doi.org/10.1126/scitranslmed.abg7504
6. Tehrani, A. Y., White, Z., Tung, L. W., Zhao, R., Milad, N., Seidman, M. A., Sauge, E.,
Theret, M., Rossi, F., Esfandiarei, M., van Breemen, C., & Bernatchez, P. (2022).
Pleiotropic activation of endothelial function by angiotensin II receptor blockers is
crucial to their protective anti-vascular remodeling effects. Scientific reports, 12(1), 9771.
https://doi.org/10.1038/s41598-022-13772-3
7. Theret, M., Rempel, L., Hashimoto, J., Ritso, M., Tung, L. W., Li, F. F., Messing, M.,
Hughes, M., McNagny, K., & Rossi, F. (2022). Elevated numbers of infiltrating
eosinophils accelerate the progression of Duchenne muscular dystrophy pathology in
mdx mice. Development (Cambridge, England), 149(8), dev200112.
https://doi.org/10.1242/dev.200112
8. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
9. White, Z.*, Theret, M.*, Milad, N.*, Tung, L.W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2022). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
muscle, 13(1), 544–560. https://doi.org/10.1002/jcsm.12879
10. Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K.,
Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity
does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life
sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
11. Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes:
Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84.
https://doi.org/10.1007/978-1-0716-1382-5_4
12. Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi,
F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors
Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment.
Journal of bone and mineral research: the official journal of the American Society for
Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
13. Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi,
F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling
pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell
science, 132(19), jcs232157. https://doi.org/10.1242/jcs.232157ttps://doi.org/10.1002/jcsm.12879
10. Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K.,
Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity
does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life
sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
11. Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes:
Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84.
https://doi.org/10.1007/978-1-0716-1382-5_4
12. Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi,
F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors
Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment.
Journal of bone and mineral research: the official journal of the American Society for
Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
13. Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi,
F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling
pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell
s that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
muscle, 10.1002/jcsm.12879. Advance online publication.
https://doi.org/10.1002/jcsm.12879
3. Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K.,
Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity
does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life
sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
4. Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes:
Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84.
https://doi.org/10.1007/978-1-0716-1382-5_4
5. Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi,
F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors
Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment.
Journal of bone and mineral research: the official journal of the American Society for
Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
6. Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi,
F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling
pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell
: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia andosition: PhD candidate
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degradian
Research s
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Ischemic heart disease (IHD) is the leading cause of mortality globally. It is characterized by
reduced blood perfusion to the cardiac tissue, which leads to irreversible myocardial cell death
and the development of non-functional scars. In Canada, about one in twelve individuals over the
age of twenty live with a diagnosed heart condition. Although current therapeutics can control
symptoms and improve the quality of life, restoration of normal cardiac function remains an
unmet need for many cardiomyopathies, including myocardial infarction. One of the reasons for
the lack of a cure is our limited understanding of the cellular environment throughout disease
progression. In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that
orchestrate tissue repair upon injury, is largely unknown. In my proposed research work, we aim
to examine MSCs using cutting-edge technologies that provide a much higher resolution than in
the past. In addition to MSCs, we will capture the behaviours of various other cell types and how
they communicate with each other in response to disease. By understanding the behaviour of
cells in proximity to areas which the disease is progressing or improving, we can identify the cell
types and specific mechanisms responsible for causing damage and facilitating recovery. From
these findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of cardiomyopathies and translate into the
development of potential therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Kajabadi, N., Low, M., Jacques, E., Lad, H., Tung, L. W., Babaeijandaghi, F., Gamu, D.,
Zelada, D., Wong, C. K., Chang, C., Yi, L., Wosczyna, M. N., Rando, T. A., Henríquez,
J. P., Gibson, W. T., Gilbert, P. M., & Rossi, F. M. V. (2023). Activation of β-catenin in
mesenchymal progenitors leads to muscle mass loss. Developmental cell, S1534-
5807(23)00051-5. https://doi.org/10.1016/j.devcel.2023.02.009
2. Groppa, E., Martini, P., Derakhshan, N., Theret, M., Ritso, M., Tung, L. W., Wang, Y.
X., Soliman, H., Hamer, M. S., Stankiewicz, L., Eisner, C., Erwan, L. N., Chang, C., Yi,
L., Yuan, J. H., Kong, S., Weng, C., Adams, J., Chang, L., Peng, A., ... Rossi, F. M. V.
