scholarly journals Placenta-derived IL-32β activates neutrophils to promote preeclampsia development

2021 ◽  
Vol 18 (4) ◽  
pp. 979-991
Author(s):  
Dan Liu ◽  
Qiang Li ◽  
Hailin Ding ◽  
Guangfeng Zhao ◽  
Zhiyin Wang ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Pregnant Mouse ◽  
Oxidase Inhibitor ◽  
Vascular Cell Adhesion ◽  
Nadph Oxidase Inhibitor ◽  
Cell Adhesion Molecule 1 ◽  
Intercellular Cell Adhesion Molecule

AbstractImmune activation at the maternal-fetal interface is a main pathogenic factor of preeclampsia (PE). Neutrophils (PMNs) are activated in PE patients, but the mechanism and consequences of PMN activation need to be further explored. Here, we demonstrated that interleukin-32 (IL-32) expression was significantly upregulated in syncytiotrophoblasts (STBs) and that IL-32β was the major isoform with increased expression in the placenta of severe PE (sPE) patients. Furthermore, the level of IL-32 expression in the placenta was correlated with its level in the serum of sPE patients, indicating that IL-32 in the serum is derived mainly from the placenta. Then, in vitro experiments showed that IL-32β could highly activate PMNs and that these IL-32β-activated PMNs were better able to adhere to endothelial cells (HUVECs) and enhance the expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) in HUVECs, which could be reversed by preincubation with the NADPH oxidase inhibitor VAS 2870. In addition, we showed that IL-32β mainly activated PMNs by binding to proteinase 3. Finally, IL-32β administration induced a PE-like phenotype in a pregnant mouse model. This study provides evidence of the involvement of IL-32β in the pathogenesis of PE.

Radix Paeoniae Rubra Ameliorates Lupus Nephritis in Lupus-Like Symptoms of Mrl Mice by Reducing Intercellular Cell Adhesion Molecule-1, Vascular Cell Adhesion Molecule-1, and Platelet Endothelial Cell Adhesion Molecule-1 Expression

2020 ◽  
Vol 23 (7) ◽  
pp. 675-683
Author(s):  
Weijie Wang ◽  
Lingyong Cao ◽  
Xinchang Wang ◽  
Yongsheng Fan
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Treated Group ◽  
Control Group ◽  
Model Group ◽  
Vascular Cell Adhesion ◽  
Platelet Endothelial Cell Adhesion ◽  
Cell Adhesion Molecule 1 ◽  
Intercellular Cell Adhesion Molecule

Objective: Vasculitis is the basic pathological change of systemic lupus erythematosus (SLE). Radix Paeoniae Rubra (RPR), a traditional Chinese herb with the function of reducing blood stasis, has anti-inflammatory and immunoregulatory properties. This study explored the effects of RPR on the kidneys of lupus-like symptoms of mrl (MRL/lpr) mice from the perspective of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1). Methods: Eighteen MRL/lpr lupus model mice were randomly divided into three groups, the model control group, prednisone-treated group, and RPR-treated group, and 6 C57BL/ 6 mice were classified as a control group. After the mice had been treated for 12 weeks, the expression of ICAM-1, VCAM-1 and PECAM-1in the kidney was determined by immunohistochemistry and Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Results: After 12 weeks, there were significant differences in body weight in the model, prednisone and RPR groups compared with the normal group (P <0.05). Pathological observation: Compared with the model group, the proliferation of inflammatory cells infiltrated glomeruli and interstitial cells in prednisone and RPR groups were reduced, and renal pathological damage was reduced. Compared with the model group, urine protein level of prednisone and RPR groups were reduced with no significance (P> 0.05). The mRNA expression levels of ICAM-1 and VCAM-1 were significantly reduced in the prednisone group and RPR group compared with the model group (P <0.05 or P <0.01). Meanwhile, the immunohistochemistry expressions of ICAM-1 and VCAM- 1 expressed in the kidney were significantly reduced in the prednisone group and RPR group (P <0.01 or P <0.05). However, The mRNA expression level and the immunohistochemistry expressions of PECAM-1 expressed in the kidney were reduced in each treatment group (prednisone group and RPR group), but these differences were not significant (P>0.05). Conclusions: ICAM-1, VCAM-1 and PECAM-1 expression in the model group was found to be significantly increased. In addition, RPR could reduce the expression of ICAM-1, VCAM-1 and PECAM-1 in MRL/lpr lupus mice as effectively as prednisone, which may result in the dosage reduction of prednisone, thus decreasing the toxicity and improving the efficacy of prednisone - based treatment of SLE.

