ライフサイエンスコーパス: NOS-II

1 NOS II protein expression and enzyme activity were clear

2 NOS-II (inducible NOS) mRNA expression was analyzed 2, 4

3 distension and increased FIO(2) may activate NOS II release at birth.

4 ned the concomitant expression of PGHS-2 and NOS II as well as the production of prostaglandin E2 (PG

5 owever, the apparent link between PGHS-2 and NOS II has not been thoroughly investigated in nontransf

6 cted into syngeneic wild-type (NOS H+/+) and NOS II-null (NOS H-/-) C57BL/6 mice.

7 s.c. and i.v. injected into NOS II(+/+) and NOS II(-/-) C57BL/6 mice.

8 into the pancreas of syngeneic NOS II+/+ and NOS II-/- C57BL/6J mice.

9 The inducing signals for astrocyte NOS II mRNA expression were in the order IL-1beta + IFN-

10 pathway in the regulation of human astrocyte NOS II is shown, suggesting a potential role for IL-1 as

11 intact (NOS II+/+) or genetically disrupted (NOS II-/-) NOS II gene.

12 w that adenoviral vectors mediated effective NOS II gene transfer into various human tumors.

13 A retroviral vector (pMFGSNOS) encoding NOS II was used to transduce primary cultures of endothe

14 uce NO and express both NO synthase enzymes, NOS II and NOS III, and DAF protein.

15 te astrocytes, but not microglia, to express NOS II belonging to the high output nitric oxide system

16 the induction of IFN-gamma was required for NOS II-mediated antitumor activity in vivo.

17 ipopolysaccharide, macrophages isolated from NOS II+/+ C57BL/6 mice produced NO-dependent cytotoxicit

18 y in sarcoma cells, whereas macrophages from NOS II-/- C57BL/6 mice did not.

19 Our data suggest that disruption of host NOS II expression enhanced the growth and metastasis of

20 We determined the role of host NOS II expression in the growth and metastasis of the B1

21 nship between nitric oxide (NO) synthase II (NOS II) expression and the metastatic ability of tumor c

22 r the induction of nitric oxide synthase II (NOS II) gene is required for IFN-beta-mediated antitumor

23 lationship between nitric oxide synthase II (NOS II) inducibility and the metastatic ability of UV-22

24 heterogeneous expression of NO synthase II (NOS II) protein.

25 II+/+) or genetically disrupted (NOS II-/-) NOS II gene.

26 In NOS II+/+ C57BL/ 6J, both parental and control vector-tr

27 In NOS II-/- C57BL/6J mice, however, IFN-beta-secreting cel

28 Higher NO induction was detected in NOS II+/+ mice that received injections with IFN-beta-se

29 he control cells, but it was not detected in NOS II-/- mice.

30 learly detected in the tumors that formed in NOS II(+/+) mice but not in those that formed in NOS II(

31 II(+/+) mice but not in those that formed in NOS II(-/-) mice.

32 ed many more experimental lung metastases in NOS II(-/-) mice than in NOS II(+/+) mice.

33 e and larger experimental lung metastases in NOS II+/+ mice than in NOS II-/- mice, whereas M5076 cel

34 and smaller experimental lung metastases in NOS II+/+ mice than in NOS II-/- mice.

35 lung metastases in NOS II(-/-) mice than in NOS II(+/+) mice.

36 larger s.c. tumors in NOS H-/- mice than in NOS II+/+ mice.

37 al lung metastases in NOS II+/+ mice than in NOS II-/- mice, whereas M5076 cells produced fewer and s

38 al lung metastases in NOS II+/+ mice than in NOS II-/- mice.

39 We conclude that increases in NOS-II mRNA following i.c.v. administration of IL-1beta

40 icroglia, cytokines and LPS failed to induce NOS II expression, while the same stimuli readily induce

41 r activity using syngeneic mice with intact (NOS II+/+) or genetically disrupted (NOS II-/-) NOS II g

42 lines were then s.c. and i.v. injected into NOS II(+/+) and NOS II(-/-) C57BL/6 mice.

43 in vitro/in vivo selection led to stable low NOS II expression and high metastatic potential.

44 the cells expressed immunodetectable murine NOS II.

45 a method to express varied levels of murine NOS II in bovine pulmonary artery endothelial cells.

