Kefeng Lv1, Yuhua Liu2, Yanbing Zheng2, Shaowen Dai2, Peifeng Yin2, Haifeng Miao3. 1. Department of Neurology, Affiliated Dongguan People's Hospital, Southern Medical University (Dongguan People's Hospital), Guangdong Province, 523059, Dongguan, People's Republic of China. 2. Department of General Practice, Affiliated Dongguan People's Hospital, Southern Medical University (Dongguan People's Hospital), 3 South Wandao Road, Wanjiang District, 523059, Dongguan, Guangdong Province, People's Republic of China. 3. Department of General Practice, Affiliated Dongguan People's Hospital, Southern Medical University (Dongguan People's Hospital), 3 South Wandao Road, Wanjiang District, 523059, Dongguan, Guangdong Province, People's Republic of China. gdmiaohf@163.com.
Abstract
BACKGROUNDS: Parkinson's disease (PD) is a common age-related neurodegenerative disorder worldwide. This research aimed to investigate the effects and mechanism underlying long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in PD. METHODS: SK-N-SH and SK-N-BE cells were treated with MPP+ to establish the MPP+-stimulated cell model of PD, and MALAT1 expression was determined. Then, the effects of MALAT1 depletion on cell proliferation and apoptosis were determined in the MPP+-stimulated cell model of PD. Besides, the correlations between microRNA-135b-5p (miR-135b-5p) and MALAT1 or glycoprotein nonmetastatic melanoma protein B (GPNMB) in MPP+-stimulated cell model of PD were explored. RESULTS: MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP+-stimulated cells. Besides, miR-135b-5p was a target of MALAT1 and directly targeted to GPNMB. Further investigation indicated that suppression of MALAT1 regulated cell proliferation and apoptosis by miR-135b-5p/GPNMB axis. CONCLUSION: Our findings reveal that MALAT1/miR-135b-5p/GPNMB axis regulated cell proliferation and apoptosis in MPP+-stimulated cell model of PD, providing a potential biomarker and therapeutic target for PD.
BACKGROUNDS: Parkinson's disease (PD) is a common age-related neurodegenerative disorder worldwide. This research aimed to investigate the effects and mechanism underlying long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in PD. METHODS:SK-N-SH and SK-N-BE cells were treated with MPP+ to establish the MPP+-stimulated cell model of PD, and MALAT1 expression was determined. Then, the effects of MALAT1 depletion on cell proliferation and apoptosis were determined in the MPP+-stimulated cell model of PD. Besides, the correlations between microRNA-135b-5p (miR-135b-5p) and MALAT1 or glycoprotein nonmetastatic melanoma protein B (GPNMB) in MPP+-stimulated cell model of PD were explored. RESULTS:MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP+-stimulated cells. Besides, miR-135b-5p was a target of MALAT1 and directly targeted to GPNMB. Further investigation indicated that suppression of MALAT1 regulated cell proliferation and apoptosis by miR-135b-5p/GPNMB axis. CONCLUSION: Our findings reveal that MALAT1/miR-135b-5p/GPNMB axis regulated cell proliferation and apoptosis in MPP+-stimulated cell model of PD, providing a potential biomarker and therapeutic target for PD.
Authors: M Shioya; S Obayashi; H Tabunoki; K Arima; Y Saito; T Ishida; J Satoh Journal: Neuropathol Appl Neurobiol Date: 2010-02-25 Impact factor: 8.090
Authors: Frank Szulzewsky; Andreas Pelz; Xi Feng; Michael Synowitz; Darko Markovic; Thomas Langmann; Inge R Holtman; Xi Wang; Bart J L Eggen; Hendrikus W G M Boddeke; Dolores Hambardzumyan; Susanne A Wolf; Helmut Kettenmann Journal: PLoS One Date: 2015-02-06 Impact factor: 3.240