(2023). Spatial compartmentalization of signaling imparts source-specific functions on
secreted factors. Cell reports, 42(2), 112051.
https://doi.org/10.1016/j.celrep.2023.112051
3. Messing, M., Sekhon, M. S., Hughes, M. R., Stukas, S., Hoiland, R. L., Cooper, J.,
Ahmed, N., Hamer, M. S., Li, Y., Shin, S. B., Tung, L. W., Wellington, C. L., Sin, D.
D., Leslie, K. B., & McNagny, K. M. (2022). Prognostic peripheral blood biomarkers at
ICU admission predict COVID-19 clinical outcomes. Frontiers in immunology, 13,
1010216. https://doi.org/10.3389/fimmu.2022.1010216
4. Babaeijandaghi F., Paiero A*., Long R.*, Tung L.W., Smith S.P., Cheng R., Smandych
J., Kajabadi N., Chang C.K., Ghassemi A., Kennedy W., Soliman H., Schutz P., & Rossi,
F. (2022). TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of
macrophages during muscle regeneration. PNAS, 119(44), e2209976119.
https://doi.org/10.1073/pnas.2209976119
5. Babaeijandaghi, F., Cheng, R., Kajabadi, N., Soliman, H., Chang, C. K., Smandych, J.,
Tung, L. W., Long, R., Ghassemi, A., & Rossi, F. (2022). Metabolic reprogramming of
skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular
dystrophy therapeutics. Science translational medicine, 14(651), eabg7504.
https://doi.org/10.1126/scitranslmed.abg7504
6. Tehrani, A. Y., White, Z., Tung, L. W., Zhao, R., Milad, N., Seidman, M. A., Sauge, E.,
Theret, M., Rossi, F., Esfandiarei, M., van Breemen, C., & Bernatchez, P. (2022).
Pleiotropic activation of endothelial function by angiotensin II receptor blockers is
crucial to their protective anti-vascular remodeling effects. Scientific reports, 12(1), 9771.
https://doi.org/10.1038/s41598-022-13772-3
7. Theret, M., Rempel, L., Hashimoto, J., Ritso, M., Tung, L. W., Li, F. F., Messing, M.,
Hughes, M., McNagny, K., & Rossi, F. (2022). Elevated numbers of infiltrating
eosinophils accelerate the progression of Duchenne muscular dystrophy pathology in
mdx mice. Development (Cambridge, England), 149(8), dev200112.
https://doi.org/10.1242/dev.200112
8. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
9. White, Z.*, Theret, M.*, Milad, N.*, Tung, L.W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2022). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
muscle, 13(1), 544–560. https://doi.org/10.1002/jcsm.12879
10. Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K.,
Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity
does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life
sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
11. Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes:
Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84.
https://doi.org/10.1007/978-1-0716-1382-5_4
12. Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi,
F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors
Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment.
Journal of bone and mineral research: the official journal of the American Society for
Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
13. Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi,
F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling
pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell
science, 132(19), jcs232157. https://doi.org/10.1242/jcs.232157ttps://doi.org/10.1002/jcsm.12879
10. Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K.,
Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity
does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life
sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
11. Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes:
Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84.
https://doi.org/10.1007/978-1-0716-1382-5_4
12. Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi,
F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors
Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment.
Journal of bone and mineral research: the official journal of the American Society for
Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
13. Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi,
F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling
pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell
s that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
muscle, 10.1002/jcsm.12879. Advance online publication.
https://doi.org/10.1002/jcsm.12879
3. Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K.,
Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity
does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life
sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
4. Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes:
Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84.
https://doi.org/10.1007/978-1-0716-1382-5_4
5. Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi,
F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors
Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment.
Journal of bone and mineral research: the official journal of the American Society for
Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
6. Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi,
F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling
pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell
: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia andosition: PhD candidate
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degradian
Research s
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
