Gene regulation of intracellular adhesion molecule-1 (ICAM-1): A molecule with multiple functions

Singh, Mona; Thakur, Mony; Mishra, Manish; Yadav, Manisha; Vibhuti, Rajkamal; Menon, Athira M.; Nagda, Girima; Dwivedi, Ved Prakash; Dakal, Tikam Chand; Yadav, Vinod Kumar

doi:10.1016/j.imlet.2021.10.007

Cited by 47 publications

(35 citation statements)

References 251 publications

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“…We had previously studied the expression of ICAM-1 with respect to platelet EVs using the same cohort [ 31 ], as ICAM-1 has been reported to play a crucial role in the pathophysiology of cardiovascular diseases by activating inflammatory responses at the endothelial level [ 43 – 45 ]. Hence, we then decided to study the influence of miR-224-5-p on endothelial surface expression of ICAM-1.Although we observed no difference between cells treated with inhibitor and mimic EVs for miR-224-5-p, there was, on the other hand, a significant increase in ICAM-1 after treating the cells with hepatic EVs regardless of whether they contained miR-224-5p or not.…”

Section: Discussionmentioning

confidence: 99%

Increased expression of miR-224-5p in circulating extracellular vesicles of patients with reduced coronary flow reserve

Bryl-Górecka

Olde

Gidlöf

et al. 2022

BMC Cardiovasc Disord

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Background Endothelial and microvascular dysfunction are pivotal causes of major adverse cardiac events predicted by coronary flow reserve (CFR). Extracellular Vesicles (EVs) have been studied extensively in the pathophysiology of coronary artery disease. However, little is known on the impact of the non-coding RNA content of EVs with respect to CFR. Methods We carried out a study among 120 patients divided by high-CFR and low-CFR to profile the miRNA content of circulating EVs. Results A multiplex array profiling on circulating EVs revealed mir-224-5p (p-value ≤ 0.000001) as the most differentially expressed miRNA in the Low-CFR group and showed a significantly independent relationship to CFR. Literature survey indicated the origin of the miR from liver cells and not of platelet, leukocyte, smooth muscle or endothelial (EC) origin. A q-PCR panel of the conventional cell type-EVs along with hepatic EVs showed that EVs from liver cells showed higher expression of the miR-224-5p. FACS analysis demonstrated the presence of liver-specific (ASGPR-1+/CD14−) EVs in the plasma of our cohort with the presence of Vanin-1 required to enter the EC barrier. Hepatic EVs with and without the miR-224-5p were introduced to ECs in-vitro, but with no difference in effect on ICAM-1 or eNOS expression. However, hepatic EVs elevated endothelial ICAM-1 levels per se independent of the miR-224-5p. Conclusion This indicated a role of hepatic EVs identified by the miR-224-5p in endothelial dysfunction in patients with Low CFR.

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Section: Discussionmentioning

confidence: 99%

Increased expression of miR-224-5p in circulating extracellular vesicles of patients with reduced coronary flow reserve

Bryl-Górecka

Olde

Gidlöf

et al. 2022

BMC Cardiovasc Disord

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“…In contrast, DCs challenged with type I parasites, which lack a functional GRA15 ( 23 ), failed to upregulate ICAM-1 and, contrary to type II infected DCs, increased motility on endothelium, suggesting reduced adhesion and therefore a reduced capability to transmigrate. Indeed, because GRA15 acts on the transcription factor NFκB ( 23 ) and ICAM-1 transcription requires the binding of NFκB ( 8 , 46 ), it is reasonable to assume that this mechanism is in play. Thus, the concerted action of GRA15 and TgWIP seem to mediate the major part of the TEM phenotype for the type II strains tested (ME49, PRU).…”

Section: Discussionmentioning

confidence: 99%

“…In the leukocyte´s approach to the site of TEM, crucial interactions between intercellular cell adhesion molecule-1 (ICAM-1) on the endothelium and leukocyte integrins, such as LFA-1 (α L β 2 ; CD11a/CD18), precede translocation ( 5 , 6 ). However, while most leukocyte subsets express ICAM-1, the putative role of leukocyte ICAM-1 in diapedesis has remained unresolved ( 7 , 8 ). Intracellular microbes hijack host cell functions and, therefore, the study of host-pathogen interactions can provide unique cues on the biology of leukocyte migration.…”

