Key result
Complement 3 maintains the undifferentiated state of smooth muscle cells from mesenchymal stem cells to generate renin, contributing to hypertension pathogenesis in spontaneously hypertensive rats.
Why the study?
To investigate the contributions of complement 3 to the development of hypertension pathogenesis by evaluating renin-producing cell formation and renin generation during differentiation of primary bone marrow-mesenchymal stem cells to smooth muscle cells.
Population
Primary bone marrow-MSCs from C57BL/6 mice, WKY rats, and SHRs
Comparison
Differentiation to SMCs with TGF-beta1, exogenous C3a, or C3a receptor antagonist SB290157 vs controls
Design
Preclinical in vitro experimental study
Authors
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C3 may promote hypertensive remodeling via local RAS in rats; leaves open human renin regulation and therapeutic targeting.
Complement 3 plays a key role in maintaining an undifferentiated state in smooth muscle cells derived from mesenchymal stem cells, promoting renin generation that may contribute to the pathogenesis of hypertension.
Chen et al. (2020) studied Hypertension. Complement 3 (C3) was evaluated on Renin generation during differentiation of MSCs to SMCs. Complement 3 maintains the undifferentiated state of smooth muscle cells from mesenchymal stem cells to generate renin, contributing to hypertension pathogenesis in spontaneously hypertensive rats.
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