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Dive into the research topics where Ying Wei Lin is active.

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Featured researches published by Ying Wei Lin.


Biochemical Pharmacology | 1994

Pyrrolidine dithiocarbamate, a potent inhibitor of nuclear factor κB (NF-κB) activation, prevents apoptosis in human promyelocytic leukemia HL-60 cells and thymocytes

Rikimaru Bessho; Kousaku Matsubara; Masaru Kubota; Katsuji Kuwakado; Haruyo Hirota; Yoshihiro Wakazono; Ying Wei Lin; Akiro Okuda; Masahiko Kawai; Ryuta Nishikomori; Toshio Heike

We examined the effect of pyrrolidine dithiocarbamate (PDTC), which potently blocks the activation of nuclear factor kappa B (NF-kappa B), on the induction of apoptosis by a variety of agents. Treatment of a human promyelocytic leukemia cell line, HL-60, with 10 micrograms/mL etoposide or 2 microM 1-beta-D-arabinofuranosylcytosine induced NF-kappa B activation within 1 hr and subsequently caused apoptosis within 3-4 hr. The simultaneous addition of 50-500 microM PDTC with these agents blocked NF-kappa B activation and completely abrogated both morphologically apoptotic changes and internucleosomal DNA fragmentation for up to 6 hr. However, PDTC failed to inhibit the endonuclease activity contained in the whole cell lysates. The inhibitory effect of PDTC was also observed in etoposide- and dexamethasone-induced apoptosis in human thymocytes at a concentration of 1-10 microM. Since PDTC has both antioxidant and metal-ion chelating activities, we tested the effects of N-acetyl-L-cysteine (NAC) (antioxidant) or o-phenanthroline (OP) (metal-ion chelator) on the induction of apoptosis. Pretreatment of HL-60 cells or thymocytes with 100-500 microM OP for 2 hr, but not 10-60 mM NAC, suppressed subsequent occurrence of apoptosis induced by etoposide. These results suggest that the activation of NF-kappa B plays an important role in the apoptotic process of human hematopoietic cells.


European Journal of Haematology | 2009

In vivo administration of granulocyte colony-stimulating factor promotes neutrophil survival in vitro

Souichi Adachi; Masaru Kubota; Ying Wei Lin; Akiro Okuda; Kousaku Matsubara; Yoshihiro Wakazono; Haruyo Hirota; Katsuji Kuwakado; Yuichi Akiyama

Abstract: We recently showed that recombinant human granulocyte‐colony stimulating factor (rhG‐CSF) maintained the viability of human neutrophils in incubation for up to 72 hours. However, it is not known whether rhG‐CSF can enhance neutrophil survival in in vivo situations. To clarify this issue, we investigated neutrophil survival in vitro following in vivo injection of rhG‐CSF. Neutrophils were obtained from 4 pediatric patients with malignancies and healthy adult volunteers before and after rhG‐CSF administration. Neutrophils obtained before rhG‐CSF treatment started to undergo apoptosis after 24 h of incubation. In contrast, the survival of neutrophils drawn after rhG‐CSF administration increased by approximately 24 h. Concomitantly, the appearance of typical ladder‐like DNA fragmentation was delayed. Such an increase in neutrophil survival was inhibited by coincubation with either H 7 (10 μmol/1) or H 8 (20 μmol/1), which worked as protein kinase C inhibitors. Although our study did not measure neutrophil survival in vivo directly, it provides us with further evidence that rhG‐CSF may function to prolong neutrophil life expectancy in vivo.


FEBS Letters | 1995

ASSOCIATION OF HIGH MOLECULAR WEIGHT DNA FRAGMENTATION WITH APOPTOTIC OR NON-APOPTOTIC CELL DEATH INDUCED BY CALCIUM IONOPHORE

Akihiro Kataoka; Masaru Kubota; Yoshihiro Wakazono; Akiro Okuda; Rikimaru Bessho; Ying Wei Lin; Ikuya Usami; Yuichi Akiyama; Kenshi Furusho

Calcium ionophore (A23187)‐induced high molecular weight (HMW) and internucleosomal DNA fragmentation were investigated in human leukemia cell lines. An apoptosis‐sensitive cell line, HL‐60, showed HMW, internucleosomal DNA fragmentation and morphological changes of apoptosis by A23187. MOLT‐4, which is resistant to apoptosis, exhibited only HMW DNA fragmentation and died of necrosis under the same conditions. Autodigestion experiments suggested the endonucleolytic activity to cause HMW fragmentation in the cytoplasm of both cell lines. The activity was more dependent on Mg2+ than Ca2+ in HL‐60, whereas it was Ca2+‐dependent in MOLT‐4. These results suggest that HMW DNA fragmentation is not specific to apoptosis.


