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Published on: September 12, 2017
Striated muscle angio-adaptation requires changes in Vasohibin-1 expression pattern
Marina Kishlyansky1, Jovana Vojnovic, Emilie Roudier
1York University, Faculty of Health, Muscle Health Research Center, Toronto, ON, Canada.
Vasohibin-1 (VASH-1) isoforms regulate muscle blood vessel adaptation. Exercise training decreased VASH-1, while unloading increased it, showing VASH-1
Area of Science:
- Physiology
- Molecular Biology
- Vascular Biology
Background:
- Vasohibin-1 (VASH-1) is a negative feedback regulator of angiogenesis.
- VASH-1 has two active isoforms: p36 and p42.
- Muscle angio-adaptation involves complex regulatory mechanisms.
Purpose of the Study:
- To investigate the expression of VASH-1 isoforms (p36 and p42) during physiological and pathological muscle angio-adaptation.
- To understand the role of VASH-1 in exercise-induced angiogenesis and unloading-induced capillary regression.
- To explore VASH-1 expression in a model of type-2 diabetes and its impact on muscle capillarization.
Main Methods:
- Analysis of VASH-1 protein expression in rat plantaris, heart, and soleus muscles.
- Utilized exercise training and hindlimb unloading models in rats.
- Investigated VASH-1 expression in Zucker Diabetic Fatty (ZDF) rats.
Main Results:
- VASH-1 expression is muscle-type specific, higher in less vascularized muscles.
- Exercise training decreased VASH-1 in plantaris and heart muscles.
- Hindlimb unloading increased VASH-1 isoforms, suggesting vessel destabilization.
- Sedentary ZDF rats showed higher VASH-1, linked to capillary loss; activity restored VASH-1 and capillarization.
Conclusions:
- Endogenous VASH-1 isoforms p36 and p42 are crucial regulators of muscle angio-adaptation.
- VASH-1 plays a significant role in both physiological (exercise) and pathological (unloading, diabetes) contexts.
- Modulation of VASH-1 levels is associated with changes in muscle vascularization.
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