lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF‑β1‑regulated RASAL1/ERK1/2 signal pathway

Liu, Xiaoming; Gao, Shanyu; Xu, Huile

doi:10.3892/mmr.2018.8807

Cited by 17 publications

(12 citation statements)

References 27 publications

(33 reference statements)

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“…19 lncRNAs are involved in modulating the proliferation and apoptosis of lung tissue cells during the development of lung organs, and play a critical role in the pathologic process of pulmonary fibrosis. 7 20 H19 is found to be upregulated and is related to the regulation of inflammation in lung tissues of BPD mice. 10 In this study, we identified that lncRNA H19 was highly expressed in lung tissues of BPD newborn mice, and downregulated H19 relieved pulmonary injury via the miR-17/STAT3 axis and attenuated p-STAT3-induced inflammatory response in BPD newborn mice.…”

Section: Discussionmentioning

confidence: 98%

Mechanism of lncRNA H19 in Regulating Pulmonary Injury in Hyperoxia-Induced Bronchopulmonary Dysplasia Newborn Mice

Zhang

Wang²,

Shen

et al. 2020

Am J Perinatol

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Objective Bronchopulmonary dysplasia (BPD) is a pulmonary injury related to inflammation and is a major cause of premature infant death. Long noncoding RNAs (lncRNAs) are important regulators in pulmonary injury and inflammation. We investigated the molecular mechanism of lncRNA H19 in pulmonary injury and inflammation in hyperoxia (Hyp)-induced BPD mice. Study Design The BPD newborn mouse model was established and intervened with H19 to evaluate the pathologic conditions and radial alveolar count (RAC) in lung tissues of mice in the room air (RA) and Hyp group on the 4th, 7th, and 14th days after birth. The levels of BPD-related biomarkers vascular endothelial growth factor (VEGF), transforming growth factor β1 (TGF-β1), and surfactant protein C (SPC) in lung tissues were detected on the 14th day after birth. The expression of and relationships among H19 and miR-17, miR-17, and STAT3 were detected and verified. Levels of interleukin (IL)-6, IL-1β, p-STAT3, and STAT3 levels in mouse lung tissues were detected on the 14th day after birth. Results Hyp-induced mice showed increased alveolar diameter, septum, and hyperemia and inflammatory cell infiltration, upregulated H19, decreased overall number and significantly reduced RAC on the 7th and 14th days after birth, which were reversed in the si-H19-treated mice. VEGF was upregulated and TGF-β1 and SPC was decreased in si-H19-treated mice. Moreover, H19 competitively bound to miR-17 to upregulate STAT3. IL-6 and IL-1β expressions and p-STAT3 and STAT3 levels were downregulated after inhibition of H19. Conclusion Downregulated lncRNA H19 relieved pulmonary injury via targeting miR-17 to downregulate STAT3 and reduced inflammatory response caused by p-STAT3 in BPD newborn mice. Key Points

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Section: Discussionmentioning

confidence: 98%

Mechanism of lncRNA H19 in Regulating Pulmonary Injury in Hyperoxia-Induced Bronchopulmonary Dysplasia Newborn Mice

Zhang

Wang²,

Shen

et al. 2020

Am J Perinatol

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“…PKC, served as the hub of multiple intracellular signal pathways, is involved in the construction of key intracellular information network and regulates a variety of in-vivo physiological and pathological processes. PKC can activate the TGF-β1 which is one of the key cytokines involved in the pathogenesis [8], and some studies also reported that ERK1/2 can interact with the TGF-β1 to be involved in the fibrosis [9, 10, 11]. Thus, it can be inferred that PKC-ERK1/2MAPK may participate in the myocardial fibrosis pathogenesis in DM, or served as the underlying regulation mechanism, through which H2S can ameliorate the myocardial fibrosis in DM.…”

Section: Introductionmentioning

confidence: 99%

H2S attenuates the myocardial fibrosis in diabetic rats through modulating PKC-ERK1/2MAPK signaling pathway