Statins reduce oxidized low-density lipoprotein levels, but do not alter soluble intercellular cell-adhesion molecule-1 and vascular cell-adhesion molecule-1 levels in subjects with hypercholesterolaemia

2004 ◽  
Vol 106 (2) ◽  
pp. 215-217 ◽  
Author(s):  
Robert S. ROSENSON ◽  
David WOLFF ◽  
Christine C. TANGNEY
Keyword(s):  
Cell Adhesion ◽  
Statin Therapy ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Vascular Cell Adhesion ◽  
Lag Times ◽  
Cell Adhesion Molecule 1 ◽  
Intercellular Cell Adhesion Molecule

ICAM-1 (intercellular cell-adhesion molecule-1) and VCAM-1 (vascular cell-adhesion molecule-1) are cell-adhesion molecules that have an essential role in monocyte recruitment. In the present study we have investigated (i) whether statins reduce soluble levels of ICAM-1 (sICAM-1) and VCAM-1 (sVCAM-1), and the relationship between resistance of LDL (low-density lipoprotein) to in vitro oxidation and sICAM-1 and sVCAM-1 levels. Whole blood samples were obtained from 55 healthy non-smoking adults (aged 35–65 years) with moderate (LDL-cholesterol, 3.4–4.9 mmol/l) hypercholesterolaemia participating in a randomized double-blinded, 8-week trial comparing pravastatin (40 mg), simvastatin (20 and 80 mg) and placebo. sICAM-1 levels (means±S.D.) increased slightly from 12.2±4.2 to 13.6±4.2 ng/ml with statin therapy, whereas, among placebo-assigned subjects, levels were unchanged (11.8±5.0 and 11.8±3.9 ng/ml). sVCAM-1 increased from 18.9±10.1 to 21.1±7.4 ng/ml among those on active therapy and slightly declined with placebo assignment (19.8±8.8 to 19.4±6.4 ng/ml). Lag times increased with statin therapy from 74.3±39.8 min to 98.3±57.8 min (P=0.003), and were unchanged in the placebo group (from 103.1±61.1 to 90.8±65.9 min; P=0.48). There were no significant changes between statin and placebo therapy for sICAM-1, sVCAM-1 or lag times (P=0.09, 0.16 and 0.067 respectively). Changes in sICAM-1 and sVCAM-1 were not correlated with the change in lag times. In contrast with the known effects of oxidized LDL on gene activation of ICAM-1 and VCAM-1, lag times did not correlate with sICAM-1 and sVCAM-1. Statin therapy improved lag times, but has no effect on sICAM-1 or sVCAM-1 levels.

scholarly journals Activated endothelium binds lymphocytes through a novel binding site in the alternately spliced domain of vascular cell adhesion molecule-1.

