NREP

Last update 08 May 2025

Basic Info

Synonyms

C5orf13, D4S114, Neuronal protein 3.1

+ [8]

Introduction

May have roles in neural function. Ectopic expression augments motility of gliomas. Promotes also axonal regeneration (By similarity). May also have functions in cellular differentiation (By similarity). Induces differentiation of fibroblast into myofibroblast and myofibroblast ameboid migration. Increases retinoic-acid regulation of lipid-droplet biogenesis (By similarity). Down-regulates the expression of TGFB1 and TGFB2 but not of TGFB3 (By similarity). May play a role in the regulation of alveolar generation.

100 Clinical Results associated with NREP

100 Translational Medicine associated with NREP

0 Patents (Medical) associated with NREP

120

Literatures (Medical) associated with NREP

01 Mar 2025·Pathology - Research and Practice

Seabuckthorn polysaccharide alleviates renal fibrosis in a mouse model of diabetic nephropathy via p311/TGFβ1/Fstl1 signaling pathway

Article

Author: Shi, Zilu ; Zheng, Dandan ; Huang, Qiuhong ; Chen, Huiqin ; Huang, Qian

BACKGROUNDDiabetic nephropathy (DN) is a primary microvascular complication of diabetes with characteristics of renal fibrosis. Seabuckthorn polysaccharide (SP) is an extract from Seabuckthron berries (Hippophae rhamnoides L.) with antioxidant, anti-fatigue, anti-inflammation, and hepatoprotective properties. This current work aimed to investigate the effect of SP on DN-induced kidney fibrosis.METHODSSTZ-induced DN mouse model was constructed by intraperitoneally injecting 50 mg/kg STZ for five days. Various doses of SP were orally administered to mice. Biochemical analysis was performed to measure blood biochemical parameters. Masson's trichrome staining of renal tissues was conducted to analyze fibrotic area. Immunofluorescence staining was performed to assess E-cadherin and α-SMA expressions in kidney samples. Serum MMP2 level was evaluated by corresponding ELISA kit, and Timp2 level was subjected to RT-qPCR analysis. PCR and western blot were conducted to quantify p311, TGFβ1, and Fstl1 levels in renal samples.RESULTSSP reversed the changes in body weight, fasting blood glucose and renal function indicators in diabetic mice. SP lessened renal fibrotic areas in diabetic mice and inhibited epithelial-mesenchymal transition (EMT) by increasing E-cadherin level and reducing α-SMA expression. Fibrotic genes MMP2 and TIMP2 were highly expressed in mice with DN, and their dysregulated expressions were reversed by SP administration. Additionally, SP suppressed the activation of p311/TGFβ1/Fstl1 signaling pathway in renal tissues of diabetic mice.CONCLUSIONSSP alleviates diabetic nephropathy by improving renal functions, alleviating renal fibrosis, and hampering EMT process via downregulation of fibrotic genes and inactivation of the p311/TGFβ1/Fstl1 pathway.

01 Feb 2025·Clinical Hemorheology and Microcirculation

Hypoxic human adipose mesenchymal stem cells-derived extracellular vesicles induce P311 expression and inhibit activation and injury of human brain microvascular endothelial cells

Article

Author: Kang, Tao ; Su, Yu ; Zhao, Hanghang ; Zhang, Yun ; Li, Li ; Yang, Shudong

ObjectiveStem cell therapy can modify angiogenic pathways. Neural protein 3.1 (P311) possesses the pro-angiogenic property. This study strived to explore the action and mechanism of human adipose mesenchymal stem cells (hADSCs) in human brain microvascular endothelial cell (hBMEC) injury by regulating P311.Methods The hADSCs of the 3 rd passage were stained with oil red O, Alizarin red, and Alcian blue to assess adipogenic, osteogenic, and chondrogenic differentiation, followed by an analysis of immune phenotype via flow cytometry. After culturing hADSCs in hypoxic (5% oxygen) and normoxic (20% oxygen) conditions, extracellular vesicles (EVs) were extracted via ultracentrifugation, followed by morphology observation by microscopy, size distribution analysis via Nanoparticle tracking analysis, and surface marker determination by Western blot. hBMECs were treated with lipopolysaccharide (LPS) and cultured with normoxia or hypoxic hADSC-EVs. The effects of normoxia and hypoxic hADSC-EVs on proliferation, migration, and tube formation of hBMECs were assessed via CCK-8, Transwell, and tube formation assays. hBMECs were transfected with pcDNA3.0-P311 or P311 siRNA to evaluate the action of P311 on hBMEC injury. ResultsHypoxic hADSC-EVs had a larger mean diameter, a wider diameter distribution range, and a higher particle concentration than normoxic hADSC-EVs. Hypoxia and normoxic hADSC-EVs were internalized by hBMECs, and hypoxic hADSC-EVs were more internalized. LPS suppressed hBMEC proliferation, migration, and tube formation and induced hBMEC injury. Hypoxia and normoxic hADSC-EVs ameliorated hBMEC injury, and hypoxic hADSC-EVs were superior to normoxic hADSC-EVs. P311 overexpression mitigated hBMEC injury, whereas P311 knockdown partly averted hypoxic hADSC-EV-exerted suppression on hBMEC injury.ConclusionHypoxic hADSC-EVs can protect against LPS-induced hBMEC injury by upregulating P311.

01 Feb 2025·DNA and Cell Biology

Pirfenidone Downregulates eIF6, P311, and TGF-β Expression and Improves Liver Fibrosis Induced by Bile Duct Ligation in Wistar Rats: Evidence for Liver Regeneration

Article

Author: Nourbakhsh, Mitra ; Yousefi, Zeynab ; Sahebghadam Lotfi, Abbas

Liver fibrosis (LF) is a clinical disorder characterized by inflammation and excessive accumulation of extracellular matrix (ECM). This study investigates the effects of the antifibrotic compound pirfenidone (PFD) on improving LF through histological changes and modulation of eukaryotic translation initiation factor 6 (eIF6), P311, and transforming growth factor beta (TGF-β) in rats with bile duct ligation (BDL)-induced LF. Rats received daily doses of PFD (200 and 500 mg/kg) for 4 weeks. The study encompassed biochemical, pathological, and immunohistochemical (IHC) analyses. mRNA levels of eIF6, P311, TGF-β, ECM deposition, hepatic stellate cell (HSC) activation, and inflammatory mediator genes were measured by RT-qPCR. Protein levels of eIF6, P311, and TGF-β were detected by western blotting. Compared with the BDL group, PFD dose-dependently reduced hydroxyproline content, liver index, biochemical parameters, fibrosis score, and fibrosis area. PFD also modulated BDL-induced hepatic inflammation, ECM accumulation, and HSC activation. IHC staining of Ki-67 and hepatocyte paraffin-1 revealed that PFD enhanced liver regeneration. The research confirmed that PFD gradually downregulated elevated eIF6, P311, and TGF-β levels in BDL-induced LF. These findings suggest that PFD could be a potential treatment for LF, as it may help attenuate fibrosis and enhance liver regeneration, possibly through the modulation of these specific markers.

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NREP

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