Abstract
Background Our previous studies demonstrated that natriuretic peptides, i.e. BNP produced by activated satellite cells within ischemic skeletal muscle, stimulate the regeneration of neighboring endothelia via endothelial GC-A/ cGMP signaling [1]. This paracrine communication might be critically involved in coordinating postischemic muscle regeneration and angiogenesis. In the retina, angiogenesis occurs as a part of normal development as well as in proliferative vascular diseases, such as diabetic retinopathy (DR) or retinopathy of prematurity (ROP) [2]. Retinal vascular development is controlled by interactions between ganglion cells, astrocytes and endothelial cells. In particular, reciprocal feedback between endothelial cells and astrocytes is crucial for proper vascular patterning. Hypoxia-induced vascular endothelial growth factor (VEGF) expression in astrocytes plays a key role in (patho)physiological retinal endothelial growth. Notably, immunohistochemistry on postnatal (P7) retinal whole-mounts revealed the expression of immunoreactive BNP in glial fibrillary acidic protein (GFAP)–expressing astrocytes. Therefore we postulated that BNP participates in this astrocyte-endothelial communication during physiological vascularization and/or pathological revascularization of the retina.
Highlights
Our previous studies demonstrated that natriuretic peptides, i.e. BNP produced by activated satellite cells within ischemic skeletal muscle, stimulate the regeneration of neighboring endothelia via endothelial GC-A/ cGMP signaling [1]
Firstly we studied whether crossing GC-Afl/fl mice with glial fibrillary acidic protein (GFAP)-CreTG mice resulted in efficient and selective inactivation of GC-A in astrocytes
ANP and BNP enhanced cGMP levels in cultured control astrocytes and these effects were significantly attenuated in astrocytes prepared from GC-Afl/fl;GFAP-Cre+/-mice
Summary
Our previous studies demonstrated that natriuretic peptides, i.e. BNP produced by activated satellite cells within ischemic skeletal muscle, stimulate the regeneration of neighboring endothelia via endothelial GC-A/ cGMP signaling [1]. This paracrine communication might be critically involved in coordinating postischemic muscle regeneration and angiogenesis. Retinal vascular development is controlled by interactions between ganglion cells, astrocytes and endothelial cells. Hypoxia-induced vascular endothelial growth factor (VEGF) expression in astrocytes plays a key role in (patho)physiological retinal endothelial growth. We postulated that BNP participates in this astrocyte-endothelial communication during physiological vascularization and/or pathological revascularization of the retina
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