Section: Introductionmentioning

confidence: 99%

Toxoplasma effector-induced ICAM-1 expression by infected dendritic cells potentiates transmigration across polarised endothelium

2022

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The obligate intracellular parasite Toxoplasma gondii makes use of infected leukocytes for systemic dissemination. Yet, how infection impacts the processes of leukocyte diapedesis has remained unresolved. Here, we addressed the effects of T. gondii infection on the trans-endothelial migration (TEM) of dendritic cells (DCs) across polarised brain endothelial monolayers. We report that upregulated expression of leukocyte ICAM-1 is a feature of the enhanced TEM of parasitised DCs. The secreted parasite effector GRA15 induced an elevated expression of ICAM-1 in infected DCs that was associated with enhanced cell adhesion and TEM. Consequently, gene silencing of Icam-1 in primary DCs or deletion of parasite GRA15 reduced TEM. Further, the parasite effector TgWIP, which impacts the regulation of host actin dynamics, facilitated TEM across polarised endothelium. The data highlight that the concerted action of the secreted effectors GRA15 and TgWIP modulate the leukocyte-endothelial interactions of TEM in a parasite genotype-related fashion to promote dissemination. In addition to the canonical roles of endothelial ICAM-1, this study identifies a previously unappreciated role for leukocyte ICAM-1 in infection-related TEM.

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“…Among the corresponding changes, ICAM1 was upregulated. ICAM1, which is a single-chain cell surface glycoprotein, is a molecule that has significant roles in the inflammatory response and in the recruitment of leukocytes to sites of inflammation ( 30 , 31 ). ICAM1 promotes adhesion at inflammatory sites and regulates the immune response, which is very beneficial in acute SCI.…”

Section: Discussionmentioning

confidence: 99%

Quantitative iTRAQ proteomics reveal the proteome profiles of bone marrow mesenchymal stem cells after cocultures with Schwann cells in vitro

Ding¹,

Li²,

Sun³

et al. 2022

Ann Transl Med

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Background: Bone marrow mesenchymal stem cells (BMSCs) combined with Schwann cells (SCs) represent a better therapeutic cell transplantation strategy for treating spinal cord injury (SCI) than transplantation with BMSCs or SCs alone. In previous studies, we demonstrated that BMSCs are able to differentiate in neuron-like cells when cocultured with SCs. The detailed mechanism underlying SCI repair that occurs during the combined transplantation of BMSCs and SCs has not yet been studied. In this study, we adopted an isobaric tag for relative and absolute quantitation (iTRAQ)-based protein identification/ quantification approach to examine the effects of the SC and BMSC coculture process on the BMSCs and then obtained and analyzed the differentially expressed proteins (DEPs) and their possible related pathways.Methods: This study included three groups based on the number of coculture days (i.e., 0, 3, and 7 days).Changes in BMSC protein expression levels were measured using the iTRAQ technique. A bioinformatics analysis of all the data was performed.Results: In total, 6,760 types of proteins were detected, corresponding to 5,181 data points with quantitative information. Of these, a total of 243 DEPs were identified, of which 169 proteins were upregulated and 74 proteins were downregulated. These DEPs were identified by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Intercellular adhesion molecule-1 (ICAM-1), integrin, and dioxygenase may play crucial roles in the repair of SCI. The data analysis indicates that the relevant biological processes may be regulated by lysosome function, cell adhesion molecules (CAMs), leukocyte transendothelial migration, and the phosphatidylinositol-3-kinase (PI3K) and peroxisome proliferator-activated receptor (PPAR) signaling pathways. Conclusions:The data provided in this study indicate that several molecular mechanisms and signaling pathways are involved in the BMSC and SC coculture process. This information may be useful for the further identification of specific targets and related mechanisms and guide new directions for SCI treatment.

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Gene regulation of intracellular adhesion molecule-1 (ICAM-1): A molecule with multiple functions

Cited by 47 publications

References 251 publications

Increased expression of miR-224-5p in circulating extracellular vesicles of patients with reduced coronary flow reserve

Increased expression of miR-224-5p in circulating extracellular vesicles of patients with reduced coronary flow reserve

Toxoplasma effector-induced ICAM-1 expression by infected dendritic cells potentiates transmigration across polarised endothelium

Quantitative iTRAQ proteomics reveal the proteome profiles of bone marrow mesenchymal stem cells after cocultures with Schwann cells in vitro

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