A Novel Glycosylphosphatidyl Inositol-Anchored Protein on Human Leukocytes: A Possible Role for Regulation of Neutrophil Adherence and Migration

Suzuki, Kichiya; Watanabe, Tadashi; Sakurai, Shin Ichi; Ohtake, Kazuhisa; Kinoshita, Taroh; Araki, Akemi; Fujita, Teizo; Takei, Hiroshi; Takeda, Yuji; Sato, Yukiko; Yamashita, T; Araki, Yoshihiko; Sendo, Fujiro

doi:10.4049/jimmunol.162.7.4277

Cited by 92 publications

(3 citation statements)

References 39 publications

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“…VNN 2 was detected high expression in kidney tissue [ 72 ]. The protein Gpi80, encoded by the VNN2, exhibited surface aggregation on activated migrating neutrophils and potentially modulated neutrophil adhesion and migration [ 73 ]. Thus, we implied that genus Marvinbryantia involved in pathological exacerbation of DN by inflammation activation.…”

Section: Discussionmentioning

confidence: 99%

Causal effect of gut microbiota and diabetic nephropathy: a Mendelian randomization study

He,

Chen,

Hao

et al. 2024

Diabetol Metab Syndr

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Background The interaction of dysbiosis of gut microbiota (GM) with diabetic nephropathy (DN) drew our attention and a better understanding of GM on DN might provide potential therapeutic approaches. However, the exact causal effect of GM on DN remains unknown. Methods We applied two-sample Mendelian Randomization (MR) analysis, including inverse variance weighted (IVW), MR-Egger methods, etc., to screen the significant bacterial taxa based on the GWAS data. Sensitivity analysis was conducted to assess the robustness of MR results. To identify the most critical factor on DN, Mendelian randomization-Bayesian model averaging (MR-BMA) method was utilized. Then, whether the reverse causality existed was verified by reverse MR analysis. Finally, transcriptome MR analysis was performed to investigate the possible mechanism of GM on DN. Results At locus-wide significance levels, the results of IVW suggested that order Bacteroidales (odds ratio (OR) = 1.412, 95% confidence interval (CI): 1.025–1.945, P = 0.035), genus Akkermansia (OR = 1.449, 95% CI: 1.120–1.875, P = 0.005), genus Coprococcus 1 (OR = 1.328, 95% CI: 1.066–1.793, P = 0.015), genus Marvinbryantia (OR = 1.353, 95% CI: 1.037–1.777, P = 0.030) and genus Parasutterella (OR = 1.276, 95% CI: 1.022–1.593, P = 0.032) were risk factors for DN. Reversely, genus Eubacterium ventriosum (OR = 0.756, 95% CI: 0.594–0.963, P = 0.023), genus Ruminococcus gauvreauii (OR = 0.663, 95% CI: 0.506–0.870, P = 0.003) and genus Erysipelotrichaceae (UCG003) (OR = 0.801, 95% CI: 0.644–0.997, P = 0.047) were negatively associated with the risk of DN. Among these taxa, genus Ruminococcus gauvreauii played a crucial role in DN. No significant heterogeneity or pleiotropy in the MR result was found. Mapped genes (FDR < 0.05) related to GM had causal effects on DN, while FCGR2B and VNN2 might be potential therapeutic targets. Conclusions This work provided new evidence for the causal effect of GM on DN occurrence and potential biomarkers for DN. The significant bacterial taxa in our study provided new insights for the ‘gut-kidney’ axis, as well as unconventional prevention and treatment strategies for DN.

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Section: Discussionmentioning

confidence: 99%

Causal effect of gut microbiota and diabetic nephropathy: a Mendelian randomization study

He,

Chen,

Hao

et al. 2024

Diabetol Metab Syndr

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“…This novel protein GPI‐80 and Vanin‐1, a GPI‐anchored protein expressed on perivascular thymic stromal cells, have been found 40% homologous with human biotinidase. This report suggested that a biotinidase superfamily of molecules may regulate leukocyte trafficking along the endothelium toward the extravascular tissues (22).…”

Section: Discussionmentioning

confidence: 99%

“…Impaired immunoregulatory function or immunodeficiency has occurred in children with biotinresponsive multiple carboxylase deficiency (20,21). However, a novel glycosylphosphatidylinositol-anchored protein (GPI-80) has been described on human leukocytes (22). This novel protein GPI-80 and Vanin-1, a GPI-anchored protein expressed on perivascular thymic stromal cells, have been found 40% homologous with human biotinidase.…”

Section: Discussionmentioning

confidence: 99%

Serum Biotinidase Activity in Children With Chronic Liver Disease and Its Clinical Significance

