Vaspin attenuates high glucose-induced vascular smooth muscle cells proliferation and chemokinesis by inhibiting the MAPK, PI3K/Akt, and NF-κB signaling pathways

Li, Yong; Peng, Wenhui; Zhuang, Jianhua; Lu, Yao; Jian, Weixia; Wei, Yidong; Li, Weiming; Xu, Yawei

doi:10.1016/j.atherosclerosis.2013.02.013

Cited by 80 publications

(69 citation statements)

References 29 publications

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“…As shown in Fig. 5A & 5B, production of ROS was increased by HG in mesenteric VSMCs, in accordance with previous findings in the literature [28,31]. …”

Section: Resultssupporting

confidence: 81%

“…Exposure of VSMCs with HG results in increased ROS production and inflammatory agents [28,31,38]. In the present study, HG-treated VSMCs caused early-elevated ROS production and down-regulation of caveolin-1, which preceded alterations of phenotype-related proteins (viz.…”

Section: Discussionmentioning

confidence: 64%

“…2A & 2B, decreased protein expression of caveolin-1 was found in mesenteric VSMCs from the GK group compared to the Wistar group. To evaluate whether mesenteric VSMCs undergo phenotypic changes, we measured protein expression of PCNA, a marker of cell proliferation [28,29,30] (Figs. 2C & 2D) and calponin (Figs.…”

Section: Resultsmentioning

confidence: 99%

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Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

Carrillo-Sepúlveda

Matsumoto

2014

Cell Physiol Biochem

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Aims: Diabetes-induced vascular complications are associated with vascular smooth muscle cell (VSMC) phenotypic modulation, switching from a contractile to a synthetic-proliferative phenotype. Loss of caveolin-1 is involved with proliferation of VSMCs. We tested the hypothesis that mesenteric VSMCs from type 2 diabetic Goto-Kakizaki (GK) rat undergo phenotypic modulation and it is linked to decreased caveolin-1 expression. Methods: VSMCs were isolated from mesenteric arteries from GK rats and age-matched control Wistar rats. Western blotting was used to determine expression of target proteins such as caveolin-1, calponin (marker of differentiation), and proliferating cell nuclear antigen (PCNA, marker of proliferation). In addition, we measured intracellular reactive oxygen species (ROS) production using H2DCF-DA and activation of extracellular signal-regulated kinase (ERK1/2) by western blotting in VSMCs from GK stimulated with lipopolysaccharide (LPS), an endotoxin upregulated in diabetes. Results: Mesenteric VSMCs from diabetic GK rats exhibited decreased caveolin-1 and calponin expression and increased PCNA expression compared to control. Increased levels of ROS and phospho-ERK1/2 expression were also found in GK VSMCs. LPS augmented ROS and phosphorylated ERK1/2 levels to a greater extent in GK VSMCs than in control. Likewise, high glucose decreased caveolin-1 and calponin expression, increased PCNA expression and augmented ROS production in control mesenteric VSMCs. Conclusion: These results suggest that mesenteric VSMCs from diabetic GK rats undergo phenotypic modulation and it is associated with decreased caveolin-1 expression. These alterations may be due to enhanced inflammatory stimuli and glucose levels present in diabetic milieu.

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“…As shown in Fig. 5A & 5B, production of ROS was increased by HG in mesenteric VSMCs, in accordance with previous findings in the literature [28,31]. …”

Section: Resultssupporting

confidence: 81%

Section: Discussionmentioning

confidence: 64%

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Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

Carrillo-Sepúlveda

Matsumoto

2014

Cell Physiol Biochem

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“…This has been proposed as a novel mechanism by which vaspin offers protection against vascular injury brought on by HG-induced insulin resistance. Vaspin has also been shown to reduce HG-stimulated vascular smooth muscle cell proliferation and chemokinesis, in vitro, by preventing the activation of reactive oxygen species, MAPK and PI3K/Akt while also blocking insulin receptor signaling and the NF-kB signaling pathway (Li et al 2013). It was concluded that the delaying effect of vaspin on vascular intimal hyperplasia could also play a possible role in the delay or prevention of carcinogenesis (Li et al 2013).…”

