RETRACTED ARTICLE: Up-regulated lncRNA5322 elevates MAPK1 to enhance proliferation of hair follicle stem cells as a ceRNA of microRNA-19b-3p

Cai, Bingjie; Wang, Xinxin; Liu, Hongtao; Ma, Shanshan; Zhang, Kun; Zhang, Yanting; Li, Qinghua; Wang, Junmin; Yao, M.; Guan, Fangxia; Yin, Guangwen

doi:10.1080/15384101.2019.1624111

Cited by 10 publications

(13 citation statements)

References 41 publications

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“…In the present study, we found that miR-214-3p can directly inhibit the expression of MAPK1, and the dual-luciferase reporter genes also confirmed the direct binding between miR-214-3p and MAPK1 gene. Cai et al showed that MAPK1 could promote HFSc proliferation, wound contraction and epidermal regeneration of mouse model [20]. Consistent with the previous study, we found that inhibition of miR-214-3p could induce HFSc differentiation, while inhibition of MAPK1 can reverse this effect, suggesting that MAPK1, as a downstream effector molecule of miR-214-3p, plays a role in promoting HFSc differentiation.…”

Section: Discussionsupporting

confidence: 92%

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DNMT1 mediated methylation silences miR-214-3p gene and promotes hair follicle stem cell differentiate into adipogenic lineages

Jin

et al. 2020

Preprint

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Background Dysfunction of the DNA methylation was associated with stem cell reprogramming. Moreover, DNA methyltransferase 1 (DNMT1) deficiency was involved in the differentiation of hair follicle stem cell (HFSc), but the molecular mechanisms remain unknown. Methods HFSc from human scalp tissues were isolated and cultured. The oil red O staining was used to detect the adipogenesis. The interaction relationship between microRNA (miR)-214-3p and mitogen-activated protein kinase 1 (MAPK1) was accessed by dual-luciferase reporter gene assay. The methylation level of miR-214-3p promoter was detected by methylation-specific PCR, and the enrichment of DNMT1 in miR-214-3p promoter was detected by chromatin immunoprecipitation assay (ChIP). The mouse model of trauma was established to observe the skin regeneration at 0, 6 and 14 days. Results Expression of DNMT1 and MAPK1 was increased in the HFSc, while the expression of miR-214-3p was reduced. Moreover, DNMT1 inhibited the expression of miR-214-3p by promoting the promoter methylation of miR-214-3p. Overexpression of DNMT1 could reduce the expression of miR-214-3p but increased the expression of MAPK1 and the extent of extracellular signal regulated kinase (ERK)1/2 phosphorylation. DNMT1 also significantly enhanced the adipogenic differentiation, and increased the proportion and markers of adipogenic cells. Importantly, DNMT1 promoted skin regeneration in vivo. Conversely, overexpression of miR-214-3p could reverse the effects of DNMT1 on adipogenesis of HFSc. Conclusion DNMT1 promotes adipogenesis of HFSc by mediating miR-214-3p/MAPK1/phosphorylated-ERK1/2 axis. This study may provide more biomarkers for the potential application in stem cell therapy.

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Section: Discussionsupporting

confidence: 92%

“…4A). More importantly, Cai et al showed that MAPK1 promotes HFSc proliferation, wound contraction and epidermal regeneration in mouse model [20]. Here, we found the expression of MAPK1 was significantly increased in HFSc by differentiation at 7d and 14d (Fig.…”

Section: The Mir-214-3p Inhibits Adipogenic Differentiation Of Hfsc Bsupporting

confidence: 59%

DNMT1 mediated methylation silences miR-214-3p gene and promotes hair follicle stem cell differentiate into adipogenic lineages

Jin

et al. 2020

Preprint

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“…In the present study, we found that miR-214-3p can directly inhibit the expression of MAPK1, and the dual-luciferase reporter gene assay also confirmed the direct binding between miR-214-3p and MAPK1 gene. Cai et al showed that MAPK1 could promote HFSc proliferation, wound contraction, and epidermal regeneration of mouse model [23]. Consistent with the previous study, we found that inhibition of miR-214-3p could induce HFSc differentiation, while inhibition of MAPK1 can reverse this effect, suggesting that MAPK1, as a downstream effector molecule of miR-214-3p, plays a role in promoting HFSc differentiation.…”

Section: Discussionsupporting

confidence: 92%

“…4 a). More importantly, Cai et al showed that MAPK1 promotes HFSc proliferation, wound contraction, and epidermal regeneration in mouse model [ 23 ]. Here, we found the expression of MAPK1 was significantly increased in HFSc by differentiation on the 7th day and the 14th day (Fig.…”

Section: Resultsmentioning

confidence: 99%

DNMT1-mediated methylation inhibits microRNA-214-3p and promotes hair follicle stem cell differentiate into adipogenic lineages