Long

Liu

et al. 2019

THC

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OBJECTIVE To investigate the roles and underlying mechanism of exogenous H S (hydrogen sulfide) in attenuating the myocardial fibrosis in diabetic rats. METHODS: A total of 40 SD rats were randomly divided into 4 groups: control group, STZ group, STZ H S group and H S group. To build the DM rat model , the rats in the STZ group and STZ H S group were injected streptozotocin (STZ) intraperitoneally, While the rats in the STZ H S group and the H S group received sodium hydrosulfide (NaHS), which provides exogenous H S. Eight weeks later, the myocardial tissues of rats were used to detecting the collagen deposition through Masson staining, as well as some protein expressions related to myocardial fibrosis and signaling pathway by western blotting. RESULTS: Comparing to control group, the collagen deposition of myocardial matrix remarkably increased in the STZ group, and almost all the proteins that are relative to myocardial fibrosis, inflammatory and signaling pathway show an overexpression, except for PPARG and NF- Bp65. When Compared with the STZ group, the collagen deposition was obviously attenuated in STZ H S group, as well as the protein expressions above-mentioned, While PPARG was up-regulated. CONCLUSION: The myocardial fibrosis in DM rats can be attenuated effectively by exogenous H S, and the underlying mechanism is likely to regulating PKC-ERK1/2MAPK signaling pathway, improving the MMPs/TIMPs expression dysregulation and inhibiting inflammatory reaction.

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“…Previous studies have shown that a prerequisite step in myogenic differentiation of SkMSCs is the activation of MyoD [18,22,40,41]. Moreover, TGFβ1 was reported to regulate the ERK signaling pathway involved in in ammation, regeneration and differentiation [42,43]. To further investigate the mechanism underlying the function of the ECM hydrogels aligned with TGFβ1 in terms of the proliferation and differentiation of SkMSCs, the EdU assays demonstrated that TGFβ1 promoted SkMSC proliferation.…”

Section: Discussionmentioning

confidence: 99%

TGFβ1 Improves the Proliferation of Decellularized and Aligned Skeletal Muscle in Extracellular Matrix Hydrogels by m6A Modification-Mediated Integrin Through Inducing ERK Phosphorylation

Zhu

Qin

Yang

et al. 2021

Preprint

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Background: The purpose of this study was to illustrate the characteristics of skeletal muscle ECM hydrogels and assess the function and underlying mechanisms of hydrogels combined with TGFβ1 for the myogenesis of skeletal muscle stem cells (SkMSCs). Methods: Six methods were used to obtain extracellular matrix (ECM) from rat skeletal muscle. Hydrogel components and cytocompatibility were assessed by Masson’s trichrome staining, scanning electron microscopy, the sulfated glycosaminoglycan (s-GAG) and bFGF contents and a cell viability assay. Satellite cells were sorted, identified and seeded into skeletal muscle ECM hydrogels with TGFβ1. To determine the function of decellularized aligned skeletal muscle ECM hydrogels with TGFβ1 for the proliferation and differentiation of SkMSCs, a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 5-ethynyl-2′-deoxyuridine (EdU) analysis and immunofluorescence staining were conducted. RNA stability assay and Gene set enrichment analysis (GSEA) were used to further investigated the mechanism underlying the function. Results: Our study established a highly efficient method for the decellularization of skeletal muscle and fabricated an ECM hydrogel without cell components that preserves the rich ECM composition. This hydrogel formed a three-dimensional microstructure and showed good biocompatibility. We found that the decellularized aligned ECM scaffold with TGFβ1 promoted SkMSC proliferation and suppressed SkMSC differentiation through extracellular signal-regulated kinase (ERK) signaling. Our study suggested that TGFβ1 increases the m6A methylation of the integrin mRNA 3’UTR, thereby inducing the phosphorylation of ERK and promoting SkMSCs proliferation and differentiation.Conclusions: Our study explored a highly efficient method for the decellularization of skeletal muscle and fabricated an ECM hydrogel with a three-dimensional microstructure and good biocompatibility. Furthermore, we demonstrated that decellularized aligned ECM scaffolds with TGFβ1 promoted SkMSC proliferation and differentiation through enhancing the m6A methylation of the integrin mRNA 3’UTR, which may serve as a potential therapeutic strategy for the acute and chronic muscle injuries

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lncRNAPCAT29 inhibits pulmonary fibrosis via the TGF‑β1‑regulated RASAL1/ERK1/2 signal pathway

Cited by 17 publications

References 27 publications

Mechanism of lncRNA H19 in Regulating Pulmonary Injury in Hyperoxia-Induced Bronchopulmonary Dysplasia Newborn Mice

Mechanism of lncRNA H19 in Regulating Pulmonary Injury in Hyperoxia-Induced Bronchopulmonary Dysplasia Newborn Mice

H2S attenuates the myocardial fibrosis in diabetic rats through modulating PKC-ERK1/2MAPK signaling pathway

TGFβ1 Improves the Proliferation of Decellularized and Aligned Skeletal Muscle in Extracellular Matrix Hydrogels by m6A Modification-Mediated Integrin Through Inducing ERK Phosphorylation

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