CSF angiotensin II and angiotensin-converting enzyme levels in anti-aquaporin-4 autoimmunity

Takuya Matsushita, Noriko Isobe, M. Kawajiri, M. Mogi, K. Tsukuda, M. Horiuchi, Y. Ohyagi, Jun-Ichi Kira

研究成果: ジャーナルへの寄稿記事

10 引用 (Scopus)

抄録

Background: Anti-aquaporin-4 (AQP4) antibody targets perivascular astrocyte foot processes, which contain abundant angiotensinogen, a precursor of angiotensin II, angiotensin-converting enzyme (ACE) and ACE2. Objective: To disclose any abnormality in the intrathecal angiotensin II metabolic pathway in Japanese patients with neuromyelitis optica (NMO) or NMO spectrum disorders (NMOs) and positive for anti-AQP4 antibody. Methods: We measured CSF angiotensin II, ACE and ACE2 levels in 15 anti-AQP4 antibody-positive patients with NMO or NMOs, 21 anti-AQP4 antibody-negative multiple sclerosis (MS) patients, 32 patients with other neurological diseases (OND) and 24 non-neurologic controls, using established ELISAs. Results: CSF angiotensin II levels were lower in patients with NMO/NMOs (2.01 ± 1.82 pg/ml) and those with MS (3.15 ± 1.67 pg/ml) than in the OND (5.41 ± 2.34 pg/ml) and control groups (6.71 ± 2.65 pg/ml) (Pcorr < 0.005). The difference in CSF angiotensin II levels between NMO/NMOs and MS patients was nearly significant (Puncorr = 0.052). In NMO/NMOs and MS patients, angiotensin II levels were negatively correlated with CSF/serum albumin ratio (P < 0.05). ACE levels in CSF were lower in patients with NMO/NMOs (34.3 ± 5.61 ng/ml) than in MS patients (42.5 ± 8.19 ng/ml, Pcorr = 0.035) and controls (44.7 ± 4.02 ng/ml, Pcorr < 0.0003) while ACE2 levels were lower in NMO/NMOs (1.13 ± 0.49 ng/ml) and MS (1.75 ± 0.86 ng/ml) patients than in controls (2.76 ± 0.23 ng/ml, Pcorr < 0.001 for both). Conclusion: CSF angiotensin II, ACE, and ACE2 levels are decreased in NMO/NMOs patients with anti-AQP4 antibody, reflecting severe destruction of perivascular astrocytes.

元の言語英語
ページ(範囲)41-45
ページ数5
ジャーナルJournal of the Neurological Sciences
295
発行部数1-2
DOI
出版物ステータス出版済み - 8 15 2010

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Aquaporin 4
Neuromyelitis Optica
Peptidyl-Dipeptidase A
Autoimmunity
Angiotensin II
Multiple Sclerosis
Antibodies
Astrocytes
Angiotensinogen
Metabolic Networks and Pathways
Serum Albumin

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Neurology

これを引用

CSF angiotensin II and angiotensin-converting enzyme levels in anti-aquaporin-4 autoimmunity. / Matsushita, Takuya; Isobe, Noriko; Kawajiri, M.; Mogi, M.; Tsukuda, K.; Horiuchi, M.; Ohyagi, Y.; Kira, Jun-Ichi.

:: Journal of the Neurological Sciences, 巻 295, 番号 1-2, 15.08.2010, p. 41-45.

研究成果: ジャーナルへの寄稿記事

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title = "CSF angiotensin II and angiotensin-converting enzyme levels in anti-aquaporin-4 autoimmunity",
abstract = "Background: Anti-aquaporin-4 (AQP4) antibody targets perivascular astrocyte foot processes, which contain abundant angiotensinogen, a precursor of angiotensin II, angiotensin-converting enzyme (ACE) and ACE2. Objective: To disclose any abnormality in the intrathecal angiotensin II metabolic pathway in Japanese patients with neuromyelitis optica (NMO) or NMO spectrum disorders (NMOs) and positive for anti-AQP4 antibody. Methods: We measured CSF angiotensin II, ACE and ACE2 levels in 15 anti-AQP4 antibody-positive patients with NMO or NMOs, 21 anti-AQP4 antibody-negative multiple sclerosis (MS) patients, 32 patients with other neurological diseases (OND) and 24 non-neurologic controls, using established ELISAs. Results: CSF angiotensin II levels were lower in patients with NMO/NMOs (2.01 ± 1.82 pg/ml) and those with MS (3.15 ± 1.67 pg/ml) than in the OND (5.41 ± 2.34 pg/ml) and control groups (6.71 ± 2.65 pg/ml) (Pcorr < 0.005). The difference in CSF angiotensin II levels between NMO/NMOs and MS patients was nearly significant (Puncorr = 0.052). In NMO/NMOs and MS patients, angiotensin II levels were negatively correlated with CSF/serum albumin ratio (P < 0.05). ACE levels in CSF were lower in patients with NMO/NMOs (34.3 ± 5.61 ng/ml) than in MS patients (42.5 ± 8.19 ng/ml, Pcorr = 0.035) and controls (44.7 ± 4.02 ng/ml, Pcorr < 0.0003) while ACE2 levels were lower in NMO/NMOs (1.13 ± 0.49 ng/ml) and MS (1.75 ± 0.86 ng/ml) patients than in controls (2.76 ± 0.23 ng/ml, Pcorr < 0.001 for both). Conclusion: CSF angiotensin II, ACE, and ACE2 levels are decreased in NMO/NMOs patients with anti-AQP4 antibody, reflecting severe destruction of perivascular astrocytes.",
author = "Takuya Matsushita and Noriko Isobe and M. Kawajiri and M. Mogi and K. Tsukuda and M. Horiuchi and Y. Ohyagi and Jun-Ichi Kira",
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T1 - CSF angiotensin II and angiotensin-converting enzyme levels in anti-aquaporin-4 autoimmunity