46 ng mutant NOS II genes that expressed mutant NOS II proteins with defined levels of enzymatic activit

47 eries of adenoviral vectors harboring mutant NOS II genes that expressed mutant NOS II proteins with

48 n cytokine-treated human astrocytes, neither NOS II mRNA/protein expression nor nitrite production wa

49 The nitric oxide synthases (NOS-I, neuronal, NOS-II, inducible, and NOS-III, endothelial) are the mos

50 In the present study, three NOS II-null (NOS II(-/-)) tumor cell lines, KX-dw1, KX-dw4, and KX-dw

51 Consistent with the absence of NOS II expression in the tumor stroma, KX-dw1, KX-dw4, a

52 Therefore, physiological expression of NOS II in host cells directly inhibits tumor growth and

53 Stable expression of NOS II was assessed by measuring nitrite accumulation in

54 Inhibition of NOS II activity in vivo significantly promoted distant l

55 tagonist exerted near complete inhibition of NOS II mRNA and nitrite induction.

56 cells, concomitant with an enhanced level of NOS II activity.

57 scites, whereas those having a high level of NOS II expression did not.

58 ata indicate that a low to moderate level of NOS II expression directly correlates with metastatic ab

59 eic C57BL/6 mice, clones with a low level of NOS II expression produced tumors in pancreas, metastasi

60 tastatic variants exhibited a lower level of NOS II expression than the parental Panc02 cell line did

61 ntal Panc02 cells exhibiting a high level of NOS II expression, these variants had a decreased level

62 ion, these variants had a decreased level of NOS II expression.

63 metastatic clones exhibited higher levels of NOS II than did poorly metastatic clones in response to

64 onal sublines expressing different levels of NOS II were then established using a limited dilution te

65 Overexpression of NOS II in a highly metastatic clone by transfection with

66 However, the phenotypes of NOS II induction and metastatic ability were unstable.

67 Finally, to further confirm the role of NOS II expression derived from tumor cells in metastasis

68 tissue, that the anatomical distribution of NOS-II mRNA is consistent with the distribution of NO pr

69 Increased expression of NOS-II mRNA was observed surrounding the microinjection

70 of inducible nitric oxide synthase (iNOS or NOS II).

71 of inducible nitric oxide synthase (iNOS or NOS-II) leading to the production of large amounts of ni

72 However, the impact of this physiological NOS II expression in host cells on tumor growth and meta

73 t birth, we studied the effects of selective NOS II antagonists N-(3-aminomethyl) benzylacetamidine d

74 We conclude that selective NOS II inhibition is as effective as nonselective NOS bl

75 (LPS) were greatly reduced by two selective NOS II inhibitors, L-NIL and SMT.

76 mained intact after treatment with selective NOS II antagonists but not after treatment with nonselec

77 res revealed an approximately 130-kDa single NOS II band that was expressed strongly at 48 and 72 h (

78 Specific NOS II immunoreactivity was detected in cytokine-treated

79 were injected into the pancreas of syngeneic NOS II(-/-) mice, and groups of mice received i.p. injec

80 lly implanted into the pancreas of syngeneic NOS II+/+ and NOS II-/- C57BL/6J mice.

81 rmine whether type II nitric oxide synthase (NOS II) contributes to the NO-mediated fall in pulmonary

82 trated that inducible nitric oxide synthase (NOS II) expression and nitric oxide (NO) production are

83 e (NO*), generated by nitric oxide synthase (NOS II) from immunostimulated cells during infection, pl

84 tion of the inducible nitric oxide synthase (NOS II) gene requires a combination of interferon-gamma

85 h augmented inducible nitric oxide synthase (NOS II).

86 Immunostaining analyses indicated that NOS II expression was apparent in the metastases growing

87 Based upon these results, we propose that NOS II is a mediator of the vascular response to oxygen

88 PCR analysis of the whole lung revealed that NOS II expression appeared to be similar in both of the

89 Collectively, these data show that NOS II expression is highly heterogeneous and dynamicall

90 ary vasodilation at birth and speculate that NOS II activity contributes to NO-mediated pulmonary vas

91 The NOS II-transduced endothelial cells were cultured on the

92 w and high FIO(2) to a similar degree as the NOS II antagonists.

93 To test the selectivity of the NOS II antagonists, we studied the effects of acetylchol

94 However, use of the NOS II gene in cancer therapy is problematic because of

95 Tumor cells transduced with these NOS II genes produced NO at different levels, which dire

96 In the present study, three NOS II-null (NOS II(-/-)) tumor cell lines, KX-dw1, KX-d

97 Also, induction of IFN-gamma correlated with NOS II gene expression and NO production in IFN-gamma(+/

98 highly metastatic clone by transfection with NOS II gene retarded tumor growth and completely suppres