Plasma MicroRNA Expression Profiles in Psoriasis

Xiao, Shiju; Liu, Xin; Wang, Xiaoxu; Lv, Hongpeng; Zhao, Junbo; Guo, Xinwei; Xian, Fuyang; Ji, Yunrun; Zhang, Guangzhong

doi:10.1155/2020/1561278

Cited by 15 publications

(17 citation statements)

References 77 publications

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“…Our previous study shows several specific plasma miRNA-targeted pathways associated with psoriasis, such as the VEGF, PI3K/Akt, and WNT signaling pathways, which are regulating angiogenesis in psoriasis [ 3 ]. We also found the amelioration in angiogenesis restricted the occurrence, persistence, and recurrence of psoriasis.…”

Section: Introductionmentioning

confidence: 99%

Yangxue Jiedu Fang Ameliorates Psoriasis by Regulating Vascular Regression via Survivin/PI3K/Akt Pathway

Liu

Chen

et al. 2021

Journal of Immunology Research

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Background. Psoriasis (PA) is a chronic autoimmune disease of the skin that adversely affects patients’ quality of life. Yangxue Jiedu Fang (YXJD) has been used for decades to treat psoriasis in China. However, its antipsoriatic mechanisms are still poorly understood. In this study, we explored the effects of YXJD on angiogenesis and apoptosis of microvessels in PA, the underlying mechanisms in HUVEC cells transfected by Survivin overexpression plasmid and in a mouse model of imiquimod-induced psoriasis and the relationship between VEGF (vascular endothelial growth factor) and Survivin. Methods. A BALB/c mouse model of imiquimod- (IMQ-) induced PA was established, and the mice were treated with YXJD. Cell viability was assessed by CCK8 assay. Apoptosis was detected by annexin V–FITC/PI double-staining and caspase-3 assays. The PI3K/Akt/β-catenin pathway was analyzed by western blotting, ELISA, and immunochemical analysis. Results. YXJD ameliorated symptoms and psoriasis area and severity index (PASI) scores and also reduced the number of microvessels, as determined by the microvessel density (MVD). The expression of apoptotic protein Survivin in endothelial cells, autophagy-related proteins p62, and angiogenic proteins VEGF was inhibited by YXJD, and the repressed expression of LC3II/I increased by YXJD. The proteins related to the PI3K/Akt pathway and β-catenin expression and the nuclear entry of β-catenin were reduced in IMQ-induced PA mice treated with YXJD. In HUVEC cells transfected by Survivin overexpression plasmid, we observed YXJD regulated the expression of Survivin, LC3II/I, and p62, VEGF, and PI3K/Akt pathway-relative proteins and the nuclear entry of β-catenin. Conclusions. YXJD inhibited the expression of Survivin via PI3K/Akt pathway to adjust apoptosis, autophagy, and angiogenesis of microvessels and thus improve the vascular sustainability in psoriasis. YXJD may represent a new direction of drug research and development for immunomodulatory therapy for psoriasis.

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Section: Introductionmentioning

confidence: 99%

Yangxue Jiedu Fang Ameliorates Psoriasis by Regulating Vascular Regression via Survivin/PI3K/Akt Pathway

Liu

Chen

et al. 2021

Journal of Immunology Research

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“…Notably, this miRNA has been reported to affect the pathogenesis of psoriasis. miR-214-3p has been among miRNAs with the highest degree in the network analyses of dysregulated miRNAs and their targets in plasma samples of patients with psoriasis (Xiao et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Association analysis of MALAT1 polymorphisms and risk of psoriasis among Iranian patients

Ghafouri‐Fard

Gholipour

Abak

et al. 2021

Int J Immunogenetics

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MALAT1 is a long non-coding transcript that affects immune reactions, thus being involved in the pathoaetiology of immune-related conditions. We investigated the associations between two genetic variants in MALAT1 and susceptibility to psoriasis in the Iranian population. The G allele of rs619586 has been shown to be less common among cases versus controls (odds ratios (OR; 95% confidence intervals (CI)) = 0.57 (0.36-0.9)), adjusted p = .02). This single nucleotide polymorphism has been associated with the risk of psoriasis in a dominant model (AG + GG vs. AA: OR (95% CI) = 0.56 (0.35-0.92), adjusted p = .04) as well as log-additive model (OR (95% CI) = 0.59 (0.38-0.92), adjusted p = .04). The rs3200401 was not associated with psoriasis in any of the supposed inheritance models. This study potentiates rs619586 as a risk locus for psoriasis in the Iranian population.

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“…upregulated in the MNCs from the two trial groups with fold change > 2 are associated with cell proliferation, migration, and inflammation [19,20]. Moreover, numerous miRNAs (hsa-miR-185-5p, -151a-3p, -320b, -4521, -548o-3p, -7-5p, -942-5p, -30a-3p, and -30e-3p) that were observed to increase with fold change of 1.5-3 in the MNCs from the TIME and LateTIME trials group are associated with inflammation [21][22][23][24][25][26][27].…”

Section: Plos Onementioning

confidence: 99%

Impaired therapeutic efficacy of bone marrow cells from post-myocardial infarction patients in the TIME and LateTIME clinical trials

Wang

Chacon²,

Derakhshandeh

et al. 2020

PLoS ONE

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Implantation of bone marrow-derived cells (BMCs) into mouse hearts post-myocardial infarction (MI) limits cardiac functional decline. However, clinical trials of post-MI BMC therapy have yielded conflicting results. While most laboratory experiments use healthy BMC donor mice, clinical trials use post-MI autologous BMCs. Post-MI mouse BMCs are therapeutically impaired, due to inflammatory changes in BMC composition. Thus, therapeutic efficacy of the BMCs progressively worsens after MI but recovers as donor inflammatory response resolves. The availability of post-MI patient BM mononuclear cells (MNCs) from the TIME and LateTIME clinical trials enabled us to test if human post-MI MNCs undergo a similar period of impaired efficacy. We hypothesized that MNCs from TIME trial patients would be less therapeutic than healthy human donor MNCs when implanted into post-MI mouse hearts, and that therapeutic properties would be restored in MNCs from LateTIME trial patients. Post-MI SCID mice received MNCs from healthy donors, TIME patients, or LateTIME patients. Cardiac function improved considerably in the healthy donor group, but neither the TIME nor LateTIME group showed therapeutic effect. Conclusion: post-MI human MNCs lack therapeutic benefits possessed by healthy MNCs, which may partially explain why BMC clinical trials have been less successful than mouse studies.

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Plasma MicroRNA Expression Profiles in Psoriasis

Cited by 15 publications

References 77 publications

Yangxue Jiedu Fang Ameliorates Psoriasis by Regulating Vascular Regression via Survivin/PI3K/Akt Pathway

Yangxue Jiedu Fang Ameliorates Psoriasis by Regulating Vascular Regression via Survivin/PI3K/Akt Pathway

Association analysis of MALAT1 polymorphisms and risk of psoriasis among Iranian patients

Impaired therapeutic efficacy of bone marrow cells from post-myocardial infarction patients in the TIME and LateTIME clinical trials

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