Section: Discussionmentioning

confidence: 99%

“…Vaspin has also been shown to reduce HG-stimulated vascular smooth muscle cell proliferation and chemokinesis, in vitro, by preventing the activation of reactive oxygen species, MAPK and PI3K/Akt while also blocking insulin receptor signaling and the NF-kB signaling pathway (Li et al 2013). It was concluded that the delaying effect of vaspin on vascular intimal hyperplasia could also play a possible role in the delay or prevention of carcinogenesis (Li et al 2013). However, to date, no papers have been published regarding this matter, and there is a need for further studies investigating the pathogenic mechanisms involved in carcinogenesis, at a molecular level.…”

Section: Discussionmentioning

confidence: 99%

Evaluating vaspin and adiponectin in postmenopausal women with endometrial cancer

Erdoğan

Sezer

Başer

et al. 2013

Endocrine-Related Cancer

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Insulin resistance is a well-documented risk factor for the development of endometrial cancer. Adiponectin and vaspin are insulin-sensitizing proteins that are secreted from adipose tissue. A clear association between serum levels of adipokines and endometrial cancer has yet to be established. The study group consisted of postmenopausal women with confirmed endometrial cancer, whereas patients with benign endometrial conditions constituted the control group. The two groups were compared in terms of insulin resistance and serum levels of adiponectin and vaspin. A total of 60 patients with confirmed endometrial cancer and 70 controls with benign endometrial conditions (polyps and atrophy) were enrolled. Median homeostasis model assessment of insulin resistance value was significantly higher in the study group compared with the control group (2.93 vs 1.27, P!0.0001), whereas mean quantitative insulin sensitivity check index value was significantly lower (0.33G0.02 vs 0.37G0.37, P!0.0001). Median values for both adiponectin and vaspin were significantly lower in patients with endometrial cancer compared with the control group (4.09 vs 17.13 mg/ml, P!0.0001 and 0.21 vs 0.39 ng/ml, P!0.0001 respectively). Low levels of both adiponectin and vaspin were found to be significantly associated with an increased risk for endometrial cancer. Following adjustment for confounding factors, the respective odds ratios for endometrial cancer in patients in the first tertile compared with those in the third tertile were 10.80 (2.76-42.24; PZ0.001) and 13.23 (2.94-59.64; PZ0.001). Our results show that lower levels of circulating adiponectin and vaspin levels are associated with an increased risk of developing endometrial cancer.

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Microtubule affinity regulating kinase 4: A promising target in the pathogenesis of atherosclerosis

Qin

Wang

et al. 2021

Journal Cellular Physiology

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Microtubule affinity regulating kinase 4 (MARK4), an important member of the serine/ threonine kinase family, regulates the phosphorylation of microtubule-associated proteins and thus modulates microtubule dynamics. In human atherosclerotic lesions, the expression of MARK4 is significantly increased. Recently, accumulating evidence suggests that MARK4 exerts a proatherogenic effect via regulation of lipid metabolism (cholesterol, fatty acid, and triglyceride), inflammation, cell cycle progression and proliferation, insulin signaling, and glucose homeostasis, white adipocyte browning, and oxidative stress. In this review, we summarize the latest findings regarding the role of MARK4 in the pathogenesis of atherosclerosis to provide a rationale for future investigation and therapeutic intervention.

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Vaspin attenuates high glucose-induced vascular smooth muscle cells proliferation and chemokinesis by inhibiting the MAPK, PI3K/Akt, and NF-κB signaling pathways

Cited by 80 publications

References 29 publications

Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

Evaluating vaspin and adiponectin in postmenopausal women with endometrial cancer

Microtubule affinity regulating kinase 4: A promising target in the pathogenesis of atherosclerosis

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