scholarly journals Hydrogen sulfide inhibits the calcification and osteoblastic differentiation of vascular smooth muscle cells

2011 ◽  
Vol 80 (7) ◽  
pp. 731-739 ◽  
Author(s):  
Erzsébet Zavaczki ◽  
Viktória Jeney ◽  
Anupam Agarwal ◽  
Abolfazl Zarjou ◽  
Melinda Oros ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Osteoblastic Differentiation

scholarly journals Globular adiponectin inhibits osteoblastic differentiation of vascular smooth muscle cells through the PI3K/AKT and Wnt/β-catenin pathway

2021 ◽  
Author(s):  
Yun Zhou ◽  
Li-Long Wei ◽  
Rui-Ping Zhang ◽  
Cheng-Wu Han ◽  
Yongtong Cao
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Osteoblastic Differentiation ◽  
Alizarin Red S ◽  
Regulation Mechanism ◽  
Alizarin Red ◽  
Globular Adiponectin

AbstractLipid metabolism is closely related to the improvement of vascular calcification (VC) in chronic kidney disease (CKD). Globular adiponectin (gAd) has been reported to be involved in the development of VC in CKD, but the detailed regulatory role remains unclear. The present study is aimed to investigate the biological function and the underlying regulation mechanism of gAd in the process of VC during CKD. Vascular smooth muscle cells (VSMCs) calcification was determined by Alizarin Red S staining. Protein signaling related with VC was tested by western blotting. The expression and intracellular localization of runt-related transcription factor 2 (Runx2) was detected by immunofluorescence and uraemic rat with VC was established by a two-step nephrectomy. Combined with the results of Alizarin Red S staining, we discovered that β-glycerophosphate (β-Gp)-induced the osteoblastic differentiation of VSMCs was significantly reversed by gAd treatment. Along with the VSMCs calcification and the increase of Runx2 in β-Gp-exposed VSMCs, the activities of protein kinase B (AKT) and Wnt/β-catenin pathway were enhanced, but that were counteracted by the exposure of gAd in rat and human VSMCs. After administration with agonists of the Wnt (SKL2001) and AKT (SC79), there appeared more osteoblastic differentiation and higher expression of Runx2 in gAd-treated VSMCs, but showing lower impact in the presence of SC79 than that in the presence of SKL2001. In the in vivo experiments, intravenous injection of gAd also significantly inhibited VC and Runx2 level in uraemic rat in a dose-dependent manner, possibly through regulating Wnt/β-catenin pathway. This study demonstrates that gAd ameliorates osteoblastic differentiation of VSMCs possibly by blocking PI3K/AKT and Wnt/β-catenin signaling transduction. The findings provide an important foundation for gAd in treating VC in kidney diseases.

scholarly journals BMP-9 regulates the osteoblastic differentiation and calcification of vascular smooth muscle cells through an ALK1 mediated pathway

2014 ◽  
Vol 19 (1) ◽  
pp. 165-174 ◽  
Author(s):  
Dongxing Zhu ◽  
Neil Charles Wallace Mackenzie ◽  
Catherine M. Shanahan ◽  
Rukshana C. Shroff ◽  
Colin Farquharson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Osteoblastic Differentiation

scholarly journals SP362EFFECT OF IRON CITRATE ON MATRIX AND SIMIL-OSTEOBLASTIC DIFFERENTIATION IN HIGH PHOSPHATE TREATED VASCULAR SMOOTH MUSCLE CELLS

2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii233-iii233
Author(s):  
Paola Ciceri ◽  
Francesca Elli ◽  
Monica Falleni ◽  
Delfina Tosi ◽  
Gaetano Bulfamante ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Osteoblastic Differentiation ◽  
Iron Citrate ◽  
High Phosphate

Interaction of Methylglyoxal and Hydrogen Sulfide in Rat Vascular Smooth Muscle Cells

2010 ◽  
Vol 12 (9) ◽  
pp. 1093-1100 ◽  
Author(s):  
Tuanjie Chang ◽  
Ashley Untereiner ◽  
Jianghai Liu ◽  
Lingyun Wu
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

Vasoconstrictive effect of hydrogen sulfide involves downregulation of cAMP in vascular smooth muscle cells

2008 ◽  
Vol 295 (5) ◽  
pp. C1261-C1270 ◽  
Author(s):  
Jia Jia Lim ◽  
Yi-Hong Liu ◽  
Ester Sandar Win Khin ◽  
Jin-Song Bian
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nitric Oxide Synthase Inhibitor ◽  
Vasorelaxant Effect ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Hydrogen sulfide (H2S), a new endogenous mediator, produces both vasorelaxation and vasoconstriction. This study was designed to examine whether cAMP mediates the vasoconstrictive effect of H2S. We found that NaHS at a concentration range of 10–100 μM (yields ∼3–30 μM H2S) concentration-dependently reversed the vasodilation caused by isoprenaline and salbutamol, two β-adrenoceptor agonists, and forskolin, a selective adenylyl cyclase activator, in phenylephrine-precontracted rat aortic rings. Pretreatment with NaHS (10–100 μM) for 5 min also significantly attenuated the vasorelaxant effect of salbutamol and forskolin. More importantly, NaHS (5–100 μM) significantly reversed forskolin-induced cAMP accumulation in vascular smooth muscle cells. However, NaHS produced significant, but weaker, vasoconstriction in the presence of NG-nitro-l-arginine methyl ester (100 μM), a nitric oxide synthase inhibitor, or in endothelium-denuded aortic rings. Blockade of ATP-sensitive potassium channels with glibenclamide (10 μM) failed to attenuate the vasoconstriction induced by H2S. Taken together, we demonstrated for the first time that the vasoconstrictive effect of H2S involves the adenyly cyclase/cAMP pathway.

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