AU - Matsushita, Takuya

AU - Isobe, Noriko

AU - Kawajiri, M.

AU - Mogi, M.

AU - Tsukuda, K.

AU - Horiuchi, M.

AU - Ohyagi, Y.

AU - Kira, Jun-Ichi

PY - 2010/8/15

Y1 - 2010/8/15

N2 - Background: Anti-aquaporin-4 (AQP4) antibody targets perivascular astrocyte foot processes, which contain abundant angiotensinogen, a precursor of angiotensin II, angiotensin-converting enzyme (ACE) and ACE2. Objective: To disclose any abnormality in the intrathecal angiotensin II metabolic pathway in Japanese patients with neuromyelitis optica (NMO) or NMO spectrum disorders (NMOs) and positive for anti-AQP4 antibody. Methods: We measured CSF angiotensin II, ACE and ACE2 levels in 15 anti-AQP4 antibody-positive patients with NMO or NMOs, 21 anti-AQP4 antibody-negative multiple sclerosis (MS) patients, 32 patients with other neurological diseases (OND) and 24 non-neurologic controls, using established ELISAs. Results: CSF angiotensin II levels were lower in patients with NMO/NMOs (2.01 ± 1.82 pg/ml) and those with MS (3.15 ± 1.67 pg/ml) than in the OND (5.41 ± 2.34 pg/ml) and control groups (6.71 ± 2.65 pg/ml) (Pcorr < 0.005). The difference in CSF angiotensin II levels between NMO/NMOs and MS patients was nearly significant (Puncorr = 0.052). In NMO/NMOs and MS patients, angiotensin II levels were negatively correlated with CSF/serum albumin ratio (P < 0.05). ACE levels in CSF were lower in patients with NMO/NMOs (34.3 ± 5.61 ng/ml) than in MS patients (42.5 ± 8.19 ng/ml, Pcorr = 0.035) and controls (44.7 ± 4.02 ng/ml, Pcorr < 0.0003) while ACE2 levels were lower in NMO/NMOs (1.13 ± 0.49 ng/ml) and MS (1.75 ± 0.86 ng/ml) patients than in controls (2.76 ± 0.23 ng/ml, Pcorr < 0.001 for both). Conclusion: CSF angiotensin II, ACE, and ACE2 levels are decreased in NMO/NMOs patients with anti-AQP4 antibody, reflecting severe destruction of perivascular astrocytes.

AB - Background: Anti-aquaporin-4 (AQP4) antibody targets perivascular astrocyte foot processes, which contain abundant angiotensinogen, a precursor of angiotensin II, angiotensin-converting enzyme (ACE) and ACE2. Objective: To disclose any abnormality in the intrathecal angiotensin II metabolic pathway in Japanese patients with neuromyelitis optica (NMO) or NMO spectrum disorders (NMOs) and positive for anti-AQP4 antibody. Methods: We measured CSF angiotensin II, ACE and ACE2 levels in 15 anti-AQP4 antibody-positive patients with NMO or NMOs, 21 anti-AQP4 antibody-negative multiple sclerosis (MS) patients, 32 patients with other neurological diseases (OND) and 24 non-neurologic controls, using established ELISAs. Results: CSF angiotensin II levels were lower in patients with NMO/NMOs (2.01 ± 1.82 pg/ml) and those with MS (3.15 ± 1.67 pg/ml) than in the OND (5.41 ± 2.34 pg/ml) and control groups (6.71 ± 2.65 pg/ml) (Pcorr < 0.005). The difference in CSF angiotensin II levels between NMO/NMOs and MS patients was nearly significant (Puncorr = 0.052). In NMO/NMOs and MS patients, angiotensin II levels were negatively correlated with CSF/serum albumin ratio (P < 0.05). ACE levels in CSF were lower in patients with NMO/NMOs (34.3 ± 5.61 ng/ml) than in MS patients (42.5 ± 8.19 ng/ml, Pcorr = 0.035) and controls (44.7 ± 4.02 ng/ml, Pcorr < 0.0003) while ACE2 levels were lower in NMO/NMOs (1.13 ± 0.49 ng/ml) and MS (1.75 ± 0.86 ng/ml) patients than in controls (2.76 ± 0.23 ng/ml, Pcorr < 0.001 for both). Conclusion: CSF angiotensin II, ACE, and ACE2 levels are decreased in NMO/NMOs patients with anti-AQP4 antibody, reflecting severe destruction of perivascular astrocytes.

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