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Two Methods of AuNPs Synthesis Induce Differential Vascular Effects. The Role of the Endothelial Glycocalyx.

ABSTRACT: AuNPs are synthesized through several methods to tune their physicochemical properties. Although AuNPs are considered biocompatible, a change in morphology or properties can modify their biological impact. In this work, AuNPs (~12 to 16 nm) capping with either sodium citrate (CA) or gallic acid (GA) were evaluated in a rat aorta ex vivo model, which endothelial inner layer surface is formed by glycocalyx (hyaluronic acid, HA, as the main component), promoting vascular processes, most of them dependent on nitric oxide (NO) production. Results showed that contractile effects were more evident with AuNPsCA, while dilator effects predominated with AuNPsGA. Furthermore, treatments with AuNPsCA and AuNPsGA in the presence or absence of glycocalyx changed the NO levels, differently. This work contributes to understanding the biological effects of AuNPs with different capping agents, as well as the key role that of HA in the vascular effects induced by AuNPs in potential biomedical applications.

SUBMITTER: Maldonado-Ortega DA

PROVIDER: S-EPMC9277019 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Two Methods of AuNPs Synthesis Induce Differential Vascular Effects. The Role of the Endothelial Glycocalyx.

Maldonado-Ortega Daniel Alberto DA Martínez-Castañón Gabriel G Palestino Gabriela G Navarro-Tovar Gabriela G Gonzalez Carmen C

Frontiers in medicine 20220629

AuNPs are synthesized through several methods to tune their physicochemical properties. Although AuNPs are considered biocompatible, a change in morphology or properties can modify their biological impact. In this work, AuNPs (~12 to 16 nm) capping with either sodium citrate (CA) or gallic acid (GA) were evaluated in a rat aorta <i>ex vivo</i> model, which endothelial inner layer surface is formed by glycocalyx (hyaluronic acid, HA, as the main component), promoting vascular processes, most of t ...[more]

PMID: 35847820

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Project description:PURPOSE:In 2007 the two senior authors wrote a review on the structure and function of the endothelial glycocalyx layer (Weinbaum in Annu Rev Biomed Eng 9:121-167, 2007). Since then there has been an explosion of interest in this hydrated gel-like structure that coats the luminal surface of endothelial cells that line our vasculature due to its important functions in (A) basic vascular physiology and (B) vascular related diseases. This review will highlight the major advances that have occurred since our 2007 paper. METHODS:A literature search mainly focusing on the role of the glycocalyx in the two major areas described above was performed using electronic databases. RESULTS:In part (A) of this review, the new formulation of the century old Starling principle, now referred to as the Michel-Weinbaum glycoclayx model or revised Starling hypothesis, is described including new subtleties and physiological ramifications. New insights into mechanotransduction and release of nitric oxide due to fluid shear stress sensed by the glycocalyx are elaborated. Major advances in understanding the organization and function of glycocalyx components, and new techniques for measuring both its thickness and spatio-chemical organization based on super resolution, stochastic optical reconstruction microscopy (STORM) are presented. As discussed in part (B) of this review, it is now recognized that artery wall stiffness associated with hypertension and aging induces glycocalyx degradation, endothelial dysfunction and vascular disease. In addition to atherosclerosis and cardiovascular diseases, the glycocalyx plays an important role in lifestyle related diseases (e.g., diabetes) and cancer. Infectious diseases including sepsis, Dengue, Zika and Corona viruses, and malaria also involve the glycocalyx. Because of increasing recognition of the role of the glycocalyx in a wide range of diseases, there has been a vigorous search for methods to protect the glycocalyx from degradation or to enhance its synthesis in disease environments. CONCLUSION:As we have seen in this review, many important developments in our basic understanding of GCX structure, function and role in diseases have been described since the 2007 paper. The future is wide open for continued GCX research.

Project description:BackgroundDegradation of the endothelial glycocalyx is critical for sepsis-associated lung injury and pulmonary vascular permeability. We investigated whether sulodexide, a precursor for the synthesis of glycosaminoglycans, plays a biological role in glycocalyx remodeling and improves endothelial barrier dysfunction in sepsis.MethodsThe number of children with septic shock that were admitted to the PICU at Children's Hospital of Fudan University who enrolled in the study was 28. On days one and three after enrollment, venous blood samples were collected, and heparan sulfate, and syndecan-1 (SDC1) were assayed in the plasma. We established a cell model of glycocalyx shedding by heparinase III and induced sepsis in a mouse model via lipopolysaccharide (LPS) injection and cecal ligation and puncture (CLP). Sulodexide was administrated to prevent endothelial glycocalyx damage. Endothelial barrier function and expression of endothelial-related proteins were determined using permeability, western blot and immunofluorescent staining. The survival rate, histopathology evaluation of lungs and wet-to-dry lung weight ratio were also evaluated.ResultsWe found that circulating SDC1 levels were persistently upregulated in the non-alive group on days 1 and 3 and were positively correlated with IL-6 levels. Receiver operating characteristic curve analysis showed that SDC1 could distinguish patients with mortality. We showed that SDC1-shedding caused endothelial permeability in the presence of heparinase III and sepsis conditions. Mechanistically, sulodexide (30 LSU/mL) administration markedly inhibited SDC1 shedding and prevented endothelial permeability with zonula occludens-1 (ZO-1) upregulation via NF-κB/ZO-1 pathway. In mice with LPS and CLP-induced sepsis, sulodexide (40 mg/kg) administration decreased the plasma levels of SDC1 and increased survival rate. Additionally, sulodexide alleviated lung injury and restored endothelial glycocalyx damage.ConlusionsIn conclusion, our data suggest that SDC1 predicts prognosis in children with septic shock and sulodexide may have therapeutic potential for the treatment of sepsis-associated endothelial dysfunction.

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Two Methods of AuNPs Synthesis Induce Differential Vascular Effects. The Role of the Endothelial Glycocalyx.

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Two Methods of AuNPs Synthesis Induce Differential Vascular Effects. The Role of the Endothelial Glycocalyx.

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