Mutation Research-dna Repair | 1994

Somatic mutations at T-cell antigen receptor and glycophorin a loci in pediatric leukemia pateints following chemotherapy: comparison with HPRT locus mutation

Haruyo Hirota; Masaru Kubota; Souichi Adachi; Akiro Okuda; Ying Wei Lin; Rikimaru Bessho; Yoshihiro Wakazono; Kousaku Matsubara; Katsuji Kuwakado; Yuichi Akiyama; Tsutomu Tsutsui

Frequencies of somatic mutations in pediatric patients with leukemia were evaluated following intensive treatment at three different loci: the hypoxanthine-guanine phosphoribosyl transferase (HPRT), T-cell antigen receptor (TCR), and glycophorin A (GPA) gene. Thirty-two children with acute lymphoblastic leukemia (ALL), nine children with acute myelogenous leukemia (AML), and 20 age-matched healthy controls were included in the study of mutant frequencies (Mfs) at the HPRT and TCR loci. Among these patients and controls, individuals with heterozygous MN blood type, i.e., 14 children with ALL, three children with AML, and nine healthy controls, served for the further assessment of variant frequency (Vf) at the GPA locus. In ALL patients, geometric mean Mfs and Vfs at these loci were significantly higher than in healthy controls. The high Mf value at the HPRT locus persisted for up to 8 years after the end of chemotherapy. On the other hand, the Mf values at the TCR locus and Vf values at the GPA locus declined gradually with time. In AML patients, on the other hand, the geometric mean Mf only at the TCR locus was significantly higher than in the controls, albeit to a lesser degree than in ALL patients. These data suggest that anti-cancer therapy induces somatic mutations at various loci and that ALL patients are more susceptible to mutagenic intervention than are AML patients.


Biochemical Pharmacology | 1998

Role of Protein Tyrosine Phosphorylation in Etoposide-Induced Apoptosis and NF-κB Activation

Ikuya Usami; Masaru Kubota; Rikimaru Bessho; Akihiro Kataoka; Seiji Koishi; Ken-ichiro Watanabe; Machiko Sawada; Ying Wei Lin; Yuichi Akiyama; Kenshi Furusho

Abstract When a human myeloid cell line, U937, was incubated with etoposide (10 μg/mL), morphologically apoptotic cells first appeared at 3 hr and increased with time to 50% at 6 hr. Pretreatment of U937 cells for 30 min with a potent tyrosine kinase inhibitor, herbimycin A (10 μM), significantly suppressed the appearance of apoptotic morphological changes. Concomitantly, herbimycin A pretreatment prevented both high molecular weight and internucleosomal DNA fragmentation induced by etoposide. Two major bands at 30 and 66 kDa with enhanced tyrosine phosphorylation inhibited by herbimycin A were detectable after 30 min of incubation with etoposide. In addition, herbimycin A prevented etoposide-induced NF-κB activation. The expressions of Bcl-2 and Bax, on the other hand, were not affected by herbimycin A pretreatment. Herbimycin A was also found to inhibit 1-β- d -arabinofuranosylcytosine-induced apoptotic changes and NF-κB activation. These results suggest that activation of tyrosine kinase(s) may play an important role in apoptotic processes induced by a variety of anti-cancer drugs.


Journal of Cellular Physiology | 1996

Methotrexate inhibits superoxide production and chemotaxis in neutrophils activated by granulocyte colony-stimulating factor

Akiro Okuda; Masaru Kubota; Machiko Sawada; Seiji Koishi; Akihiro Kataoka; Rikimaru Bessho; Ikuya Usami; Ying Wei Lin; Souichi Adachi; Kenshi Furusho

Treatment of circulating human neutrophils with recombinant human granulocyte colony‐stimulating factor (rhG‐CSF) for 30 min augmented superoxide generation and chemotaxis induced by N‐formylmethionyl‐leucyl‐phenylalanine (fMLP) in a dose dependent manner. When neutrophils were treated with 1 μM of methotrexate (MTX) for 60 min after incubation with rhG‐CSF (10 ng/ml), the effects of rhG‐CSF on superoxide generation and chemotaxis were inhibited by approximately 49 and 29%, respectively. Although inhibitory effects of MTX were also seen in neutrophils not pretreated with rhG‐CSF, the degree of inhibition was much less. The addition of either hypoxanthine or guanosine at a concentration of 100 μM to the culture medium significantly attenuated the effects of MTX. However, in neutrophils obtained from a patient with Lesch‐Nyhan syndrome, which lacked hypoxanthine‐guanine phosphoribosyl transferase activity, neither hypoxanthine nor guanosine had any rescue effect. These results suggest that MTX inhibits superoxide generation and chemotaxis in rhG‐CSF‐activated neutrophils, at least in part, by disturbing purine nucleotide biosynthesis.


