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Potential mechanisms that may contribute to the cardiovascular benefit affo...
Published: 11 January 2022
Figure 2 Potential mechanisms that may contribute to the cardiovascular benefit afforded by GLP-1Ra. GLP-1Ra-mediated cardioprotection likely results from multiple contributing factors, including a reduction in inflammatory processes and body weight, improvements in vascular function that decrease... More
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<em>A</em>: Overview of C-peptide’s cytoprotective, antiapoptotic, ...
Published: 14 March 2012
FIG. 3. A: Overview of C-peptide’s cytoprotective, antiapoptotic, and anti-inflammatory effects. B: Leukocyte adherence in the rat mesenteric microvasculature after superfusion of the mesentery with 0.5 units/mL thrombin. Bars show number of adhering leukocytes per 100 μm postcapillary venular endothelium after an intravenous bolus administration of C-peptide (red bars) or scrambled C-peptide (orange bar). Data are means ± SE for number of adherent cells observed at 120 min in each group (n = 6). **P < 0.01 vs. control (blue bar). Data are from Ref. 34 . C: Effect of C-peptide on binding activity of NF-κB p50. Human aortic endothelial cells were cultured in low (5.6 mmol/L) or high (25 mmol/L) glucose in the presence or absence of 0.5 nmol/L C-peptide. In cells exposed to high glucose (blue bar), there was a twofold increase in NF-κB p50 nuclear translocation compared with cells in low glucose (yellow bar). A decrease in NF-κB p50 nuclear translocation was observed in the presence of C-peptide (red bar) (*P < 0.05 vs. high glucose alone), while heat-inactivated C-peptide (orange bar) had no significant effect. Data are from Ref. 35 . D: C-peptide reduces high glucose–induced proliferation of umbilical artery smooth muscle cells. Cells were incubated with 5.6 or 25 mmol/L glucose (yellow and blue bars, respectively) in the presence or absence of C-peptide and assayed for cell proliferation. C-peptide (red bars) reduced high glucose–induced umbilical artery smooth muscle cell proliferation (**P < 0.01 vs. high glucose), while addition of scrambled C-peptide (orange bar) had no significant effect. Data are from Ref. 37 . E: C-peptide induces vascular smooth muscle proliferation. Human aortic smooth muscle cells were stimulated with different concentrations of human C-peptide (red bars) for 24 h before cell proliferation was assessed by [3H]thymidine incorporation. Scrambled C-peptide (10 nmol/L; orange bar) was used as a negative and platelet-derived growth factor (10 ng/mL) as a positive control. Data are expressed as fold induction of unstimulated cells. *P < 0.05 vs. control. Data are from Ref. 40 . ROS, reactive oxygen species; ICAM-1, intercellular adhesion molecule 1; VCAM-1, vascular adhesion molecule 1; MCP-1, monocyte chemoattractant protein 1; VSMC, vascular smooth muscle cell; CP, C-peptide; Scr, scrambled; HI, heat inactivated; UASMC, umbilical artery smooth muscle cells; VSM, vascular smooth muscle; PDGF, platelet-derived growth factor; PI-3K, phosphoinositide 3-kinase. FIG. 3. A: Overview of C-peptide’s cytoprotective, antiapoptotic, and anti-inflammatory effects. B: Leukocyte adherence in the rat mesenteric microvasculature after superfusion of the mesentery with 0.5 units/mL thrombin. Bars show number of adhering leukocytes per 100 μm postcapillary venular endothelium after an intravenous bolus administration of C-peptide (red bars) or scrambled C-peptide (orange bar). Data are means ± SE for number of adherent cells observed at 120 min in each group (n = 6). **P < 0.01 vs. control (blue bar). Data are from Ref. 34. C: Effect of C-peptide on binding activity of NF-κB p50. Human aortic endothelial cells were cultured in low (5.6 mmol/L) or high (25 mmol/L) glucose in the presence or absence of 0.5 nmol/L C-peptide. In cells exposed to high glucose (blue bar), there was a twofold increase in NF-κB p50 nuclear translocation compared with cells in low glucose (yellow bar). A decrease in NF-κB