Ursolic acid suppresses leptin-induced cell proliferation in rat vascular smooth muscle cells

2017 ◽  
Vol 95 (7) ◽  
pp. 811-818 ◽  
Author(s):  
Ya-Mei Yu ◽  
Chiang-Chin Tsai ◽  
Yu-Wen Tzeng ◽  
Weng-Cheng Chang ◽  
Su-Yin Chiang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Ursolic Acid ◽  
Vascular Smooth Muscle Cells ◽  
Biological Effects ◽  
Muscle Cells ◽  
Laser Scanning Microscopy ◽  
Matrix Metalloproteinase 2

Accumulating lines of evidence indicate that high leptin levels are associated with adverse cardiovascular health in obese individuals. Proatherogenic effects of leptin include endothelial cell activation and vascular smooth muscle cell proliferation and migration. Ursolic acid (UA) has been reported to exhibit multiple biological effects including antioxidant and anti-inflammatory properties. In this study, we investigated the effect of UA on leptin-induced biological responses in rat vascular smooth muscle cells (VSMCs). A-10 VSMCs were treated with leptin in the presence or absence of UA. Intracellular reactive oxygen species (ROS) was probed by 2′,7′-dichlorofluorescein diacetate. The expression of extracellular signal-regulated kinase (ERK)1/2, phospho-(ERK)1/2, nuclear factor-kappa B (NF-κB) p65 and p50, and matrix metalloproteinase-2 (MMP2) was determined by Western blotting. Immunocytochemistry and confocal laser scanning microscopy were also used for the detection of NF-κB. The secretion of MMP2 was detected by gelatin zymography. UA exhibited antioxidant activities in vitro. In rat VSMCs, UA effectively inhibited cell growth and the activity of MMP2 induced by leptin. These suppressive effects appeared by decreasing the activation of (ERK)1/2, the nuclear expression and translocation of NF-κB, and the production of ROS. UA appeared to inhibit leptin-induced atherosclerosis, which may prevent the development of obesity-induced cardiovascular diseases.

scholarly journals Integrin β3 Targeting Biomaterial Preferentially Promotes Secretion of bFGF and Proliferation of iPSC-Derived Vascular Smooth Muscle Cells

2021 ◽  
Author(s):  
Biraja C. Dash ◽  
Kaiti Duan ◽  
Themis R. Kyriakides ◽  
Henry C. Hsia
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Matrix Metalloproteinase 2 ◽  
Αvβ3 Integrin ◽  
Integrin Β3

AbstractHuman-induced pluripotent stem cell-derived-vascular smooth muscle cells (hiPSC-VSMC) have been shown to promote angiogenesis and wound healing. However, there is a paucity of research on how the extracellular matrix (ECM) microenvironment may impact the hiPSC-VSMC’s function. In this study, our objective was to understand the effect of specific ECM ligand-integrin interaction on hiPSC- VSMC’s paracrine secretion, cell proliferation, and morphology. We here showed a precise modulation of hiPSC-VSMC in a fibronectin functionalized fibrillar collagen scaffold by targeting their integrin β3. The secretion of proangiogenic growth factor, basic fibroblast growth factor (bFGF) was found to be fibronectin dependent via αvβ3 integrin interactions. Also, our data indicate the possible role of a positive feedback loop between integrin β3, bFGF, and matrix metalloproteinase-2 in regulating hiPSC- VSMC’s morphology and cell proliferation. Finally, the secretome with improved proangiogenic activity shows potential for future regenerative applications.

scholarly journals Troglitazone and pioglitazone attenuate agonist-dependent Ca2+ mobilization and cell proliferation in vascular smooth muscle cells

1999 ◽  
Vol 128 (3) ◽  
pp. 673-683 ◽  
Author(s):  
Michiko Asano ◽  
Toshiaki Nakajima ◽  
Kuniaki Iwasawa ◽  
Toshihiro Morita ◽  
Fumitaka Nakamura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

Trimethylamine But Not Trimethylamine Oxide Increases With Age in Rat Plasma and Affects Smooth Muscle Cells Viability

2019 ◽  
Vol 75 (7) ◽  
pp. 1276-1283 ◽  
Author(s):  
Kinga Jaworska ◽  
Marek Konop ◽  
Tomasz Hutsch ◽  
Karol Perlejewski ◽  
Marek Radkowski ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cardiovascular Risk ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Biological Effects ◽  
Muscle Cells ◽  
Gut Bacteria ◽  
Sprague Dawley ◽  
Trimethylamine Oxide

Abstract It has been suggested that trimethylamine oxide (TMAO), a liver oxygenation product of gut bacteria-produced trimethylamine (TMA), is a marker of cardiovascular risk. However, mechanisms of the increase and biological effects of TMAO are obscure. Furthermore, the potential role of TMAO precursor, that is TMA, has not been investigated. We evaluated the effect of age, a cardiovascular risk factor, on plasma levels of TMA and TMAO, gut bacteria composition, gut-to-blood penetration of TMA, histological and hemodynamic parameters in 3-month-old and 18-month-old, male, Sprague–Dawley and Wistar–Kyoto rats. Cytotoxicity of TMA and TMAO was studied in human vascular smooth muscle cells. Older rats showed significantly different gut bacteria composition, a significantly higher gut-to-blood TMA penetration, and morphological and hemodynamic alterations in intestines. In vitro, TMA at concentration of 500 µmol/L (2-fold higher than in portal blood) decreased human vascular smooth muscle cells viability. In contrast, TMAO at 1,000-fold higher concentration than physiological one had no effect on human vascular smooth muscle cells viability. In conclusion, older rats show higher plasma level of TMA due to a “leaky gut”. TMA but not TMAO affects human vascular smooth muscle cells viability. We propose that TMA but not TMAO may be a marker and mediator of cardiovascular risk.

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