Leukemia Research | 1995

Augmentation by aphidicolin of 1-β-d-arabinofuranosylcytosine-induced c-jun and NF-κB activation in a human myeloid leukemia cell line: Correlation with apoptosis

Katsuji Kuwakado; Masaru Kubota; Rikimaru Bessho; Akihiro Kataoka; Ikuya Usami; Ying Wei Lin; Akiro Okuda; Yoshihiro Wakazono

Abstract 1-β- d -arabinofuranosylcytosine (ara-C) (2 μM) can induce apoptosis in a human myeloid leukemia cell line, U937, after 4 h of incubation. Pretreatment of cells with aphidicolin (2 μM) augments ara-C-induced apoptosis, since it was first observed at 0.4 μM ara-C and became more intense at 2 and 10 μM. Although aphidicolin itself had a marginal effect on c- jun expression, it significantly augmented ara-C induced c- jun upregulation by shortening the lag time and lowering ara-C concentrations necessary for the induction of detectable c- jun transcripts. Aphidicolin and ara-C acted synergistically to increase NF-κB DNA binding activity as determined by an electrophoretic mobility shift assay. Expression of c- myc was slightly increased through the DNA degradative phase, and was then downregulated. Thus, the activation of NF-κB and c- jun expression seems to be well correlated with the potentiation by aphidicolin of ara-C-induced apoptosis.


Pediatrics International | 1991

Familial Juvenile Nephronophthisis in Two Siblings — Histological Findings at an Early Stage —

Kousaku Matsubara; Kei Suzuki; Ying Wei Lin; Toshiyuki Yamamoto; Shigeru Ohta

We present two female siblings with familial juvenile nephronophthisis (FJN) which was diagnosed at the early stage of renal failure. Diagnosis was made during the investigation of anemia in case 1 and by a subsequent family survey in case 2. Most patients with FJN are not identified until the terminal stage of renal failure and such cases have rarely been reported in Japan. Case 2 had a reduction in the maximum urinary concentration ability but no azotemia, and among the FJN patients reported in Japan so far she has the least advanced renal disease. Histological examination of the renal biopsy in case 1 showed typical findings of FJN, such as thickening and lamination of the tubular basement membrane (TBM), interstitial fibrosis, and round cell infiltration of the interstitium. In case 2, renal biopsy revealed an irregular marked thickening of the TBM with trivial interstitial changes and a normal glomerular appearance. The histology of these two cases suggests that the TBM may be the primary site affected in FJN.


European Journal of Haematology | 2009

Inhibition of superoxide production and chemotaxis by methotrexate in neutrophils primed by TNF-α or LPS

Akiro Okuda; Masaru Kubota; Ken-ichiro Watanabe; Machiko Sawada; Seiji Koishi; Akihiro Kataoka; Ikuya Usami; Ying Wei Lin; Kenshi Furusho

Abstract: We have demonstrated recently that methotrexate (MTX) inhibits superoxide generation and chemotaxis induced by N‐formylmethionyl‐leucyl‐phenylalanine (fMLP) in neutrophils primed by granulocyte colony‐stimulating factor (G–CSF). To extend these observations, we examined the in vitro effect of MTX on fMLP‐stimulated superoxide generation and chemotaxis in neutrophils primed by either tumor necrosis factor α (TNF‐α) or bacterial lipopolysaccharide (LPS). MTX inhibited superoxide generation and chemotaxis more efficiently in TNF‐α‐or LPS‐primed neutrophils than in unprimed neutrophils. When either hypoxanthine or guanosine was added to the culture medium, the effects of MTX were partially counteracted. Furthermore, MTX caused a significant inhibition of both superoxide production induced by phorbol 12‐myristate‐13‐acetate and chemotaxis induced by interleukin 8 in G‐CSF‐primed neutrophils. These results may support the hypothesis that neutrophils primed by different stimuli are more susceptible to the inhibitory effects of MTX on superoxide generation and chemotaxis irrespective of chemoattractants. Such an effect can be partly attributed to the perturbation of purine nucleotide biosynthesis.


Cancer Letters | 1997

Constitutive endonuclease to induce high molecular weight or internucleosomal DNA fragmentation in freshly isolated leukemia cells

Akihiro Kataoka; Masaru Kubota; Ikuya Usami; Akiro Okuda; Ying Wei Lin; Seiji Koishi; Machiko Sawada; Yuichi Akiyama; Kenshi Furusho

Using an autodigestion method, we investigated endogenous endonuclease(s) in leukemia cells freshly obtained from pediatric patients with various types of leukemia. Endonucleolytic activity was found to cause both high molecular weight and internucleosomal DNA fragmentation at a neutral pH in whole cell lysates of all common acute lymphoblastic leukemia (cALL) blasts, which was Mg2+-dependent and Ca2+-independent. Whole lysates from most acute myeloblastic leukemia (AML) cells possessed similar endonuclease activity, but both Mg2+ and Ca2+ were required for the activity. Our results suggest that leukemia cells of different lineages have distinct constitutive endonucleases, which may play a role in the occurrence of apoptosis in these cells.

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