p50 nuclear translocation was observed in the presence of C-peptide (red bar) (*P < 0.05 vs. high glucose alone), while heat-inactivated C-peptide (orange bar) had no significant effect. Data are from Ref. 35. D: C-peptide reduces high glucose–induced proliferation of umbilical artery smooth muscle cells. Cells were incubated with 5.6 or 25 mmol/L glucose (yellow and blue bars, respectively) in the presence or absence of C-peptide and assayed for cell proliferation. C-peptide (red bars) reduced high glucose–induced umbilical artery smooth muscle cell proliferation (**P < 0.01 vs. high glucose), while addition of scrambled C-peptide (orange bar) had no significant effect. Data are from Ref. 37. E: C-peptide induces vascular smooth muscle proliferation. Human aortic smooth muscle cells were stimulated with different concentrations of human C-peptide (red bars) for 24 h before cell proliferation was assessed by [3H]thymidine incorporation. Scrambled C-peptide (10 nmol/L; orange bar) was used as a negative and platelet-derived growth factor (10 ng/mL) as a positive control. Data are expressed as fold induction of unstimulated cells. *P < 0.05 vs. control. Data are from Ref. 40. ROS, reactive oxygen species; ICAM-1, intercellular adhesion molecule 1; VCAM-1, vascular adhesion molecule 1; MCP-1, monocyte chemoattractant protein 1; VSMC, vascular smooth muscle cell; CP, C-peptide; Scr, scrambled; HI, heat inactivated; UASMC, umbilical artery smooth muscle cells; VSM, vascular smooth muscle; PDGF, platelet-derived growth factor; PI-3K, phosphoinositide 3-kinase. More
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Hypothesized contributions from Nox2-generated oxidative stress to the proc...
Published: 17 May 2013
FIG. 1. Hypothesized contributions from Nox2-generated oxidative stress to the process of atherosclerosis. When NADPH donates electrons to molecular oxygen via Nox2, O2· generation occurs. Oxidative stress occurs when O2· production exceeds the antioxidant capacity of the immediate environment. Oxidative stress can contribute to atherosclerosis progression by various mechanisms ( 7 ). ↑, increase; ↓, decrease. Mice with endothelial cell–specific insulin resistance (ESMIRO and IR+/− mice) exhibit increased Nox2-mediated O2· generation to an extent that evokes endothelial dysfunction. Treatment of ESMIRO and IR+/− mice with the Nox inhibitor gp91ds-tat (+gp91ds-tat) or endothelial cell–specific knockout of Nox2 in ESMIRO mice (ESMIRO / Nox2y/−) reduces O2· production and restores endothelial function. *Endothelial function was assessed in the current study (3), but the influence of endothelial cell–specific Nox2 deletion on other potential contributors to atherosclerosis depicted in the figure has not been investigated. VSMC, vascular smooth muscle cell; MMPs, matrix metalloproteinases. FIG. 1. Hypothesized contributions from Nox2-generated oxidative stress to the process of atherosclerosis. When NADPH donates electrons to molecular oxygen via Nox2, O2·− generation occurs. Oxidative stress occurs when O2·− production exceeds the antioxidant capacity of the immediate environment. Oxidative stress can contribute to atherosclerosis progression by various mechanisms (7). ↑, increase; ↓, decrease. Mice with endothelial cell–specific insulin resistance (ESMIRO and IR+/− mice) exhibit increased Nox2-mediated O2·− generation to an extent that evokes endothelial dysfunction. Treatment of ESMIRO and IR+/− mice with the Nox inhibitor gp91ds-tat (+gp91ds-tat) or endothelial cell–specific knockout of Nox2 in ESMIRO mice (ESMIRO / Nox2y/−) reduces O2·− production and restores endothelial function. *Endothelial function was assessed in the current study (3), but the influence of endothelial cell–specific Nox2 deletion on other potential contributors to atherosclerosis depicted in the figure has not been investigated. VSMC, vascular smooth muscle cell; MMPs, matrix metalloproteinases. More
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Electron microscopy for quantitative analysis of caveolae. <em>A</em>...
