Autocrine Human Urotensin II Enhances Macrophage-Derived Foam Cell Formation in Transgenic Rabbits

Song, Zhao; Li, Yafeng; Gao, Shoucui; Wang, Xiaojing; Sun, Lijing; Cheng, Daxing; Bai, Liang; Guan, Hua; Wang, Rong; Fan, Jianglin; Liu, Enqi

doi:10.1155/2015/843959

Cited by 13 publications

(6 citation statements)

References 29 publications

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“…The entire aortic tree was fixed in 10% neutral buffered formalin and stained with Sudan IV (Yongsheng Chemical Co., Ji'nan, China) as previously described [21]. The area of the atherosclerotic lesion (sudanophilic area) was measured using image analysis software (WinROOF 6.5, Mitani Co. Ltd., Tokyo, Japan).…”

Section: Atherosclerotic Lesion Analysismentioning

confidence: 99%

Salusin-α Inhibits Proliferation and Migration of Vascular Smooth Muscle Cell via Akt/mTOR Signaling

Gao

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: The proliferation and migration of vascular smooth muscle cells (VSMCs) are key steps in the progression of atherosclerosis. The aim of the present study was to investigate the potential roles of salusin-α in the functions of VSMCs during the development of atherosclerosis. Methods: In vivo, the effects of salusin-α on atherogenesis were examined in rabbits fed a cholesterol diet. The aortas were en face stained with Sudan IV to evaluate the gross atherosclerotic lesion size. The cellular components of atherosclerotic plaques were analyzed by immunohistochemical methods. In vitro, Cell Counting Kit-8 and wound-healing assays were used to assess the effects of salusin-α on VSMC proliferation and migration. In addition, western blotting was used to evaluate the total and phosphorylated levels of Akt (also known as protein kinase B) and mammalian target of rapamycin (mTOR) in VSMCs. Results: Salusin-α infusion significantly reduced the aortic lesion areas of atherosclerosis, with a 39% reduction in the aortic arch, a 71% reduction in the thoracic aorta, and a 71% reduction in the abdominal aorta; plasma lipid levels were unaffected. Immunohistochemical staining showed that salusin-α decreased both macrophage- and VSMC-positively stained areas in atherosclerotic lesions by 54% and 69%, cell proliferative activity in the intima and media of arteriosclerotic lesions, and matrix metalloproteinase 2 (MMP-2) and MMP-9 expression in plaques. Studies using cultured VSMCs showed that salusin-α decreased VSMC migration and proliferation via reduced phosphorylation of Akt and mTOR. Conclusion: Our data indicate that salusin-α suppresses the development of atherosclerosis by inhibiting VSMC proliferation and migration through the Akt/mTOR pathway.

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Section: Atherosclerotic Lesion Analysismentioning

confidence: 99%

Salusin-α Inhibits Proliferation and Migration of Vascular Smooth Muscle Cell via Akt/mTOR Signaling

Gao

Zhang

et al. 2018

Cell Physiol Biochem

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“…10 27 Proinflammatory cytokines such as interleukin (IL)-6, IL-1β, and interferon (IFN)-γ in atherosclerotic plaques, which are secreted by macrophages and lymphocytes, upregulate the expression of U-II, and the specific receptor UT which accelerates the formation of atherosclerotic plaques with autocrine/paracrine effects. 28 Moreover, U-II induces proliferation of vascular smooth muscle cells 10 and cardiomyocytes. 11 Indeed, previous studies have indicated the presence of cardiac hypertrophy 29 and altered cardiac function 30 in SGA infants.…”

Section: Discussionmentioning

confidence: 99%

Birth Weight Standard Deviation Score is a Significant Determinant of Serum Urotensin-II Levels at Term-Equivalent Age in Preterm Infants

et al. 2020

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Objective Urotensin II (U-II) is a potent vasoconstrictor peptide, and increased U-II levels are associated with atherosclerosis and hypertension in adults. Low birth weight (LBW) infants have higher risks of such diseases in the future. A small number of nephrons is one of possible mechanism underlying these risks in LBW infants, while vascular elasticity and cardiac function might be another important factor. The objective of this study is to evaluate U-II levels in preterm LBW infants at an early stage of life and determine perinatal factors associated with U-II levels. Study Design The study population consisted of 57 preterm LBW infants (26 males and 31 females), including 49 appropriate for gestational age (AGA) and 8 small for gestational age (SGA) infants, born at a gestational age of ≤34 weeks with a mean birth weight of 1,589 g. Serum U-II levels were measured at term-equivalent age to evaluate perinatal factors related to serum U-II levels. Results Preterm SGA infants had significantly higher serum U-II levels than preterm AGA infants at term-equivalent age (p = 0.019). Serum U-II levels in preterm LBW infants at term-equivalent age were inversely correlated with birth weight standard deviation (SD) score in a simple regression analysis (r = − 0.395, p = 0,002) and the correlation was maintained in the multiple regression analysis. Conclusion Our results indicate that birth weight SD score might be associated with serum U-II levels in preterm LBW infants at term-equivalent age. Further studies are required to determine whether U-II levels at an early stage of life might influence the risk of atherosclerosis and hypertension. Key Points

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“…Transgenic (Tg) mice of C57BL/6 N background were generated in our laboratory as previously reported [ 26 , 27 ]. The DNA construct used for microinjection contained mouse SFRP4 cDNA under the control of the liver-specific sequences containing partial apoE and liver-specific region of the apoE/apoCI gene locus [ 28 ], along with four copies of the chicken β globin insulator ( Figure 1(a )), to prevent position effects of transgene insulators [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

Effects of SFRP4 overexpression on the production of adipokines in transgenic mice

Zhang

Guan

et al. 2020

Adipocyte

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Secreted frizzled-related protein (SFRP) 4 is an extracellular antagonist of Wnt signalling that regulates adipogenesis, and is highly in the visceral adipose tissue of obese individuals. However, it is still unclear how exactly SFRP4 regulates the secretion of adipokines in the adipose tissue in vivo, an event that is closely related to the pathogenesis of obesity and insulin resistance. In this study, we generated transgenic (Tg) mice overexpressing SFRP4 in the liver and investigated SFRP4 role in adipokine secretion in mice on a regular normal diet. In Tg mice, SFRP4 protein was overexpressed in the liver, as compared to wild-type littermates (non-Tg), and released into the blood. Moreover, the size of adipocytes was smaller in the visceral adipose tissue of Tg mice compared to controls. Additionally, SFRP4 overexpression affected the expression of genes related to adipocyte differentiation, causing the upregulation of adiponectin and glucose transporter 4, and the downregulation of CCAAT/enhancer-binding protein-β, in both visceral and subcutaneous adipose tissue. However, there was no difference in body weight or body composition between Tg and non-Tg mice. In summary, our data showed that SFRP4 overexpression altered adipocyte size and adipokine secretion, possibly affecting adipocyte differentiation, obesity, and glucose metabolism.

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Autocrine Human Urotensin II Enhances Macrophage-Derived Foam Cell Formation in Transgenic Rabbits

Cited by 13 publications

References 29 publications

Salusin-α Inhibits Proliferation and Migration of Vascular Smooth Muscle Cell via Akt/mTOR Signaling

Salusin-α Inhibits Proliferation and Migration of Vascular Smooth Muscle Cell via Akt/mTOR Signaling

Birth Weight Standard Deviation Score is a Significant Determinant of Serum Urotensin-II Levels at Term-Equivalent Age in Preterm Infants

Effects of SFRP4 overexpression on the production of adipokines in transgenic mice

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