
Name: Elena Groppa
Position: Postdoctoral Research Fellow (Swiss National Science Foundation Early Mobility
Postdoctoral Fellowship)
Nationality: Italian
PhD: Vascular Biology
Bachelor and master degree: Biotechnology
Research summary:
Adult skeletal muscle usually regenerates very efficiently. However, when regeneration fails, for
example due to repeated damage or changes in the inflammatory milieu associated with muscle
disorders, deposition of fibrotic matrix infiltrated with adipocytes takes place and initiates a
vicious circle that prevents functional restoration and interferes with therapeutic
approaches. Hence, the comprehension of the mechanisms by which reparative disorders are
caused appear crucial to apply modifications to the muscle environment for halting or
attenuating the progression of the muscle degeneration, as well as for improving the efficacy of
possible therapies. It is now recognized that muscle regeneration is led by myogenic cells that
directly contribute to tissue repair, but also by non-myogenic cells from other developmental
sources, which act as pivotal accessory players, e.g. revascularization enhances proper muscle
differentiation and function (Mounier et al, 2011). Moreover, non-myogenic mesenchymal
population resident in skeletal muscle in a perivascular position and named fibro/adipogenic
progenitors (FAPs) can proliferate in response to muscle injury to transiently establish an
environment that enhances myogenic differentiation (Joe et al, 2010).
My interest is characterizing the vascular remodeling during skeletal muscle regeneration to
establish correlations between the various phases of angiogenesis and the activity of other
cellular components of the regenerative process, such as FAPs, and dissect the underlying
paracrine mechanisms.
Personal summary:
During my PhD, I acquired extensive experience with myoblast-mediated delivery of angiogenic
genes to skeletal muscle (Banfi et al, 2002). This method is based on the retroviral transduction
of syngeneic myoblasts and provides robust expression of the transgene that is stable over time.
Taking advantage of such cell-based ex vivo approach to gene delivery, we explored the biology
of Vascular Endothelial Growth Factor (VEGF), which is the master regulator of angiogenesis i.e.
the formation of new capillaries from preexisting ones. We previously found that VEGF can
induce either normal capillaries or aberrant angioma-like structures depending strictly on its
dose in the microenvironment around each producing cell in vivo, and not on the total amount
(Ozawa et al, 2004). However, stimulation of pericyte recruitment by coexpression of PDGF-BB
could increase the number of pericytes enrolled to the area of neo-angiogenesis and prevent the
aberrant angiogenic phenotype induced by high VEGF levels (Banfi et al, 2012). In term of
vascular stability, VEGF-sustained delivery of 4 weeks was required to maintain newly induced
normal capillaries upon VEGF-signaling abrogation, whereas aberrant vascular structures never
became VEGF-independent. The aim of my project was to further investigate the cellular and
molecular mechanisms regulating 1) the switch between normal and aberrant angiogenesis and
2) the achievement of vascular stabilization in the presence of increasing VEGF doses, in order to
identify novel and potentially more specific molecular targets to improve both the safety and the
efficacy of VEGF-based strategies for therapeutic angiogenesis (Reginato et al, 2011).
Hobbies:
I love practicing both indoor and outdoor sports, and my favorite one is the (European)
Handball! I love travelling, reading books, cooking, and hanging out with friends and know new
people.
Position: Postdoctoral Research Fellow (Swiss National Science Foundation Early Mobility
Postdoctoral Fellowship)
Nationality: Italian
PhD: Vascular Biology
Bachelor and master degree: Biotechnology
Research summary:
Adult skeletal muscle usually regenerates very efficiently. However, when regeneration fails, for
example due to repeated damage or changes in the inflammatory milieu associated with muscle
disorders, deposition of fibrotic matrix infiltrated with adipocytes takes place and initiates a
vicious circle that prevents functional restoration and interferes with therapeutic
approaches. Hence, the comprehension of the mechanisms by which reparative disorders are
caused appear crucial to apply modifications to the muscle environment for halting or
attenuating the progression of the muscle degeneration, as well as for improving the efficacy of
possible therapies. It is now recognized that muscle regeneration is led by myogenic cells that
directly contribute to tissue repair, but also by non-myogenic cells from other developmental
sources, which act as pivotal accessory players, e.g. revascularization enhances proper muscle
differentiation and function (Mounier et al, 2011). Moreover, non-myogenic mesenchymal
population resident in skeletal muscle in a perivascular position and named fibro/adipogenic
progenitors (FAPs) can proliferate in response to muscle injury to transiently establish an
environment that enhances myogenic differentiation (Joe et al, 2010).
My interest is characterizing the vascular remodeling during skeletal muscle regeneration to
establish correlations between the various phases of angiogenesis and the activity of other
cellular components of the regenerative process, such as FAPs, and dissect the underlying
paracrine mechanisms.
Personal summary:
During my PhD, I acquired extensive experience with myoblast-mediated delivery of angiogenic
genes to skeletal muscle (Banfi et al, 2002). This method is based on the retroviral transduction
of syngeneic myoblasts and provides robust expression of the transgene that is stable over time.
Taking advantage of such cell-based ex vivo approach to gene delivery, we explored the biology
of Vascular Endothelial Growth Factor (VEGF), which is the master regulator of angiogenesis i.e.
the formation of new capillaries from preexisting ones. We previously found that VEGF can
induce either normal capillaries or aberrant angioma-like structures depending strictly on its
dose in the microenvironment around each producing cell in vivo, and not on the total amount
(Ozawa et al, 2004). However, stimulation of pericyte recruitment by coexpression of PDGF-BB
could increase the number of pericytes enrolled to the area of neo-angiogenesis and prevent the
aberrant angiogenic phenotype induced by high VEGF levels (Banfi et al, 2012). In term of
vascular stability, VEGF-sustained delivery of 4 weeks was required to maintain newly induced
normal capillaries upon VEGF-signaling abrogation, whereas aberrant vascular structures never
became VEGF-independent. The aim of my project was to further investigate the cellular and
molecular mechanisms regulating 1) the switch between normal and aberrant angiogenesis and
2) the achievement of vascular stabilization in the presence of increasing VEGF doses, in order to
identify novel and potentially more specific molecular targets to improve both the safety and the
efficacy of VEGF-based strategies for therapeutic angiogenesis (Reginato et al, 2011).
Hobbies:
I love practicing both indoor and outdoor sports, and my favorite one is the (European)
Handball! I love travelling, reading books, cooking, and hanging out with friends and know new
people.