BACKGROUND: Biglycan (BGN), an extracellular matrix proteoglycan, has been shown to convey pro-inflammatory signals. In the present study we investigated BGN expression and its correlation with plasma levels of inflammatory markers in hypertensive subjects with or without alteration of carotid intima media thickness (IMT). METHODS: We evaluated 123 untreated essential hypertensives with no additional risk factors for atherosclerosis nor signs of cardiovascular disease and 40 controls. Hypertensives were classified according to a normal (< or =1 mm) or increased (>1 mm) IMT. BGN-mRNA and protein expression were measured in unstimulated, LPS- and Angiotensin II (Ang-II)-stimulated blood monocytes. Plasma concentrations of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha) and high sensitivity-C-reactive protein (hs-CRP) were also measured. RESULTS: We found increased levels of IL-6, TNF-alpha, hs-CRP, and BGN-mRNA and protein in hypertensives vs controls (1.72+/-0.60 vs 1 n-fold, and 3.60+/-0.75 vs 1 n-fold, both p<0.001). However, BGN expression was not significantly different between hypertensives with IMT < or =1 mm and >1 mm. Furthermore, in vitro addition of Ang II enhanced basal BGN-mRNA (in hypertensives: 3.57+/-1.08 vs 1.72+/-0.60 n-fold, p<0.001) and protein (in hypertensives: 4.92+/-0.42 vs 3.41+/-0.75, p<0.001) expression in monocytes. CONCLUSIONS: Our data provide evidence of an enhanced expression of BGN in essential hypertension. In addition we suggest that Ang II can mediate monocyte BGN production.
BACKGROUND:Biglycan (BGN), an extracellular matrix proteoglycan, has been shown to convey pro-inflammatory signals. In the present study we investigated BGN expression and its correlation with plasma levels of inflammatory markers in hypertensive subjects with or without alteration of carotid intima media thickness (IMT). METHODS: We evaluated 123 untreated essential hypertensives with no additional risk factors for atherosclerosis nor signs of cardiovascular disease and 40 controls. Hypertensives were classified according to a normal (< or =1 mm) or increased (>1 mm) IMT. BGN-mRNA and protein expression were measured in unstimulated, LPS- and Angiotensin II (Ang-II)-stimulated blood monocytes. Plasma concentrations of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha) and high sensitivity-C-reactive protein (hs-CRP) were also measured. RESULTS: We found increased levels of IL-6, TNF-alpha, hs-CRP, and BGN-mRNA and protein in hypertensives vs controls (1.72+/-0.60 vs 1 n-fold, and 3.60+/-0.75 vs 1 n-fold, both p<0.001). However, BGN expression was not significantly different between hypertensives with IMT < or =1 mm and >1 mm. Furthermore, in vitro addition of Ang II enhanced basal BGN-mRNA (in hypertensives: 3.57+/-1.08 vs 1.72+/-0.60 n-fold, p<0.001) and protein (in hypertensives: 4.92+/-0.42 vs 3.41+/-0.75, p<0.001) expression in monocytes. CONCLUSIONS: Our data provide evidence of an enhanced expression of BGN in essential hypertension. In addition we suggest that Ang II can mediate monocyte BGN production.
Authors: Priscila G Pereira; Kíssila Rabelo; Jemima F R da Silva; Bianca T Ciambarella; Juliana G C Argento; Ana L R Nascimento; Aline B Vieira; Jorge J de Carvalho Journal: Histol Histopathol Date: 2019-10-18 Impact factor: 2.303
Authors: Tatiana Martin-Rojas; Laura Mourino-Alvarez; Sergio Alonso-Orgaz; Esther Rosello-Lleti; Enrique Calvo; Luis Fernando Lopez-Almodovar; Miguel Rivera; Luis R Padial; Juan Antonio Lopez; Fernando de la Cuesta; Maria G Barderas Journal: Sci Rep Date: 2015-12-01 Impact factor: 4.379