Albumin functions as an inhibitor of T cell adhesion in vitro

Kim, Yu-Lee; Im, Young Jin; Lee, Yun-Kyung; Ha, Nam Chul; Bae, Yoe Sik; Lim, Soo Min; Okajima, Fumikazu; Im, Dong‐Soon

doi:10.1016/j.bbrc.2006.10.143

Cited by 12 publications

(9 citation statements)

References 18 publications

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“…We find it important that the effect of BSA be controlled by including an experimental group with identical concentrations of BSA and organic solvent used to dissolve the FA. However, as we have discussed throughout this manuscript, albumin has biological effects itself [136; 138; 139], including lipid quenching, that should be considered specifically for each model. If endogenous lipid quenching occurs, determining an appropriate concentration of serum or titrating low quantities of FA to inhibit lipid quenching by FA-free BSA are possible solutions to prevent this undesired effect.…”

Section: Discussionmentioning

confidence: 99%

Cell culture models of fatty acid overload: Problems and solutions

Alsabeeh

Chausse

Kakimoto

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

120

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High plasma levels of fatty acids occur in a variety of metabolic diseases. Cellular effects of fatty acid overload resulting in negative cellular responses (lipotoxicity) are often studied in vitro, in an attempt to understand mechanisms involved in these diseases. Fatty acids are poorly soluble, and thus usually studied when complexed to albumins such as bovine serum albumin (BSA). The conjugation of fatty acids to albumin requires care pertaining to preparation of the solutions, effective free fatty acid concentrations, use of different fatty acid species, types of BSA, appropriate controls and ensuring cellular fatty acid uptake. This review discusses lipotoxicity models, the potential problems encountered when using these cellular models, as well as practical solutions for difficulties encountered.

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Section: Discussionmentioning

confidence: 99%

Cell culture models of fatty acid overload: Problems and solutions

Alsabeeh

Chausse

Kakimoto

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

120

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“…Interestingly, HSA may behave differently under different pathological or physiological conditions. In vitro experiments (Kim et al 2006) have shown that albumin can inhibit T cell adhesion. Graner et al (2004) found that albumin expressed in mouse tumours can inhibit T cell activation and response in vivo and in vitro, promoting tumour progression.…”

Section: Anti-inflammatory Effectsmentioning

confidence: 99%

Impaired albumin function: a novel potential indicator for liver function damage?

et al. 2019

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Albumin is the most abundant plasma protein and albumin infusion is commonly used. Conventionally, the biologic and therapeutic effects of albumin have been thought to be due to its oncotic properties. However, albumin has a variety of biologic functions, including molecular transport, anti-oxidation, anti-inflammation, endothelial stabilisation, anti-thrombotic effects, and the adjustment of capillary permeability. Despite this, the functions of albumin have not been thoroughly investigated. Recent studies have shown non-alcoholic fatty liver disease (NAFLD), viral hepatitis, cirrhosis, and liver failure to be associated with impairments in albumin function, which are associated with impairments in liver function and disease prognosis. Post-translational modifications of albumin cause structural modifications that affect protein function. Recently, the concentration of albumin associated with normal function, the 'efficient albumin concentration', has been attracting more interest. In addition, although many biologic markers, including albumin concentration, are widely used for the assessment of early liver dysfunction in patients with liver diseases, the predictive values are unsatisfactory. However, clinical evidence has suggested that albumin function may represent a novel biomarker of early impairment in liver function. In this review, we summarise the factors affecting albumin function and discuss the clinical significance of impairments in albumin function in various liver diseases. KEY MESSAGES1. The importance of albumin depends not only on its concentration, but also on its various physiological functions. 2. Impaired albumin function has been reported in a variety of liver diseases, and is associated with disease severity and prognosis, thereby proposing the concept of 'effective albumin concentration'. 3. Albumin dysfunction occurs earlier than other conventional indicators, and albumin dysfunction may be a new biomarker of early impairment in liver function. 4. Many exogenous and endogenous factors lead to post-translational modifications of albumin, which alters the three-dimensional structure of albumin, resulting in a decrease in its biological activity.

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“…For eosin Y staining, cells that adhered to the wells were fixed overnight with 2% formaldehyde and stained with eosin Y for 30 min. Eosin Y was then extracted by the addition of a mixture of 1% of acetic acid and 50% ethanol, and the absorbance was measured at 570 nm (Kim et al, 2006).…”

Section: Cell Adhesionmentioning

confidence: 99%

“…Jurkat T cells or human primary T cells adhered to a tissue culture flask when 10% fetal bovine serum (FBS) was withdrawn (Kim et al, 2006), and T cell adhesion was inhibited by bovine serum albumin (BSA) in FBS (Kim et al, 2006). To test whether this effect of albumin is common in hematopoietic cells, we investigated the effects of FBS and albumin on cell adhesion in U-937 monocytes, THP-1 monocytes, K-562 promyelocytic leukemia cells, and HL-60 human leukemia cells.…”

Section: Inhibitory Effect Of Albumin On Adhesion Of Hematopoietic Cellsmentioning

confidence: 99%

“…However, cell adhesion and migration of inactivated hematopoietic cells has been poorly investigated. In the previous study, we reported that bovine serum albumin (BSA), the most studied and well-understood protein in plasma, inhibited the adhesion of T cells, such as the human Jurkat T cell line and primary cultured human T cells, probably independent of integrin-mediated signaling (Kim et al, 2006). In the present study, we tested whether this effect of albumin is common in hematopoietic cells by using U-937 human monocytes, THP-1 monocytes, K-562 promyelocytic leukemia cells, and HL-60 human leukemia cells and also whether oxidative signaling is involved in cell adhesion by using various antioxidants such as (-)-epigallocatechin-3-gallate (EGCG), morin, and α-tocopherol, because oxidative signaling has been implicated in inflammation-mediated cell adhesion (Chen et al, 2006;Sen and Roy, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Albumin and Antioxidants Inhibit Serum-deprivation-induced Cell Adhesion in Hematopoietic Cells

Han¹,

Lim²,

Kim³

et al. 2008

Biomolecules and Therapeutics

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− Previously, we identified albumin as an inhibitory factor in serum for cell adhesion of T cells such as human Jurkat T and primary cultured human T cells. In the present study, we found that other hematopoietic cell lines including U-937 human monocytes, THP-1 human monocytes, K-562 promyelocytic leukemia cells, and HL-60 human leukemia cells, also adhere to tissue culture flasks when serum is withdrawn, and albumin exerts an inhibitory effect on cell adhesion by those cells, implying that this inhibition is a common phenomenon in hematopoietic cells. Furthermore, we found that cell adhesion is inhibited by antioxidants such as (-)-epigallocatechin-3-gallate (EGCG), morin, and a-tocopherol. Our results suggest that albumin may inhibit basal cell adhesion of hematopoietic cells and that the oxidative balance in the plasma may be important for cell adhesion of hematopoietic cells in vivo.

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Albumin functions as an inhibitor of T cell adhesion in vitro

Cited by 12 publications

References 18 publications

Cell culture models of fatty acid overload: Problems and solutions

Cell culture models of fatty acid overload: Problems and solutions

Impaired albumin function: a novel potential indicator for liver function damage?

Albumin and Antioxidants Inhibit Serum-deprivation-induced Cell Adhesion in Hematopoietic Cells

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