Published: 13 March 2014
Figure 5 Electron microscopy for quantitative analysis of caveolae. A: Scheme for analysis of the electron microscopy images. Endothelial cells (ECs) were identified as those regions adjacent to erythrocytes (RBC). VSMC, vascular smooth muscle cell (left). A photo editor was used to establish a threshold gate to assist in identifying caveolae in multiple regions of interest (ROIs) (middle). Caveolae (black arrowheads) within endothelial cells were defined as apical or basal invaginations open to the surface, and membranes for analysis had to contain at least one caveolae (right). B: Representative electron micrograph illustration of the coronary endothelium in non-DM (top, white arrowheads point at caveolea) and DM patients (bottom, black arrowheads point at caveolea). Scale bar, 0.5 µm. C: Summary data show comparison of the number of endothelial membrane caveolae per µm2 in non-DM (○, data are from 53 membrane regions from three patients) and DM patients (●, data are from 46 membrane regions from three patients). Electron micrograph illustration (D) and summary data (E) demonstrate the effects of increasing concentrations (1–100 μmol/L) of exogenous ONOO on the number of coronary endothelial caveolae. Scale bar, 0.5 µm. Black arrows point at caveolae. Data are means ± SEM. *, non-DM vs. DM patients; #, significant effect of ONOO treatment. P < 0.05. Figure 5. Electron microscopy for quantitative analysis of caveolae. A: Scheme for analysis of the electron microscopy images. Endothelial cells (ECs) were identified as those regions adjacent to erythrocytes (RBC). VSMC, vascular smooth muscle cell (left). A photo editor was used to establish a threshold gate to assist in identifying caveolae in multiple regions of interest (ROIs) (middle). Caveolae (black arrowheads) within endothelial cells were defined as apical or basal invaginations open to the surface, and membranes for analysis had to contain at least one caveolae (right). B: Representative electron micrograph illustration of the coronary endothelium in non-DM (top, white arrowheads point at caveolea) and DM patients (bottom, black arrowheads point at caveolea). Scale bar, 0.5 µm. C: Summary data show comparison of the number of endothelial membrane caveolae per µm2 in non-DM (○, data are from 53 membrane regions from three patients) and DM patients (●, data are from 46 membrane regions from three patients). Electron micrograph illustration (D) and summary data (E) demonstrate the effects of increasing concentrations (1–100 μmol/L) of exogenous ONOO− on the number of coronary endothelial caveolae. Scale bar, 0.5 µm. Black arrows point at caveolae. Data are means ± SEM. *, non-DM vs. DM patients; #, significant effect of ONOO− treatment. P < 0.05. More
Journal Articles
Journal: Diabetes
Diabetes 1997;46(1):138–142
Published: 01 January 1997
... growth. A novel member of endothelium-specific growth factors, hepatocyte growth factor (HGF), is produced in vascular cells. To investigate the effects of high glucose on vascular cells, we examined 1) the effects of high glucose on endothelial cell and vascular smooth muscle cell (VSMC) growth...
Journal Articles
Journal: Diabetes
Diabetes 1997;46(4):659–664
Published: 01 April 1997
... blood pressure in humans and rodents. Because troglitazone has insulinlike effects on a number of tissues, we hypothesized that it may reduce vascular tone through stimulation of endothelial-derived nitric oxide (NO) production or by diminution of vascular smooth muscle cell (VSMC) intracellular calcium...
Journal Articles
Journal: Diabetes
Diabetes 2003;52(10):2562–2569
Published: 01 October 2003
...Cecilia C. Low Wang; Inga Gurevich; Boris Draznin Insulin maintains vascular smooth muscle cell (VSMC) quiescence yet can also promote VSMC migration. The mechanisms by which insulin exerts these contrasting effects were examined using α-smooth muscle actin (α-SMA) as a marker of VSMC phenotype...
Journal Articles
Journal: Diabetes
Diabetes 1996;45(Supplement_3):S47–S51
Published: 01 July 1996
... regulating [Ca2+]j metabolism is plasma membrane Na+-K+-ATPase. Decreased Na+-K+- Investigations conducted over the past several years ATPase activity may lead to an accumulation of Na+, and have demonstrated that vascular smooth muscle cells because of the subsequent changes in Na+-Ca2+ exchange, (VSMCs...
Meeting Abstracts
Journal: Diabetes
Diabetes 1998;47(6):931–936
Published: 01 June 1998
...T Kuroki; T Inoguchi; F Umeda; F Ueda; H Nawata Gap junction is thought to have a crucial role in maintaining tissue homeostasis. We examined the effect of a high glucose level on gap junctional intercellular communication (GJIC) activity in cultured vascular smooth muscle cells (VSMCs) using...
