Effect of MiR-133 on myocardial cell apoptosis in rats with myocardial infarction through the Notch1 signaling pathway

2021 ◽  
Vol 112 (2) ◽  
Author(s):  
Bei ZHANG ◽  
Haiyan ZHOU ◽  
Chunqi QIAN ◽  
Niwen HUANG ◽  
Ying GU ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Myocardial Cell ◽  
Notch1 Signaling ◽  
Notch1 Signaling Pathway

scholarly journals Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Jiewei Lin ◽  
Zhiwei Xu ◽  
Junjie Xie ◽  
Xiaxing Deng ◽  
Lingxi Jiang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathway ◽  
Density Lipoprotein ◽  
Human Pancreatic Cancer ◽  
Luciferase Reporter ◽  
Notch1 Signaling ◽  
In Vivo Experiments ◽  
Notch1 Signaling Pathway

AbstractAPOL1 encodes a secreted high-density lipoprotein, which has been considered as an aberrantly expressed gene in multiple cancers. Nevertheless, the role of APOL1 in the regulatory mechanisms of pancreatic cancer remains unknown and should be explored. We identified APOL1 was abnormally elevated in human pancreatic cancer tissues compared with that in adjacent tissues and was associated with poor prognosis. The effects of APOL1 in PC cell proliferation, cell cycle, and apoptosis was verified via functional in vitro and in vivo experiments. The results showed that knockdown of APOL1 significantly inhibited the proliferation and promoted apoptosis of pancreatic cancer. In addition, we identified APOL1 could be a regulator of NOTCH1 signaling pathway using bioinformatics tools, qRT-PCR, dual-luciferase reporter assay, and western blotting. In summary, APOL1 could function as an oncogene to promote proliferation and inhibit apoptosis through activating NOTCH1 signaling pathway expression in pancreatic cancer; therefore, it may act as a novel therapeutic target for pancreatic cancer.

scholarly journals Long non-coding RNA TUG1 knockdown hinders the tumorigenesis of multiple myeloma by regulating the microRNA-34a-5p/NOTCH1 signaling pathway

2020 ◽  
Vol 15 (1) ◽  
pp. 284-295
Author(s):  
Yongtian Zhang ◽  
Dandan Zhao ◽  
Shumei Li ◽  
Meng Xiao ◽  
Hongjing Zhou ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Signaling Pathway ◽  
Notch Receptor ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Notch1 Signaling ◽  
Non Coding Rna ◽  
Notch1 Signaling Pathway ◽  
Long Non Coding Rna

AbstractMultiple myeloma (MM) is a serious health issue in hematological malignancies. Long non-coding RNA taurine-upregulated gene 1 (TUG1) has been reported to be highly expressed in the plasma of MM patients. However, the functions of TUG1 in MM tumorigenesis along with related molecular basis are still undefined. In this study, increased TUG1 and decreased microRNA-34a-5p (miR-34a-5p) levels in MM tissues and cells were measured by the real-time quantitative polymerase reaction assay. The expression of relative proteins was determined by the Western blot assay. TUG1 knockdown suppressed cell viability, induced cell cycle arrest and cell apoptosis in MM cells, as shown by Cell Counting Kit-8 and flow cytometry assays. Bioinformatics analysis, luciferase reporter assay, and RNA pull-down assay indicated that miR-34a-5p was a target of TUG1 and directly bound to notch receptor 1 (NOTCH1), and TUG1 regulated the NOTCH1 expression by targeting miR-34a-5p. The functions of miR-34a-5p were abrogated by TUG1 upregulation. Moreover, TUG1 loss impeded MM xenograft tumor growth in vivo by upregulating miR-34a-5p and downregulating NOTCH1. Furthermore, TUG1 depletion inhibited the expression of Hes-1, Survivin, and Bcl-2 protein in MM cells and xenograft tumors. TUG1 knockdown inhibited MM tumorigenesis by regulating the miR-34a-5p/NOTCH1 signaling pathway in vitro and in vivo, deepening our understanding of the TUG1 function in MM.

scholarly journals Interleukin-22 attenuates renal tubular cells inflammation and fibrosis induced by TGF-β1 through Notch1 signaling pathway

Renal Failure ◽  
2020 ◽  
Vol 42 (1) ◽  
pp. 381-390 ◽  
Author(s):  
Rong Tang ◽  
Xiangcheng Xiao ◽  
Yang Lu ◽  
Huihui Li ◽  
Qiaoling Zhou ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Tubular Cells ◽  
Interleukin 22 ◽  
Renal Tubular Cells ◽  
Notch1 Signaling ◽  
Renal Tubular ◽  
Notch1 Signaling Pathway ◽  
Tgf Β1

PEDF Induces Native Coronary Collateral Microcirculation Remodeling in a Manner Similar to That of FSS Through Activing Canonical and Non-canonical Notch1 Signaling Pathway Simultaneously

