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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 충북대학교 동물의학연구소 Journal of Biomedical and Translational Research Journal of Biomedical and Translational Research 제21권 제4호
- 발행연도
- 2020.1
- 수록면
- 143 - 151 (9page)
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초록· 키워드
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Amyotrophic lateral sclerosis (ALS) is progressive neurological disease that results in the death of motor neurons in the brain and spinal cord, leading to a decrease in skeletal muscle size and muscle weakness, wasting, or paralysis. Most research on ALS has focused on motor neuron death, and the underlying mechanisms are not well understood. This study examined the molecular mechanisms underlying muscle degeneration. We compared the protein and cytokine profiles of gastrocnemius muscle in ALS model hSOD1G93A mice at pre-symptomatic and symptomatic stages by western blotting. Pro-inflammatory factors including tumor necrosis factor-α, interleukin (IL)-1β and IL-6, and cluster of differentiation 11b were upregulated in the muscle of symptomatic as compared to pre-symptomatic mice. Additionally, the levels of oxidative stress-related proteins, heme oxygenase-1 and ferritin, were increased in muscle from symptomatic as compared to pre-symptomatic mice. We also observed increased autophagy dysfunction and metabolic dysregulation in the muscles of symptomatic hSOD1G93A as compared to non-Tg and pre-symptomatic hSOD1G93A mice, which was accompanied by upregulation of thrombospondin-1, Prospero-related homeobox 1, glial fibrillary acidic protein, and DNA-damage-inducible 45α. Increased inflammation, oxidative stress, and autophagy contribute to motor neuron death and muscle atrophy in ALS, and the factors involved in these processes are potential therapeutic targets for treatment of this disease.
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참고문헌 (41)
참고문헌 신청
Rosen DR / 1993 / Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis / Nature 362:59~62
Paez-Colasante X / 2015 / Amyotrophic lateral sclerosis : mechanisms and therapeutics in the epigenomic era / Nat Rev Neurol 11:266~279
Cai M / 2016 / Ginsenoside re attenuates neuroinflammation in a symptomatic ALS animal model / Am J Chin Med 44:401~413
Chiu IM / 2008 / T lymphocytes potentiate endogenous neuroprotective inflammation in a mouse model of ALS / Proc Natl Acad Sci USA 105:17913~17918
Tjust AE / 2017 / Impact of amyotrophic lateral sclerosis on slow tonic myofiber composition in human extraocular muscles / Invest Ophthalmol Vis Sci 58:3708~3715
Paez-Colasante X / 2015 / Amyotrophic lateral sclerosis : mechanisms and therapeutics in the epigenomic era / Nat Rev Neurol 11:266~279
Cai M / 2016 / Ginsenoside re attenuates neuroinflammation in a symptomatic ALS animal model / Am J Chin Med 44:401~413
Chiu IM / 2008 / T lymphocytes potentiate endogenous neuroprotective inflammation in a mouse model of ALS / Proc Natl Acad Sci USA 105:17913~17918
Tjust AE / 2017 / Impact of amyotrophic lateral sclerosis on slow tonic myofiber composition in human extraocular muscles / Invest Ophthalmol Vis Sci 58:3708~3715
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