Autoantibody Against one of the Antioxidant Repair Enzymes, Methionine Sulfoxide Reductase A (MSRA), in Systemic Sclerosis: Association with Pulmonary Fibrosis and Vascular Damage

Purpose: For protecting oxidative injuries, cell contains multiple antioxidant mechanisms. Methionine sulfoxide reductase A (MSRA) is one of the antioxidant enzyme peptides, which repairs oxidized methionine, methionine sulfoxide, into methionine. Recently, MSRA is suggested to play a protective rol...

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Published inNihon Rinsho Men'eki Gakkai Sokai Shorokushu Vol. 35; p. 41
Main Authors 小川, 文秀, 小村, 一浩, 原, 肇秀, 佐藤, 伸一, 清水, 和宏, 室井, 栄治
Format Journal Article
LanguageJapanese
Published 日本臨床免疫学会 2007
The Japan Society for Clinical Immunology
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Online AccessGet full text
ISSN1880-3296
DOI10.14906/jscisho.35.0.41.0

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Abstract Purpose: For protecting oxidative injuries, cell contains multiple antioxidant mechanisms. Methionine sulfoxide reductase A (MSRA) is one of the antioxidant enzyme peptides, which repairs oxidized methionine, methionine sulfoxide, into methionine. Recently, MSRA is suggested to play a protective role against oxidative stress including ischemic/hypoxic injury.Methods: Serum anti-MSRA autoantibody (Ab) levels were examined in 70 patients with SSc by ELISA.Results: Serum anti-MSRA Ab levels were significantly elevated in SSc patients compared to normal controls (mean ± SD; 0.70 ± 0.29, n=70 vs. 0.52 ± 0.15, n=23; p<0.01). Regarding the disease subset, anti-MSRA Ab levels were similar between patients with diffuse cutaneous SSc (n=40) and those with limited cutaneous SSc (n=30). Concerning clinical correlation, anti-MSRA Ab levels significantly increased in SSc patients with pulmonary fibrosis (p<0.05), cardiac involvement (p<0.05), or decreased total antioxidant power (p<0.05) compared with those without pulmonary fibrosis, cardiac disease, or decreased total anti oxidant power. Furthermore, anti-MSRA Ab levels correlated negatively with %VC (r=-0.37, p<0.05) and %DLco (r=-0.26, p<0.05), and positively with renal vascular resistance determined as the PI value (r=0.31, p<0.05). MSRA activity was significantly inhibited by anti-MSRA Ab in the serum of SSc patients.Conclusion: These results suggest that anti-MSRA Ab contributes to the development of the disease severity and activity in SSc by inhibiting one of the antioxidant repair enzymes, MSRA.
AbstractList Purpose: For protecting oxidative injuries, cell contains multiple antioxidant mechanisms. Methionine sulfoxide reductase A (MSRA) is one of the antioxidant enzyme peptides, which repairs oxidized methionine, methionine sulfoxide, into methionine. Recently, MSRA is suggested to play a protective role against oxidative stress including ischemic/hypoxic injury.Methods: Serum anti-MSRA autoantibody (Ab) levels were examined in 70 patients with SSc by ELISA.Results: Serum anti-MSRA Ab levels were significantly elevated in SSc patients compared to normal controls (mean ± SD; 0.70 ± 0.29, n=70 vs. 0.52 ± 0.15, n=23; p<0.01). Regarding the disease subset, anti-MSRA Ab levels were similar between patients with diffuse cutaneous SSc (n=40) and those with limited cutaneous SSc (n=30). Concerning clinical correlation, anti-MSRA Ab levels significantly increased in SSc patients with pulmonary fibrosis (p<0.05), cardiac involvement (p<0.05), or decreased total antioxidant power (p<0.05) compared with those without pulmonary fibrosis, cardiac disease, or decreased total anti oxidant power. Furthermore, anti-MSRA Ab levels correlated negatively with %VC (r=-0.37, p<0.05) and %DLco (r=-0.26, p<0.05), and positively with renal vascular resistance determined as the PI value (r=0.31, p<0.05). MSRA activity was significantly inhibited by anti-MSRA Ab in the serum of SSc patients.Conclusion: These results suggest that anti-MSRA Ab contributes to the development of the disease severity and activity in SSc by inhibiting one of the antioxidant repair enzymes, MSRA.
Purpose: For protecting oxidative injuries, cell contains multiple antioxidant mechanisms. Methionine sulfoxide reductase A (MSRA) is one of the antioxidant enzyme peptides, which repairs oxidized methionine, methionine sulfoxide, into methionine. Recently, MSRA is suggested to play a protective role against oxidative stress including ischemic/hypoxic injury. Methods: Serum anti-MSRA autoantibody (Ab) levels were examined in 70 patients with SSc by ELISA. Results: Serum anti-MSRA Ab levels were significantly elevated in SSc patients compared to normal controls (mean ± SD; 0.70 ± 0.29, n=70 vs. 0.52 ± 0.15, n=23; p<0.01). Regarding the disease subset, anti-MSRA Ab levels were similar between patients with diffuse cutaneous SSc (n=40) and those with limited cutaneous SSc (n=30). Concerning clinical correlation, anti-MSRA Ab levels significantly increased in SSc patients with pulmonary fibrosis (p<0.05), cardiac involvement (p<0.05), or decreased total antioxidant power (p<0.05) compared with those without pulmonary fibrosis, cardiac disease, or decreased total anti oxidant power. Furthermore, anti-MSRA Ab levels correlated negatively with %VC (r=-0.37, p<0.05) and %DLco (r=-0.26, p<0.05), and positively with renal vascular resistance determined as the PI value (r=0.31, p<0.05). MSRA activity was significantly inhibited by anti-MSRA Ab in the serum of SSc patients. Conclusion: These results suggest that anti-MSRA Ab contributes to the development of the disease severity and activity in SSc by inhibiting one of the antioxidant repair enzymes, MSRA.
Author 清水, 和宏
小川, 文秀
小村, 一浩
室井, 栄治
佐藤, 伸一
原, 肇秀
Author_FL 小村 一浩
原 肇秀
佐藤 伸一
小川 文秀
清水 和宏
室井 栄治
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Nihon Rinsho Men'eki Gakkai Sokai Shorokushu
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The Japan Society for Clinical Immunology
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Snippet Purpose: For protecting oxidative injuries, cell contains multiple antioxidant mechanisms. Methionine sulfoxide reductase A (MSRA) is one of the antioxidant...
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SubjectTerms methionine sulfoxide reductase A
Oxidative stress
pulmonary fibrosis
Systemic sclerosis
vascular damage
Title Autoantibody Against one of the Antioxidant Repair Enzymes, Methionine Sulfoxide Reductase A (MSRA), in Systemic Sclerosis: Association with Pulmonary Fibrosis and Vascular Damage
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