2020 ◽  
Author(s):  
Jiali Chen ◽  
Xiucheng Liu ◽  
Xichun Qin ◽  
Hao Zhang ◽  
Zhiwei Liu ◽  
...  
Keyword(s):  
Blood Flow ◽  
Signaling Pathway ◽  
Fluid Shear Stress ◽  
Adherens Junctions ◽  
Pigment Epithelium ◽  
Butyl Ester ◽  
Specific Mechanism ◽  
Notch1 Signaling ◽  
Coronary Collateral ◽  
Notch1 Signaling Pathway

Abstract Background Our previous studies showed that the coronary collateral microcirculation reserve (CCMR) in rat hearts is abundant, but the structure is naturally flawed, which preventing it from continuously providing alternative blood flow to the ischemic myocardium. Further research indicated that pigment epithelium-derived factor (PEDF) can induce CCMR vessels remodeling in a manner similar to that of fluid shear stress (FSS), thus improving compensatory blood flow. However, the specific mechanism remained unclear. Methods We established the rat model of PEDF overexpression in the myocardium and the cardiac explant angiogenesis model in matrigel to identify the role of the canonical and non-canonical Notch1 signaling pathway in the process of PEDF-induced CCMR remodeling. Results: We found that pharmaceutical blockage of Notch1 pathway via γ-secretase inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) would effectively abrogate the remodeling process, including the diameter expansion and adherens junctions reorganization of CCMR induced by PEDF. In vitro, western blot and enzyme activity assay analysis indicated that PEDF treatment simultaneously active the canonical Notch1 pathway (NICD/AKT/eNOS/NO) and non-canonical Notch1 pathway (TMD/VE-cadherin-LAR-Trio complex). To our amusement, using L-Nitromonomethylarginine (L-NMMA) acetate to inhibit endothelial nitric oxide synthase (eNOS) activity could significantly block PEDF-induced the diameter expansion of the nascent blood vessels, but it had little effect on the reassembly of adherens junctions. While activation of non-canonical Notch1 pathway seems to be the cause of adherens junctions remodeling. Blocking of the non-canonical Notch1 pathway canceled PEDF-driven adherens junctions assembly. Conclusions We demonstrate the specific mechanism of PEDF-induced native collateral microcirculation remodeling. PEDF can active the canonical Notch1 pathway signaling pathway to promote lumenal remodeling and, Simultaneously, active non-canonical Notch1 signaling pathway responsible for adherens junctions assembly.

α5‐nAChR modulates melanoma growth through the Notch1 signaling pathway

2020 ◽  
Vol 235 (11) ◽  
pp. 7816-7826 ◽  
Author(s):  
NingNing Dang ◽  
Xianguang Meng ◽  
Guojing Qin ◽  
Yunhe An ◽  
QianQian Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Notch1 Signaling ◽  
Notch1 Signaling Pathway ◽  
Melanoma Growth

scholarly journals Platelet-Rich Plasma with Endothelial Progenitor Cells Accelerates Diabetic Wound Healing in Rats by Upregulating the Notch1 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Cheng Zhang ◽  
Yu Zhu ◽  
Shengdi Lu ◽  
Wanrun Zhong ◽  
Yanmao Wang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factors ◽  
Signaling Pathway ◽  
Platelet Rich Plasma ◽  
Diabetic Wound ◽  
Endothelial Progenitor ◽  
Notch1 Signaling ◽  
Diabetic Wound Healing ◽  
Notch1 Signaling Pathway ◽  
Diabetic Wounds

Diabetic wounds, as a kind of refractory wound, are very difficult to heal. Both endothelial progenitor cell (EPC) transplantation and platelet-rich plasma (PRP) can improve diabetic wound healing to some extent. However, PRP application cannot provide reparative cells, while EPC transplantation cannot replenish the required growth factors for wound healing. Thus, when applied alone, neither of these factors is sufficient for effective wound healing. Furthermore, the proliferation, differentiation, and fate of the transplanted EPCs are not well known. Therefore, in this study, we examined the efficacy of combined PRP application with EPC transplantation in diabetic wound healing. Our results indicated that PRP application improved EPC proliferation and migration. The Notch signaling pathway plays a key role in the regulation of the proliferation and differentiation of stem cells and angiogenesis in wound healing. The application of PRP upregulated the Notch pathway-related gene and protein expression in EPCs. Furthermore, experiments with shNotch1-transfected EPCs indicated that PRP enhanced the function of EPCs by upregulating the Notch1 signaling pathway. In vivo studies further indicated that the combination of PRP and EPC transplantation increased neovascularization, reduced wound size, and improved healing in rat wound models. Thus, PRP application can provide the necessary growth factors for wound healing, while EPC transplantation offers the required cells, indicating that the combination of both is a potent novel approach for treating diabetic wounds.

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