1992 ◽  
Vol 176 (1) ◽  
pp. 99-107 ◽  
Author(s):  
L Osborn ◽  
C Vassallo ◽  
C D Benjamin
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Binding Sites ◽  
Cell Adhesion Molecule ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Vascular Cell Adhesion Molecule ◽  
Cell Adhesion Molecule 1

Vascular cell adhesion molecule-1 (VCAM-1) is induced on endothelial cells by inflammatory cytokines, and binds mononuclear leukocytes through the integrin very late antigen-4 (VLA-4) (alpha 4 beta 1). This adhesion pathway has been implicated in a diverse group of physiological and pathological processes, including B cell development, leukocyte activation and recruitment to sites of inflammation, atherosclerosis, and tumor cell metastasis. The major form of VCAM-1 (VCAM-7D) has seven extracellular immunoglobulin (Ig)-like domains, of which the three NH2-terminal domains (domains 1-3) are similar in amino acid sequence to domains 4-6. By functional analysis of VCAM-7D relative to VCAM-6D (a minor 6-domain form of VCAM-1 in which domain 4 is deleted because of alternative splicing), and chimeric constructs between VCAM-1 and its structural relative intercellular adhesion molecule-1 (ICAM-1), we show that either the first or the homologous fourth domain of VCAM-1 is required for VLA-4-dependent adhesion. Either of these binding sites can function in the absence of the other. When both are present, cell binding activity is increased relative to monovalent forms of the molecule. The homologous binding regions appear to have originated by internal duplication of a portion of a monovalent ancestral gene, before the mammalian radiation. Thus VCAM-1 exemplifies evolution of a functionally bivalent cell-cell adhesion molecule by intergenic duplication. We have also produced a new class of anti-VCAM-1 monoclonal antibodies that block domain 4-dependent adhesion, and demonstrate that both binding sites participate in the adhesion function of VCAM-1 on endothelial cells in vitro. Therefore both sites must be blocked in clinical, animal, or in vitro studies depending on the use of anti-VCAM-1 antibodies to inactivate the VCAM-1/VLA-4 adhesion pathway.

scholarly journals MiR-138 ameliorates myocardial ischemia/reperfusion injury by targeting intercellular cell adhesion molecule 1

2020 ◽  
Vol 19 (3) ◽  
pp. 489-495 ◽  
Author(s):  
Zhanling Liao ◽  
Xiaoli Cheng ◽  
Chunyan Xiang ◽  
Feng Liu
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
H9c2 Cells ◽  
Myocardial Ischemia Reperfusion ◽  
Cell Adhesion Molecule 1 ◽  
Intercellular Cell Adhesion Molecule

Purpose: To explore the effect of miR-138 on regulating intercellular cell adhesion molecule 1 (ICAM-1) expression in endothelial cells to alleviate cardiac ischemia/reperfusion (I/R) injury and its related mechanisms. Methods: The left anterior descending artery of the heart was occluded for 30 min and then perfused for 2 h to induce a rat model of cardiac I/R injury. H9C2 cells were cultured in an anoxic medium without serum to establish the model of hypoxia/reoxygenation (H/R). Triphenyl tetrazolium chloride (TTC) staining was applied to measure myocardial infarction sizes in rat hearts. The mRNA expression levels of miR-138 and ICAM-1 were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). Dual luciferase reporter assay was used to identify the target of miR-138. The agomiR-138 and miR-138 mimics were transfected into H9C2 cells; exogenous ICAM-1 was also administered, and ROS accumulation, cell viability, and apoptosis were measured. Furthermore, the underlying mechanism was investigated. Results: MiR-138 was downregulated both in vitro and in vivo. AgomiR-138 reduced myocardial infarction area, decreased ROS production and suppressed cell apoptosis in a rat model of cardiac I/R injury. On the other hand, miR-138 mimics increased cell viability, enhanced ROS production and induced cell apoptosis in H/R-induced H9C2 cells. Further analysis verified ICAM-1 as a target of miR- 138. Besides, exogenous ICAM-1 inhibited the protective effect of miR-138 on H/R-induced apoptosis in vitro. Conclusion: MiR-138 may protect against injury of myocardial I/R by targeting ICAM-1. The results also provide insight into miR-138/ICAM-1 axis as new therapeutic targets for myocardial I/R injury. Keywords: Intercellular cell adhesion molecule 1, MicroRNA-138, Myocardial/ischemia reperfusion injury, Reactive oxygen species

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