From: Emerging roles and mechanisms of miR-206 in human disorders: a comprehensive review
Type of disease | Expression Pattern | Samples | Animal studies/cell lines | Downstream targets | Pathway | Function | Kaplan–Meier | Refs. |
---|---|---|---|---|---|---|---|---|
Amyotrophic Lateral Sclerosis (ALS) | Up-regulation | 27 sporadic ALS patients and 25 control subjects | – | – | – | miR-206 contributes in ALS progression, so act as a longitudinal biomarker | – | [59] |
Alzheimer’s disease (AD) | Up-regulation | 128 subjects with amnestic mild cognitive impairment (aMCI) who progressed to AD (aMCI-AD) and 330 subjects who maintained and aMCI (aMCI- aMCI) diagnosis | – | Brain-derived neurotrophic factor (BDNF) | – | miR-206 plays a key role in the progression of aMCI to AD by targeting BDNF | A significant AD conversion trend for aMCI patients having high levels of miR-206 | [60] |
Up-regulation | 24 olfactory epithelia of early dementia patients, 8 Patients with significant depression and 9 cognitively healthy controls | – | BDNF | – | miR-206 increases from the MCI stage, and shows excellent sensitivity and specificity for diagnosing CDR1 dementia | – | [61] | |
Up-regulation | – | Tg2576 AD transgenic mice, Neuro-2a | BDNF | – | miR-206 contributes in the pathogenesis of AD by suppressing BDNF expression | – | [62] | |
– | – | 36 C57 mice | BDNF | – | miR-206-3p protects neurons via up- regulation of BDNF after the onset of AD. Exogenous miR-206-3p further ameliorates the neuronal morphology, and improves the cognitive ability and memory of AD mice | – | [63] | |
Up-regulation | – | SHSy5y, APP/PS1 mice | BDNF | – | miR-206 induces cell death via downregulating the expression of BDNF | – | [64] | |
Atherosclerosis (AS) | Down-regulation (treated with ox-LDL) | – | HUVECs and 293 T | RAB22A | – | MIAT targeted miR-206 and promoted cell viability, invasion, migration, and EMT | – | [65] |
Bronchopulmonary dysplasia (BPD) | Down-regulation | – | AECII, old Sprague–Dawley female rats | – | – | miR-206 inhibits FN1 expression and proliferation | – | [66] |
Coronary Artery Disease (CAD) | Up-regulation | 78 CAD patients and 65 healthy cases | – | vascular endothelial growth factor (VEGF) | VEGF | miR-206 inhibited cell viability and invasion, promoted apoptosis, and has some protective roles in CAD | – | [67] |
Up-regulation | 53 Peripheral blood mononuclear cells CAD and 34 healthy cases | Nude mice | PIK3C2a | PI3K/Akt/eNOS | miR-206 downregulated angiogenesis by repression of the PI3K/Akt/eNOS signaling | – | [68] | |
Chronic obstructive pulmonary disease (COPD) | Up-regulation | 44 tissue samples of patients | HPMECs | Notch3, and VEGFA | Notch and VEGFA | Up-regulation of miR-206 promoted cell apoptosis by repressing Notch3, and VEGFA | – | [69] |
Duchene muscular dystrophy (DMD) | Up-regulation | – | Mdx mice | Notch3, Igfbp5 | – | miR -206 induced satellite cell differentiation into muscle fibers through inhibiting negative myogenesis regulators. miR-206 slows progression of DMD | – | [70] |
Up-regulation | 39 DMD patients and 36 healthy controls | – | – | – | miR-206, related to low muscle strength, muscle function, and quality of life | – | [71] | |
Epilepsy | Down-regulation | – | Male Sprague–Dawley rats | C–C Motif Chemokine Ligand 2 (CCL2) | – | miR-206 suppresses epilepsy and seizure-induced brain damage through targeting CCL2 | – | [72] |
Non-alcoholic fatty liver disease (NAFLD) | Down-regulation | – | 24 high-fat diet (HFD) feeding mouse, Huh-7 and HepG2 | ROCK1 | ROCK1/AMPK | miR-206 inhibited lipogenesis via targeting ROCK1 and repressed triglyceride secretion which contributed to NAFLD development and progression | – | [73] |
Hirschsprung (HSCR) | Down-regulation | 80 HSCR cases and 80 matched controls | 293 T and SH-SY5Y | SDPR (serum deprivation response), FN1(fibronectin 1) and PAX3(paired box 3) | – | miR-206 inhibited cell migration and proliferation by up-regulation of SDPR | – | [74] |
Legg-Calvé-Perthes disease (LCPD) | Up-regulation | 20 LSPD tissue and 20 normal patients with repair surgery after fracture | TC28 | SOX9 | – | Up-regulation of miR-206 promoted cell apoptosis by repressing SOX9 | – | [75] |
Limb-girdle muscular dystrophies (LGMD) | Up-regulation | 11 LGMD patients | – | – | – | Up-regulation of miR-206 occurs during skeletal muscle regeneration | – | [76] |
Muscular dystrophies | Up-regulation (in BMD and DMD patient) | 48 patients with DMD, DM1, LGMD, LGMD2B, FSHD, BMD, and DMRV and healthy controls | C57Bl/10SnSlc mice, mdx mice | – | – | miR-206 levels in mouse serum are up-regulated upon skeletal muscle regeneration | – | [77] |
Pulmonary arterial hypertension (PAH) | Down-regulation | – | HPASMCs,mice | Notch3 | Up-regulation of miR-206 inhibited migration, proliferation, contraction and enhanced apoptosis in PASMC’s of hypoxia induced PAH mice | – | [78] | |
Sepsis | Up-regulation | 63 blood samples of Sepsis and 30 Septic Shock and 28 healthy controls | – | Cx43 | – | miR-206 regulates the barrier function of ATII cells in sepsis-related acute lung injury through regulating expression of Cx43 | – | [79] |
Spinal muscular atrophy (SMA) | Up-regulation | – | 80 WT mice and 74 SMA mice, PC12 | SLC8A2 | – | miR-206 decreases severity of SMA pathology, progression, increases survival rate and improved behavioral performance of mice | – | [80] |
Ulcerative colitis (UC) | Down-regulation (In mesalamine-treated patients) | 10 established UC patients | HT29 | A3 adenosine receptor (A3AR) | – | miR-206 acts as a pro-inflammatory factor through direct suppression of A3AR expression | – | [81] |