Pabuçcuoğlu,

Aydoğdu,

Baş

2002

J. pediatr. gastroenterol. nutr.

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BackgroundBiotinidase is the enzyme responsible for liberating the vitamin biotin from biocytin and dietary protein–bound vitamin. Individuals lacking biotinidase activity become biotin deficient. Because the liver is the major source of plasma biotinidase, chronic liver diseases can lead to decreased serum biotinidase activity and biotin deficiency. The aim of this study is to determine serum biotinidase activity values in children with chronic liver disease and to investigate the relation among enzyme activity, certain liver function tests, and degree of liver damage.MethodIn this study, using a spectrophotometric method, biotinidase activity was determined in sera from 62 children with chronic liver diseases (median age, 9.73 years; range, 8 months to 18 years) and from 27 healthy controls. Diagnoses of the patient group were as follows: noncirrhotic chronic hepatitis B virus infection (n = 12), metabolic liver diseases (n = 16), autoimmune hepatitis (n = 6), intrahepatic and extrahepatic cholestasis (n = 14), fulminant hepatitis (n = 5), cryptogenic cirrhosis n = 5), prehepatic portal hypertension (n = 4). Meanwhile, serum albumin, total bilirubin, alkaline phosphatase, alanine aminotransferase, and γ‐glutamyltransferase concentrations and prothrombine time were determined for each patient and the results were correlated with serum biotinidase activity.ResultsThere was significant difference between mean enzyme activity of the controls (7.6 ± 1.2 nmol · min −1 · mL −1 ) and of all patients with chronic liver disease (6.3 ± 2.5 nmol · min −1 · mL −1 ) (P < 0.05). Serum biotinidase activity in patients with noncirrhotic chronic liver diseases (chronic viral hepatitis, prehepatic portal hypertension, glycogen storage disease, Gaucher disease) was within the normal ranges. However, serum biotinidase activity in patients with cirrhosis and Wilson disease was significantly less than that of the control group (P < 0.05). The lowest enzyme activities were detected in patients with fulminant hepatitis.ConclusionIn this study, serum biotinidase activity was significantly lower in patients with cirrhosis, particularly in the patients with decompensated cirrhosis and fulminant hepatitis who exhibited no clinical symptoms related to biotin deficiency. The decreased serum biotinidase activity in chronic liver diseases was associated with severe impairment of hepatocellular function.

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Glycosyl‐phosphatidyl‐inositol‐defective granulocytes from paroxysmal nocturnal haemoglobinuria patients show increased bacterial ingestion but reduced respiratory burst induction

et al. 2006

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Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by the emergence of a GPI-defective clonal hematopoiesis. Its clinical features are hemolytic anemia, cytopenia, and thrombosis. Circulating monocytes and granulocytes are largely GPI-defective in PNH patients. This study aims to investigate the granulocyte functional properties in PNH. We analyzed bacterial-dependent intracellular ingestion and the consequent activation of oxidative burst in GPI-defective granulocytes from four neutropenic PNH patients. Our data show a significant increase in the ability of GPI-defective granulocytes to ingest opsonized bacteria. In addition, an impaired respiratory burst effectiveness in response to two independent bacterial stimuli, the N-formyl-MetLeuPhe (fMLP) synthetic bacterial peptide and E. coli, was revealed. The occurrence of neutropenia and the severe impairment of oxidative burst, occurring in chronic granulomatosis disease, were unable to significantly affect phagocytosis. Thus, additional mechanisms, able to differentially affect ingestion ability and respiratory burst effectiveness, have to be hypothesized. The reduced burst effectiveness of GPIdefective granulocytes was maintained after treatment with phorbol 12-myristate 13-acetate, a pharmacological stimulus able to extensively recruit and to trigger intracellular protein kinase C (PKC). Moreover, blocking of PKC has been observed to severely affect granulocyte respiratory burst with a mild effect on the phagocytosis. These data suggest a role for a modulation of intracellular PKC in the pathogenesis of the impaired granulocyte oxidative burst. Am. J. Hematol. 82:98-107, 2007. V V C 2006 Wiley-Liss, Inc.

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A Novel Glycosylphosphatidyl Inositol-Anchored Protein on Human Leukocytes: A Possible Role for Regulation of Neutrophil Adherence and Migration

Cited by 92 publications

References 39 publications

Causal effect of gut microbiota and diabetic nephropathy: a Mendelian randomization study

Causal effect of gut microbiota and diabetic nephropathy: a Mendelian randomization study

Serum Biotinidase Activity in Children With Chronic Liver Disease and Its Clinical Significance

Glycosyl‐phosphatidyl‐inositol‐defective granulocytes from paroxysmal nocturnal haemoglobinuria patients show increased bacterial ingestion but reduced respiratory burst induction

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