Heparan sulfate potentiates leukocyte adhesion on cardiac fibroblast by enhancing Vcam-1 and Icam-1 expression

Olivares-Silva, Francisco; Landaeta, Rodolfo; Aránguiz, Pablo; Bolívar, Samir; Humeres, Claudio; Anfossi, Renatto; Vivar, Raúl; Boza, Pía; Muñoz, Claudia; Pardo-Jiménez, V.; Peiró, Concepción; Sánchez‐Ferrer, Carlos F.; Díaz‐Araya, Guillermo

doi:10.1016/j.bbadis.2017.12.002

Cited by 31 publications

(16 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…VCAM-1 is a cell surface sialoglycoprotein originally identified to be expressed in activated endothelial cells and mediating adhesion of leukocytes during the inflammation process [39]. VCAM-1 is expressed in a variety of human tissues and organs, including dendritic cells, macrophages, cardiac fibroblasts, synoviocytes, as well as in several types of malignant cells and its expression has been associated with pathophysiological conditions such as autoimmune disorders, cardiovascular disease, and infections [39][40][41]. Because VEGF-A signaling mediates VCAM-1 expression [42,43], we investigated VCAM-1 levels in periodontal tissues during EP in animals treated with antiresorptives.…”

Section: Discussionmentioning

confidence: 99%

Vasculature submucosal changes at early stages of osteonecrosis of the jaw (ONJ)

Gkouveris

Hadaya

Soundia

et al. 2019

Bone

View full text Add to dashboard Cite

Osteonecrosis of the Jaw (ONJ), a rare, but potentially severe side effect of anti-resorptive medications, presents as exposed bone in the maxillofacial region lasting for at least 8 weeks. While clinical experience and animal models concur in finding that systemic antiresorptive treatment in conjunction with local risk factors, such as tooth extraction or dental disease may lead to ONJ development, the subclinical molecular changes that precede bone exposure remain poorly understood. The identification of these changes is not only important in understanding disease pathophysiology, but could provide potential for treatment development. Here, we evaluated the early stages of ONJ utilizing a model of experimental periodontitis (EP) in mice treated with two different types of antiresorptives, targeting potential changes in vasculature, hypoxia, oxidative stress, and apoptosis. Antiresorptive treatment in animals with EP increased levels of empty osteocytic lacunae and increased ONJ prevalence compared to Veh animals. The arteriole and venule network seen around EP areas was diminished in animals treated with antiresorptives. Higher levels of vascular endothelial growth factor A (VEGF-A) and vascular cell adhesion protein-1 (VCAM-1) were observed 1-week following EP in treated animals. Finally, levels of hypoxia, oxidative stress, and apoptosis remained high in antiresorptive treated animals with EP through the duration of the experiment. Together, our data point to subclinical vasculature organizational disturbances that subsequently affect levels of hypoxia, oxidative stress, and apoptosis in the area of developing ONJ.

show abstract

Section: Discussionmentioning

confidence: 99%

Vasculature submucosal changes at early stages of osteonecrosis of the jaw (ONJ)

Gkouveris

Hadaya

Soundia

et al. 2019

Bone

View full text Add to dashboard Cite

show abstract

“…It is identified via the expression of adhesion/inflammatory molecules, such as VCAM-1 and ICAM-1. An increase in VCAM-1 and ICAM-1 surface protein expression leads to an increase in vascular inflammation and the initiation of atherosclerotic plaque formation [37,38]. Thus, we examined the effect of Ref-1 overexpression on the expression of VCAM-1 and ICAM-1 in thrombotic carotid arteries.…”

Section: Ref-1 Inhibits Inflammatory Molecule Expression In the Carotmentioning

confidence: 99%

Ref-1 protects against FeCl₃-induced thrombosis and tissue factor expression via the GSK3β–NF-κB pathway

Lee

Nagar

Kim

et al. 2021

Korean J Physiol Pharmacol

View full text Add to dashboard Cite

“…Under the stimulation of TLR4 ligands such as LPS and DAMPs, cardiac fibroblasts can promote the transformation of monocyte phenotype into pro-inflammatory M1 macrophages, while under the stimulation of transforming growth factor-β1 (TGF-β1), cardiac fibroblasts can direct monocytes toward antiinflammatory/pro-fibrotic M2 macrophages (126). Interestingly, monocytes can adhere to cardiac fibroblasts and trigger secretion of TNF-α and TGF-β to transform fibroblasts to myofibroblasts, which also is relevant to the activation of TLR4 (127).…”

Section: Cardiac Fibroblasts and Cardiac Myofibroblastsmentioning

confidence: 99%

Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4

Zheng

Kong

Yang

et al. 2020

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Toll-like receptor 4 (TLR4), a key pattern recognition receptor, initiates the innate immune response and leads to chronic and acute inflammation. In the past decades, accumulating evidence has implicated TLR4-mediated inflammatory response in regulation of myocardium hypertrophic remodeling, indicating that regulation of the TLR4 signaling pathway may be an effective strategy for managing cardiac hypertrophy's pathophysiology. Given TLR4's significance, it is imperative to review the molecular mechanisms and roles underlying TLR4 signaling in cardiac hypertrophy. Here, we comprehensively review the current knowledge of TLR4-mediated inflammatory response and its interaction ligands and co-receptors, as well as activation of various intracellular signaling. We also describe the associated roles in promoting immune cell infiltration and inflammatory mediator secretion, that ultimately cause cardiac hypertrophy. Finally, we provide examples of some of the most promising drugs and new technologies that have the potential to attenuate TLR4-mediated inflammatory response and prevent or reverse the ominous cardiac hypertrophy outcomes.

show abstract

Heparan sulfate potentiates leukocyte adhesion on cardiac fibroblast by enhancing Vcam-1 and Icam-1 expression

Cited by 31 publications

References 50 publications

Vasculature submucosal changes at early stages of osteonecrosis of the jaw (ONJ)

Vasculature submucosal changes at early stages of osteonecrosis of the jaw (ONJ)

Ref-1 protects against FeCl₃-induced thrombosis and tissue factor expression via the GSK3β–NF-κB pathway

Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4

Contact Info

Product

Resources

About

Heparan sulfate potentiates leukocyte adhesion on cardiac fibroblast by enhancing Vcam-1 and Icam-1 expression

Cited by 31 publications

References 50 publications

Vasculature submucosal changes at early stages of osteonecrosis of the jaw (ONJ)

Vasculature submucosal changes at early stages of osteonecrosis of the jaw (ONJ)

Ref-1 protects against FeCl3-induced thrombosis and tissue factor expression via the GSK3β–NF-κB pathway

Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4

Contact Info

Product

Resources

About

Ref-1 protects against FeCl₃-induced thrombosis and tissue factor expression via the GSK3β–NF-κB pathway