Disease-specific characteristics of vascular cell adhesion molecule-1 levels in patients with peripheral artery disease

Edlinger, Christoph; Lichtenauer, Michael; Wernly, Bernhard; Pistulli, Rudin; Paar, Vera; Prodinger, Christine; Krizanic, Florian; Thieme, Marcus; Kammler, Jürgen; Jung, Christian; Hoppe, Uta C.; Schulze, P. Christian; Kretzschmar, Daniel

doi:10.1007/s00380-018-1315-1

Cited by 21 publications

(19 citation statements)

References 35 publications

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“…Under steady-state conditions, the expression levels of VCAM-1 and ICAM-1 are usually low. It has been reported that down-regulated expression of VCAM-1 and ICAM-1 could protect against disruption of BBB [20,21,51]. Findings from the current study showed that ICAM-1 and VCAM-1 were transcriptionally upregulated in the brain of 1,2-DCE-intoxicated mice through the p38 MAPK/ NF-κB signaling pathway, and also being induced by IL-1β.…”

Section: Discussionsupporting

confidence: 49%

Neuroinflammatory Reactions in the Brain of 1,2-DCE-Intoxicated Mice during Brain Edema

Jin

Wang

Liao

et al. 2019

Cells

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We previously reported that expression of matrix metalloproteinase-9 (MMP-9) mRNA and protein was upregulated during 1,2-dichloroethane (1,2-DCE) induced brain edema in mice. We also found that the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway resulted in MMP-9 overexpression and nuclear factor-κB (NF-κB) activation in mice treated with 1,2-DCE. In this study, we further hypothesized that inflammatory reactions mediated by the p38 MAPK/ NF-κB signaling pathway might be involved in MMP-9 overexpression, blood–brain barrier (BBB) disruption and edema formation in the brain of 1,2-DCE-intoxicated mice. Our results revealed that subacute poisoning by 1,2-DCE upregulates protein levels of glial fibrillary acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba-1), interleukin-1β (IL-1β), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS) and p-p65 in mouse brains. Pretreatment with an inhibitor against p38 MAPK attenuates these changes. Moreover, pretreatment with an inhibitor against NF-κB attenuates alterations in brain water content, pathological indications notable in brain edema, as well as mRNA and protein expression on levels of MMP-9, VCAM-1, ICAM-1, iNOS, and IL-1β, tight junction proteins (TJs), GFAP and Iba-1 in the brain of 1,2-DCE-intoxicated mice. Furthermore, pretreatment with an inhibitor against MMP-9 obstructs the decrease of TJs in the brain of 1,2-DCE-intoxicated mice. Lastly, pretreatment with an antagonist against the IL-1β receptor also attenuates changes in protein levels of p-p38 MAPK, p-p65, p-IκB, VCAM -1, ICAM-1, IL-1β, and Iba-1 in the brain of 1,2-DCE-intoxicated-mice. Taken together, findings from the current study indicate that the p38 MAPK/ NF-κB signaling pathway might be involved in the activation of glial cells, and the overproduction of proinflammatory factors, which might induce inflammatory reactions in the brain of 1,2-DCE-intoxicated mice that leads to brain edema.

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Section: Discussionsupporting

confidence: 49%

Neuroinflammatory Reactions in the Brain of 1,2-DCE-Intoxicated Mice during Brain Edema

Jin

Wang

Liao

et al. 2019

Cells

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“…VCAM-1 belongs to the immunoglobulin superfamily and can be expressed in endothelial cells, smooth muscle cells, and macrophages 38 . Some previous studies have observed an early increase in VCAM-1 levels within 6 h of injury, thus implying that VCAM-1 plays a role in early vascular inflammation and that the early application of a VCAM-1 antibody could inhibit the development of intimal hyperplasia 39 . Our results demonstrated that BSP inhibited early intimal hyperplasia and inflammation by inhibiting the production of VCAM-1.…”

Section: Discussionmentioning

confidence: 90%

Bletilla striata Polysaccharide Prevents Restenosis of Vein Graft Through Inhibiting Cell Proliferation in Rat Model

