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lncRNA | Tissue/model | Regulation | Pathway targeted by the lncRNAs | References |
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AS UCHL1 | (1) MN9D cells treated with MPP+ | Down | AS Uchl1 RNA, as a component of Nurr1-dependent gene network and target of cellular stress, extended the understanding on the role of antisense transcription in the brain | [28] |
(2) DA neurons from PD model treated with MPP+ |
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HAGLROS | MPTP-induced PD mice and SH-SY5Y cells treated with MPP+ | Up | Suppression of HAGLRO decreased apoptosis and autophagy in both in vivo and in vitro PD models | [29] |
HAGLRO negatively regulated miR-100 expression |
Suppression of HAGLROS alleviated MPP(+)-intoxicated SH-SY5Y cell injury by activating PI3K/AKT/mTOR pathway |
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HOTAIR | SH-SY5Y cells treated with MPP+ | Up | With HOTAIR overexpression in SH-SY5Y cells, the expression of LRRK2 increased compared with that in the control | [30] |
HOTAIR knockdown provided protection against MPP(+)-induced DA neuronal apoptosis by repressing caspase 3 activity |
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MALAT1 | MPTP-induced PD mice and SH-SY5Y cells treated with MPP+ | Up | MALAT1 knockdown attenuated MPTP-induced apoptosis of DA neurons in MPTP-induced PD mouse model | [31] |
MALAT1 interacted with miR-124 to negatively regulate its expression |
MPTP-induced PD mice and SH-SY5Y cells treated with MPP+ | Up | MALAT1 was associated with a-synuclein, leading to the increased stability of a-synuclein and its expression | [32] |
MPTP-induced PD mice and MN9D cells treated with MPP+ | Up | MALAT1/miR-205-5p axis regulates MPP(+)-induced apoptosis in MN9D cells by targeting LRRK2 | [33] |
MPTP-induced PD mice and SH-SY5Y cells treated with MPP+ | Up | MALAT1 knockdown attenuated MPP(+)-induced apoptosis of DA neurons in SH-SY5Y cells | [34] |
MALAT1 regulates DAPK1 expression by targeting miR-124-3p | |
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MAPT-AS1 | Brain tissue samples (10 patients with PD and 10 controls) | Down | MAPT-AS1 and DNMT1 have been identified as potential epigenetic regulators of MAPT expression in PD | [35] |
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Mirt2 | SY5Y cells treated with TNF-α | Down | Mirt2 exhibited anti-inflammatory properties through miR-101 suppression | [36] |
Mirt2 blocked TNFα-triggered NF-κB/p38MAPK pathway |
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NEAT1 | MPTP-induced PD mice and SH-SY5Y cells treated with MPP+ | Up | NEAT1 knockdown promoted cell viability and suppressed cell apoptosis | [37] |
Downregulation of NEAT1 also decreased the ratio of Bax/Bcl-2, the activity of caspase-3, as well as the expression of α-synuclein |
MPTP-induced PD mice and SH-SY5Y cells treated with MPP+ | Up | NEAT1 positively regulated the protein level of PINK1 through inhibition of PINK1 protein degradation | [38] |
NEAT1 knockdown could effectively suppress MPTP-induced autophagy that alleviated dopaminergic neuronal injury |
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lincRNA-p21 | SH-SY5Y cells treated with MPP+ | Up | lincRNA-p21 regulated MPP(+)-induced neuronal injury by sponging miR-625 and upregulating TRPM2 in SH-SY5Y cells | [39] |
MPTP-induced PD mice and SH-SY5Y cells treated with MPP+ | Up | lincRNA-p21 sponged miR-1277-5p and indirectly increased the expression of α-synuclein to suppress viability and activate apoptosis in SH-SY5Y cells | [40] |
MPTP-induced PD mice and SH-SY5Y cells treated with a CM transfer system were used to determine the impact of LPS-treated BV2 cells | Up | p53/lincRNA-p21, together with miR-181/PKC-δ, formed a double-negative feedback loop that facilitated sustained microglial activation and the deterioration of neurodegeneration | [41] |
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SNHG1 | MPTP-induced PD mice and SH-SY5Y cells treated with MPP+ | Up | SNHG1 could directly bind to miR-15-5p and repress miR-15-5p expression | [42] |
Upregulation of miR-15b-5p alleviated α-synuclein aggregation and apoptosis by targeting SIAH1 |
SNHG1 knockdown inhibited α-synuclein aggregation and α-synuclein-induced apoptosis |
MN9D cells treated with MPP+ | Up | SNHG1 could competitively bind to the miR-221/222 cluster and indirectly regulate the expression of p27/mTOR | [43] |
SH-SY5Y cells treated with MPP+ | Up | SNHG1 overexpression lowered viability and enhanced apoptosis in MPP(+)-treated SH-SY5Y cells. | [44] |
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H19 | MPTP-induced PD mice and human neuroblastoma cells treated with MPP+ | Down | H19 attenuates apoptosis in MPTP-induced Parkinson's disease | [45] |
H19/miR-585-3p axis regulates MPP(+)-induced apoptosis in human neuroblastoma cells cells by targeting PIK3R3 |
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UCA1 | 6-OHDA-induced PD rat | Up | Downregulation of lncRNA UCA1 ameliorates the damage of dopaminergic neurons, reduces oxidative stress and inflammation in PD rats | [46] |
Downregulation of lncRNA UCA1 inhibits the PI3K/Akt signaling pathway. |
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