Gp96/GRP94 is a putative high density lipoprotein-binding protein in liver

Crom, Rini de; Haperen, Rien van; Janssens, Rick; Visser, Pim; Willemsen, Rob; Grosveld, Frank; Kamp, Arthur van der

doi:10.1016/s1388-1981(99)00017-7

Cited by 21 publications

(10 citation statements)

References 53 publications

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“…gp96 is a molecular chaperon in the endoplasmic reticulum (Mazzarella and Green;1987). It has been shown that gp96 is a high density lipoprotein-binding protein in liver (de Crom et al, 1999). Although its precise function is not clear, gp96 may contribute to control the HDL-metabolism for maintenance of normal function on vascular endothelium.…”

Section: Discussionmentioning

confidence: 99%

Searching for Genes Involved in Arteriosclerosis: Proteomic Analysis of Cultured Human Umbilical Vein Endothelial Cells Undergoing Replicative Senescence

Kamino

Hiratsuka

Toda

et al. 2003

Cell Struct. Funct.

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ABSTRACT. It is known that replicative senescence of endothelium in vivo contributes at least partially to agerelated vascular disorders such as arteriosclerosis. However, the genes involved in this process remain to be identified. In this study, we employed a proteomics-based approach to identify candidate genes using in vitro cultured human umbilical vein endothelial cells (HUVECs) as an experimental model for replicative senescence. By comparing protein spots from young and senescent HUVECs using two-dimensional electrophoresis, we identified three up-regulated proteins and five down-regulated proteins in senescent HUVECs as compared to young HUVECs, whose alteration was not observed during replicative senescence of primary human fibroblasts. Consistent results were obtained in Western blotting analysis using specific antibodies raised against some of these proteins, whereas there were no significant changes in the mRNA levels of these genes during senescence of HUVECs. Among them, cathepsin B, a protease participating in both intracellular proteolysis and extracellular matrix remodeling was observed to be dramatically up-regulated in senescent HUVECs and whose activity is known to be up-regulated in atherosclerotic lesions with senescence-associated phenotypes in vivo. Additional proteins, including cytoskeletal proteins and proteins involved in the processes of synthesis, turnover and modification of protein, were identified, whose function in endothelium was previously unsuspected. These proteins identified by a proteomics-based approach using cultured HUVECs may be involved not only in replicative senescence but also in functional alterations in vascular endothelial cells with senescence-associated phenotypes and may serve as molecular markers for these processes.

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Section: Discussionmentioning

confidence: 99%

Searching for Genes Involved in Arteriosclerosis: Proteomic Analysis of Cultured Human Umbilical Vein Endothelial Cells Undergoing Replicative Senescence

Kamino

Hiratsuka

Toda

et al. 2003

Cell Struct. Funct.

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“…Based on previous reports, there are two possibilities for gp96 localization: the extracellular secretion of gp96 47,48 and its cell surface presentation. 21,49,50 In this study, we analyzed the culture media of WT and AIMP1 Ϫ/Ϫ MEFs for the presence of gp96 but failed to detect it (data not shown). However, gp96 was detected on cell surfaces by FACS ( Figure 4C).…”

Section: Significance Of Aimp1 In the Subcellular Localization Of Gp96mentioning

confidence: 93%

Aminoacyl-tRNA Synthetase-Interacting Multifunctional Protein 1/p43 Controls Endoplasmic Reticulum Retention of Heat Shock Protein gp96

Han

Park

Liu

et al. 2007

The American Journal of Pathology

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Aminoacyl-tRNA synthetase-interacting multifunctional protein 1 (AIMP1; previously known as p43) is a multifunctional protein that was initially found in multitRNA synthetase complex. In the present study, screening of the AIMP1-binding proteins revealed that AIMP1 can form a molecular complex with heat shock protein gp96. AIMP1 enhances gp96 dimerization and the interaction between gp96 and KDEL receptor-1 (KDELR-1), which mediates the retrieval of KDEL-containing proteins from Golgi to the endoplasmic reticulum (ER). The interaction between gp96 and KDELR-1 was reduced in AIMP1-deficient cells, and this disturbed ER retention of gp96 and increased its cell surface localization. Moreover, this localization of gp96 at the cell surface was suppressed by its interaction with AIMP1 and enhanced by the depletion of endogenous AIMP1. In addition, AIMP1-deficient mice showed dendritic cell activation attributable to increased gp96 surface presentation and lupus-like autoimmune phenotypes. These results suggest that AIMP1 acts as a regulator of the ER retention of gp96 and provide a new perspective of the regulatory mechanism underlying immune stimulation by gp96.

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“…Aortas were freshly collected and homogenized in 50 mM Tris⅐HCl, pH 7.4, con-taining 1 mM EDTA, 0.25 M sucrose, and 20 mM 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate. Western blotting was performed as described previously (20). Twenty-five micrograms of protein (BCA protein assay kit, Pierce) was applied to each lane.…”

Section: Transgenic (Tg) Micementioning

confidence: 99%

Endothelial nitric oxide synthase overexpression attenuates congestive heart failure in mice

Jones

Greer

Haperen

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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216

177

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Congestive heart failure results in cardiovascular dysfunction and diminished vascular nitric oxide (NO) production. We hypothesized that overexpression of endothelial NO synthase (eNOS) within the endothelium would reduce the extent of contractile dysfunction in a murine model of infarct-induced congestive heart failure. We generated transgenic (TG) mice overexpressing the human eNOS gene. The TG mice displayed significantly enhanced eNOS protein levels and eNOS activity levels (10-to 12-fold greater) in the aorta and the coronary vasculature. Non-TG (NTg) and eNOS TG mice were subjected to permanent left anterior descending coronary artery occlusion and then observed for 1 mo. We assessed cardiac function in vivo by using echocardiography and ultraminiature ventricular pressure catheters. Myocardial infarct size was similar between study groups (Ϸ70% of the risk zone). Survival was increased by 43% in the eNOS TG mice compared with NTg (P < 0.05). Fractional shortening and cardiac output were also significantly (P < 0.05) greater in the eNOS TG than in NTg. Interestingly, pulmonary edema was evident only in NTg mice, and no evidence of pulmonary edema was observed in the eNOS TG mice. Thus, targeted overexpression of the eNOS gene within the vascular endothelium in mice attenuates both cardiac and pulmonary dysfunction and dramatically improves survival during severe congestive heart failure.

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Gp96/GRP94 is a putative high density lipoprotein-binding protein in liver

Cited by 21 publications

References 53 publications

Searching for Genes Involved in Arteriosclerosis: Proteomic Analysis of Cultured Human Umbilical Vein Endothelial Cells Undergoing Replicative Senescence

Searching for Genes Involved in Arteriosclerosis: Proteomic Analysis of Cultured Human Umbilical Vein Endothelial Cells Undergoing Replicative Senescence

Aminoacyl-tRNA Synthetase-Interacting Multifunctional Protein 1/p43 Controls Endoplasmic Reticulum Retention of Heat Shock Protein gp96

Endothelial nitric oxide synthase overexpression attenuates congestive heart failure in mice

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