et al. 2020

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Coronary artery bypass grafting (CABG) is still the most effective method for the treatment of coronary heart disease at present. However, the restenosis of vein grafts following surgery is an important complication of CABG. In this study, Bletilla striata polysaccharide (BSP), which has anti-inflammatory and antiproliferative properties, was used to prevent or delay the proliferation of venous bridge endothelial cells in a rat model. We transplanted the autogenous jugular vein to the rat carotid artery, and wrapped it with BSP. We carried out experiments in 4 groups (with 24 rats in each group): a high-BSP dose group (the HBG group, 10 mg), a low-BSP dose group (the LBG group, 3 mg), a pluronic gel group (the gel group), and a control group. Vein grafts were then harvested after 3, 14, and 28 days. Following transplantation, we used color Doppler ultrasound to assess the patency of the transplanted vein. The grafted veins were stained with hematoxylin and eosin (H&E) and Masson to measure the thickness of the intima and media of the blood vessels. Proliferating cell nuclear antigen (PCNA) and vascular cell adhesion molecule-l (VCAM-1) were assessed in vein grafts by immunohistochemistry and western blotting. We detected a significant reduction in the proliferation of endothelial cells in the BSP group compared with the control group ( P < 0.05). H&E and Masson’s trichrome staining showed that the extent of intimal hyperplasia in transplanted veins from the high BSP group (HBS) (67.42 ± 0.54 µm) and low BSP group (LBS) (120.83 ± 1.87 µm) groups was significantly lower than that in the control group (257.03 ± 2.74 µm, P < 0.05), and that the extent of intimal hyperplasia in the HBS group was lower than that in the LBS group ( P < 0.05). We found that the effect of BSP was dose-dependent, as high-dose BSP had a more significant inhibitory effect on cell proliferation than low-dose BSP ( P < 0.05). The results of immunohistochemistry and western blotting showed that PCNA and VCAM-1 were significantly downregulated in the BSP treatment group on days 14 and 28 ( P < 0.05). BSP inhibits the proliferation of vascular endothelial cells and reduces the expression of VCAM-1, thereby inhibiting the restenosis of graft veins.

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“…Not only high plasm glucose, lipid and high blood pressure, but also aging itself can cause arterial stiffness. 14 15,16 However, we found the serum VCAM levels of hypertensive patients were lower than normotensive participants. In previous published study, serum VCAM levels were not found to be elevated in pulmonary hypertension or gestational hypertension, and low VCAM level might lead to fetal growth restriction.…”

Section: Bio-markers For Predicting Arterial Stiffness In Regressionmentioning

confidence: 54%

Differential use of pulse wave velocity and ankle-brachial index in elderly Chinese and novel serum bio-markers for predicting arterial stiffness: a cross-sectional study

Fu¹,

Yuan²,

Pan³

et al. 2019

Preprint

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Background Arterial stiffness is characterized by the loss of vessel elasticity and arterial compliance. Brachial-ankle pulse wave velocity (PWV) and ankle-brachial Index (ABI) are widely used in clinic for evaluating arterial stiffness. This study aimed to compare the efficiency of PWV and ABI in elderly Chinese and investigate novel bio-markers for aging related arterial stiffness. Methods PWV and ABI were evaluated in 169 elderly Chinese with mean age of 85.7 years. 86 of the participants had serum concentrations of angiotensin Ⅱ, vascular cell adhesion molecule (VCAM), osteopontin and glutathione peroxidase tested in further. Results Compared with normotensive participants, PWV levels elevated in both limbs of hypertensive patients ( 2219 ± 90 cm/s v.s. 1970 ± 66 cm/s, P = 0.090 and 2141 ± 52 cm/s v.s. 1932 ± 67 cm/s, P = 0.023, separately) . Compared with non- diabetes mellitus participants, ABI levels declined in both limbs of diabetes mellitus (DM) patients( 0.96 ± 0.02 v.s. 1.05 ± 0.02, P = 0.002 and 0.99 ± 0.03 v.s. 1.03 ± 0.02, P = 0.071, separately). VCAM was included in both regression models for predicting PWV in left limbs and PWV in right limbs ( Beta= - 0.307, P= 0.048; Beta= - 0.358, P= 0.020, separately). Osteopontin was included in both regression models for predicting ABI in left limbs and ABI in right limbs ( Beta= - 0.320, P= 0.039; Beta= - 0.290, P= 0.011, separately). Conclusions: Differential use of PWV and ABI should be considered in elderly with hypertension and/or DM. Serum levels of VCAM and osteopontin might be independent bio-markers for predicting arterial stiffness. KEYWORDS Arterial stiffness in elderly; Pulse wave velocity; Ankle-brachial Index; Vascular cell adhesion molecule; Osteopontin

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Disease-specific characteristics of vascular cell adhesion molecule-1 levels in patients with peripheral artery disease

Cited by 21 publications

References 35 publications

Neuroinflammatory Reactions in the Brain of 1,2-DCE-Intoxicated Mice during Brain Edema

Neuroinflammatory Reactions in the Brain of 1,2-DCE-Intoxicated Mice during Brain Edema

Bletilla striata Polysaccharide Prevents Restenosis of Vein Graft Through Inhibiting Cell Proliferation in Rat Model

Differential use of pulse wave velocity and ankle-brachial index in elderly Chinese and novel serum bio-markers for predicting arterial stiffness: a cross-sectional study

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