miR-137 Inhibits Proliferation and Metastasis of Hypertrophic Scar Fibroblasts via Targeting Pleiotrophin

Zhang, Qian; Guo, Bingyu; Qiang, Hui; Chang, Peng; Tao, Kai

doi:10.1159/000493236

Cited by 28 publications

(19 citation statements)

References 26 publications

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“…These exuberant responses start the formation of collagen and even keloids . The innovative and targeted therapeutics have recently drawn our attention by medicating the expression of miRs for curing these diseases . In the current study, we found that BAI effectively eliminated the proliferation of fibroblast cells and TGF‐β1‐induced synthesis of collagen.…”

Section: Discussionmentioning

confidence: 53%

“…17 The innovative and targeted therapeutics have recently drawn our attention by medicating the expression of miRs for curing these diseases. [18][19][20] In the current study, we found Fibroblast NIH-3T3 cells were pretreated with BAI (150 μM) for 12 hours after transfection of miR-29 inhibitor and its consistent NC. Fibroblast NIH-3T3 cells did not accept the transfection of miR-29 inhibitor or pretreatment of BAI in the CTRL.…”

Section: Discussionmentioning

confidence: 62%

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Retracted: Baicalein retards proliferation and collagen deposition by activating p38MAPK‐JNK via microRNA‐29

Yang

Jiang

2019

J of Cellular Biochemistry

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Immoderate proliferation and deposition of collagen generally result in hypertrophic scars and even keloids. microRNA‐29 (miR‐29) has been proved as a crucial regulator in these pathological processes. Although mounting evidence have proved baicalein (BAI) impairs scar formation, it is still incompletely understood whether miR‐29 participated in the underlying mechanism. In the present study, NIH‐3T3 cells were stimulated with BAI, and then cell viability was analyzed by cell counting kit‐8 (CCK‐8) and Western blot. We further analyzed total soluble collagen, collagen 1, and alpha‐smooth muscle actin (α‐SMA) in NIH‐3T3 cells, which were exposed to transforming growth factor beta 1 (TGF‐β1)/BAI, using a Sircol assay kit, quantitative reverse transcription‐PCR (qRT‐PCR) and Western blot, respectively. Besides, the miR‐29 inhibitor was transduced and its transfection efficiency was verified by qRT‐PCR. Finally, the phosphorylated p38 mitogen‐activated protein kinase (p38MAPK) and c‐Jun N‐terminal kinase (JNK) were examined by Western blot. BAI effectively retarded NIH‐3T3 proliferation in a dose‐dependent manner. Besides, TGF‐β1‐induced deposition of total soluble collagen and synthesis of collagen 1 and α‐SMA were repressed by BAI at mRNA and protein levels. However, miR‐29 inhibitor reversed the effects of BAI. Remarkably, BAI promoted phosphorylated expression of p38MAPK and JNK while miR‐29 inhibitor reversed its effects on the phosphorylated expression of p38MAPK and JNK. BAI effectively weakened the cell viability and repressed TGF‐β1‐induced total soluble collagen as well as collagen 1 and α‐SMA by upregulating miR‐29. Mechanically, BAI activates the p38MAPK/JNK pathway by promoting miR‐29.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 62%

Retracted: Baicalein retards proliferation and collagen deposition by activating p38MAPK‐JNK via microRNA‐29

Yang

Jiang

2019

J of Cellular Biochemistry

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“…in addition, an abundance of evidence has identified that mirnas were involved in numerous metabolic reactions, including cell proliferation, differentiation, autophagy and apoptosis, by directly binding to the 3'-untranslated region (3'-uTr) of their target mrnas (23)(24)(25)(26). To date, a small number of studies have suggested a potential role between mirnas and HSs; for example, the expression levels of mir-21 were reported to be upregulated in HS-derived fibroblasts (HSFBs) and inhibiting miR-21 expression significantly slowed the formation of HSs in vivo (27). Conversely, the expression levels of another miRNA, miR-137, were markedly downregulated in HSs, which induced the proliferation and metastasis of fibroblasts (28).…”

Section: Resveratrol Inhibits Hypertrophic Scars Formation Bymentioning

confidence: 99%

Resveratrol inhibits hypertrophic scars formation by activating autophagy via the miR-4654/Rheb axis