Jin

et al. 2020

Stem Cell Res Ther

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Background Dysfunction of the DNA methylation was associated with stem cell reprogramming. Moreover, DNA methyltransferase 1 (DNMT1) deficiency was involved in the differentiation of hair follicle stem cell (HFSc), but the molecular mechanisms remain unknown. Methods HFSc from human scalp tissues were isolated and cultured. The oil red O staining was used to observe the adipogenesis. The interaction relationship between microRNA (miR)-214-3p and mitogen-activated protein kinase 1 (MAPK1) was accessed by dual-luciferase reporter gene assay. The methylation level of miR-214-3p promoter was detected by methylation-specific PCR and the enrichment of DNMT1 in miR-214-3p promoter by chromatin immunoprecipitation assay. A mouse model of trauma was established to observe the skin regeneration at 0, 6, and 14 days. Results Expression of DNMT1 and MAPK1 was increased in the HFSc, while the expression of miR-214-3p was reduced. Moreover, DNMT1 inhibited the expression of miR-214-3p by promoting the promoter methylation of miR-214-3p. Overexpression of DNMT1 could reduce the expression of miR-214-3p, but increase the expression of MAPK1 and the extent of extracellular signal regulated kinase (ERK)1/2 phosphorylation, leading to enhanced adipogenic differentiation. Importantly, DNMT1 promoted skin regeneration in vivo. Conversely, overexpression of miR-214-3p could reverse the effects of DNMT1 on adipogenesis of HFSc. Conclusion DNMT1 promotes adipogenesis of HFSc by mediating miR-214-3p/MAPK1/p-ERK1/2 axis. This study may provide novel biomarkers for the potential application in stem cell therapy.

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“…In our study, miR-19b was up-regulated in HG-treated hRMECs, and miR-19b overexpression dramatically inhibited cell viability and enhanced cell apoptosis and inflammation. Similarly, according to Cai's study, inhibition of miR-19b could promote the proliferation of hair follicle stem cells (HFSCs) [21]. All these studies supported our findings.…”

Section: Discussionsupporting

confidence: 87%

Regulation of the miR-19b-mediated SOCS6-JAK2/STAT3 pathway by lncRNA MEG3 is involved in high glucose-induced apoptosis in hRMECs

Xiao

Lan

et al. 2020

Bioscience Reports

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Objective: Diabetic retinopathy (DR) is one of the most severe and common complications of diabetes mellitus. The present study aimed to investigate the molecular mechanism of MEG3, miR-19b and SOCS6 in human retinal microvascular endothelial cells (hRMECs) under high glucose conditions. Methods: HRMECs were cultured in 5 or 30 mM D-glucose medium. qRT-PCR and Western blotting were used to determine the mRNA expression and protein levels. MTT assay and flow cytometry analysis were performed to detect the viability and apoptosis of hRMECs, respectively. TNF-α, IL-6 and IL-1β levels in cell supernatants were detected by ELISA. The activity of caspase-3/7 was also determined. A luciferase reporter assay was performed to confirm the targeting relationship between miR-19b and SOCS6, as well as MEG3 and miR-19b. Results: Our study demonstrated that miR-19b was increased and SOCS6 was decreased in HG-induced hRMECs. Knockdown of SOCS6 inhibited cell viability and reversed the promotion of cell viability induced by knockdown of miR-19b. Additionally, miR-19b directly targeted and negatively regulated SOCS6. Moreover, miR-19b promoted the cell apoptosis rate and caspase-3/7 activity and increased inflammatory factors through the SOCS6-mediated JAK2/STAT3 signalling pathway. In addition, MEG3 attenuated HG-induced apoptosis of hRMECs by targeting the miR-19b/SOCS6 axis. Conclusion: These findings indicate that MEG3 inhibited HG-induced apoptosis and inflammation by regulating the miR-19b/SOCS6 axis through the JAK2/STAT3 signalling pathway in hRMECs. Thus, these findings might provide a new target for the treatment of DR.

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RETRACTED ARTICLE: Up-regulated lncRNA5322 elevates MAPK1 to enhance proliferation of hair follicle stem cells as a ceRNA of microRNA-19b-3p

Abstract: Yin (2019) Upregulated lncRNA5322 elevates MAPK1 to enhance proliferation of hair follicle stem cells as a ceRNA of microRNA-19b-3p,

Cited by 10 publications

References 41 publications

DNMT1 mediated methylation silences miR-214-3p gene and promotes hair follicle stem cell differentiate into adipogenic lineages

DNMT1 mediated methylation silences miR-214-3p gene and promotes hair follicle stem cell differentiate into adipogenic lineages

DNMT1-mediated methylation inhibits microRNA-214-3p and promotes hair follicle stem cell differentiate into adipogenic lineages

Regulation of the miR-19b-mediated SOCS6-JAK2/STAT3 pathway by lncRNA MEG3 is involved in high glucose-induced apoptosis in hRMECs

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