Journal Articles
Journal: Diabetes
Diabetes 2005;54(3):811–817
Published: 01 March 2005
...Santiago Redondo; Emilio Ruiz; Carlos G. Santos-Gallego; Eugenia Padilla; Teresa Tejerina Thiazolidinediones, such as pioglitazone, seem to exert direct antiatherosclerotic and antirestenotic effects on type 2 diabetes, in part due to an induction of vascular smooth muscle cell (VSMC) apoptosis. We...
Journal Articles
Journal: Diabetes
Diabetes 2005;54(2):540–545
Published: 01 February 2005
... treatment on serum withdrawal–induced apoptosis, expression of Bcl-2 family members, and inhibitor of apoptosis protein (IAP)-1 in vascular smooth muscle cells (VSMCs). Treatment with a high concentration of glucose (22 mmol/l) significantly attenuated apoptosis in response to serum withdrawal in cultured...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(5):1243–1251
Published: 01 May 2006
... of the balance between cell proliferation and cell death. Our aim was to study whether arteries and vascular smooth muscle cells (VSMCs) isolated from diabetic patients exhibit resistance to apoptosis induced by several stimuli. Internal mammary arteries (IMAs) were obtained from patients who had undergone...
Journal Articles
Journal: Diabetes
Diabetes 2007;56(5):1445–1453
Published: 01 May 2007
...Bei You; Aixia Ren; Guijun Yan; Jianxin Sun Vascular smooth muscle cell (VSMC) apoptosis plays an essential role in vascular development and atherosclerosis. Hyperglycemia inhibits VSMC apoptosis, which may contribute to the development of diabetic vasculopathy. In the present study, we analyzed...
Meeting Abstracts
Journal: Diabetes
Diabetes 1998;47(5):801–809
Published: 01 May 1998
... peroxidation, implying significant differences in The aim of this study was to compare the extent of glu- intracellular responses to glucose between contractile cose-induced oxidative stress in both vascular smooth cells in the macro- and microvasculature. Diabetes muscle cells (VSMCs) and pericytes...
Journal Articles
Journal: Diabetes
Diabetes 2002;51(4):1194–1200
Published: 01 April 2002
.... Of the many animal models used in the study of non-insulin-dependent (type 2) diabetes, the JCR:LA-cp rat is unique in that it develops insulin resistance in the presence of obesity and manifests both peripheral and coronary vasculopathies. In this animal model, arterial vascular smooth muscle cells (VSMCs...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(9):2611–2619
Published: 01 September 2006
... experimental animal models of diabetes. We examined our hypothesis that macrophages and short-term cultured vascular smooth muscle cells (VSMCs) derived from obese, insulin-resistant, and diabetic db/db mice would exhibit increased proatherogenic responses relative to those from control db...
Journal Articles
Journal: Diabetes
Diabetes 2003;52(9):2381–2388
Published: 01 September 2003
... kinase 2 (JAK2) is essential for the Ang II–induced proliferation of vascular smooth muscle cells (VSMCs) and that high glucose augments Ang II–induced proliferation of VSMCs by increasing signal transduction through activation of JAK2. Here, we demonstrate that S100B, a ligand for the receptor...
Journal Articles
Journal: Diabetes
Diabetes 2001;50(5):1171–1179
Published: 01 May 2001
.... To define the role of GLUT1 in vascular biology, we established cultured vascular smooth muscle cells (VSMCs) with constitutive upregulation of GLUT1, which led to a threefold increase in glucose uptake as well as significant increases in both nonoxidative and oxidative glucose metabolism as assessed...
Journal Articles
Journal: Diabetes
Diabetes 2003;52(2):519–526
Published: 01 February 2003
...Malcolm Campbell; William E. Allen; Jonathan A. Silversides; Elisabeth R. Trimble The aim of this study was to investigate the effects of elevated d-glucose concentrations on vascular smooth muscle cell (VSMC) expression of the platelet-derived growth factor (PDGF)β receptor and VSMC...
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(12):2178–2189
Published: 01 December 2000
...O A Sandu; L Ragolia; N Begum Our laboratory has demonstrated that insulin rapidly stimulates myosin-bound phosphatase (MBP) activity in vascular smooth muscle cells (VSMCs). In this study, we examined whether diabetes is accompanied by alterations in MBP activation and elucidated the components...