Abstract

BackgroundsParkinson’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.MethodsSK-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.ResultsMALAT1 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.ConclusionOur 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.

Highlights

  • Parkinson’s disease (PD) is the second-most common neurodegenerative disease characterized by static tremors, bradykinesia, and cognitive dysfunction [1, 2]

  • Further investigation indicated that suppression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) regulated cell proliferation and apoptosis by miR135b-5p/glycoprotein nonmetastatic melanoma protein B (GPNMB) axis

  • 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

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Summary

Introduction

Parkinson’s disease (PD) is the second-most common neurodegenerative disease characterized by static tremors, bradykinesia, and cognitive dysfunction [1, 2]. Approximately 1.7% of the Chinese population older than 65 years suffer from PD, which brings a heavy burden to patients’ families and society [3]. Mounting evidence suggested that PD is associated with multiple factors, such as inflammatory. Lv et al Biol Res (2021) 54:10 response, oxidative stress, and cell apoptosis [4]. There is numerous evidence suggesting that neuroinflammation is related to neurodegeneration in diverse neurological diseases [5]. Despite several alternative therapies used in clinical medicine, effective treatment for PD is still limited [6]. A better understanding of mechanism underlying PD and finding effective strategies for PD is urgently needed

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