Pang

Tang

et al. 2020

Mol Med Rep

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Hypertrophic scars (HSs) are a type of pathological scar which are induced by surgery, burn injuries or trauma during the healing process. Due to the high recurrence rates and strong invasive properties, HSs have become a major clinical issue. Resveratrol has been identified as a potential agent to suppress scar formation; however, the underlying mechanism of action remains unclear. Therefore, the present study aimed to investigate the effect of resveratrol on HS-derived fibroblasts (HSFBs) in vitro . MTT assay was performed to evaluate cell viability following the resveratrol treatment. Western blot and RT-qPCR analysis was used to identify the expression levels and the relationship among autophagic markers, miR-4654 and resveratrol treatment. Finally, GFP-LC3 stable HSFBs cells were generated to further assess the effect of resveratrol. The results revealed that resveratrol significantly induced cell death in a dose-dependent manner and induced autophagy by downregulating the expression levels of Rheb in HSFBs. Notably, microRNA-4654 (miR-4654) was significantly decreased in the HSFBs and re-upregulated by resveratrol treatment dose-dependently. Through the bioinformatic analysis and luciferase assay, miR-4654 was identified to directly target Rheb. Transfection studies showed that miR-4654 negative correlated with Rheb expression, suggesting that the autophagic process may be altered by the miR-4654/Rheb axis under the control of resveratrol. In conclusion, the results of the present study suggested that resveratrol may promote autophagy by upregulating miR-4654, which in turn may suppress Rheb expression via directly binding to the 3′-untranslated region of Rheb. These findings provided a novel insight into the development of potential therapeutic targets for HSs.

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“…By mediating post-transcriptional regulation, they exert various biological functions, including proliferation, apoptosis, and invasion (2). For instance, Zhang et al reported that the downregulation of miR-137 expression can induce the proliferation and metastasis of skin fibroblasts, and promote HS formation and development (3). Furthermore, a study by Wu et al showed that miR-155 was downregulated in both HS tissues and HS-derived fibroblasts, and therefore suggested it as a potential therapeutic target for HS (4).…”

Section: Introductionmentioning

confidence: 99%

microRNA-181a promotes the proliferation of hypertrophic scar fibroblasts and inhibits their apoptosis via targeting phosphatase and tensin homolog

Zhou¹,

Shi²,

Li³

et al. 2021

Ann Palliat Med

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Background: This study aimed to compare the expression of microRNA (miR)-181a and phosphatase and tensin homolog (PTEN) in hypertrophic scar tissue and cells and to explore the effects of miR-181a and PTEN on the proliferation and apoptosis of the human scar fibroblast cell line HSFb.Methods: HSFb cells were transfected with miR-negative control (miR-NC), miR-181a mimics, miR-181a inhibitor, pcDNA3.1-PTEN (pc-PTEN), or small interfence-PTEN (si-PTEN) plasmid using a Lipofectamine 2000 transfection kit. The effects of miR-181a and PTEN on the proliferation and apoptosis of HSFb were determined using a Cell Counting Kit (CCK)-8 experiment and flow cytometry, respectively.The effects of miR-181a and PTEN on the expression of apoptosis-related proteins in HSFb, including type I collagen (Col-1) and type III collagen (Col-3), were measured by western blot. Finally, the relationship between miR-181a and PTEN was explored by the dual-luciferase reporter gene experiment. Results:The miR-181a in hypertrophic scar tissues and HSFb were significantly up-regulated compared to embryo skin fibroblast (ESF-1) cells and normal tissues (P<0.05), whereas the opposite results were seen for PTEN expression (P<0.05). Inhibiting miR-181a or upregulating the expression of PTEN significantly suppressed the proliferation of HSFb (P<0.05) and induced their apoptosis (P<0.05). Western blot revealed that inhibiting and upregulating miR-181a and PTEN, respectively, decreased the expression of the B-cell lymphoma-2 (Bcl-2), Col-1, and Col-3 proteins in HSFb, but significantly up-regulated the expression of Bcl-2-associated X protein (Bax), cleaved caspase-3 (c-caspase-3), and cleaved caspase-9 (c-caspase-9) (P<0.05). The dual-luciferase reporter gene experiment results confirmed PTEN to be the downstream target gene of miR-181a. Simultaneous upregulation of miR-181a and PTEN expression had no significant effect on the proliferation and apoptosis of HSFb.Conclusions: miR-181a promotes the up-regulation of Col-1 and Col-3, and regulates the proliferation and apoptosis of HSFb by targeting PTEN, thereby enhancing the formation of hypertrophic scarring (HS).Therefore, miR-181a and PTEN may be potential therapeutic targets for the treatment of HS.

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miR-137 Inhibits Proliferation and Metastasis of Hypertrophic Scar Fibroblasts via Targeting Pleiotrophin

Cited by 28 publications

References 26 publications

Retracted: Baicalein retards proliferation and collagen deposition by activating p38MAPK‐JNK via microRNA‐29

Retracted: Baicalein retards proliferation and collagen deposition by activating p38MAPK‐JNK via microRNA‐29

Resveratrol inhibits hypertrophic scars formation by activating autophagy via the miR-4654/Rheb axis

microRNA-181a promotes the proliferation of hypertrophic scar fibroblasts and inhibits their apoptosis via targeting phosphatase and tensin homolog

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