Last update 01 Nov 2024

NOSTRIN

Last update 01 Nov 2024

Basic Info

Synonyms

BM247 homolog, eNOS-trafficking inducer, MGC20702

+ [4]

Introduction

Multivalent adapter protein which may decrease NOS3 activity by inducing its translocation away from the plasma membrane.

100 Clinical Results associated with NOSTRIN

100 Translational Medicine associated with NOSTRIN

0 Patents (Medical) associated with NOSTRIN

Literatures (Medical) associated with NOSTRIN

01 Oct 2024·Plant Physiology and Biochemistry

Regulation of arsenate stress by nitric oxide and hydrogen sulfide in Oryza sativa seedlings: Implication of sulfur assimilation, glutathione biosynthesis, and the ascorbate-glutathione cycle and its genes

Article

Author: Sharma, Shivesh ; Singh, Vijay Pratap ; Tripathi, Durgesh Kumar ; Mishra, Vipul ; Rai, Padmaja

Seed priming by nitric oxide (NO) and hydrogen sulphide (H₂S) in combating against abiotic stress in plants is well documented. However, knowledge of fundamental mechanisms of their crosstalk is scrambled. Therefore, the reported study examined the probable role of NO and H₂S in the mitigation of arsenate toxicity (As(V)) in rice seedlings and whether their potential signalling routes crossover. Results report that As(V) toxicity limited shoot and root length growth with more As accumulation in roots. As(V) further caused elevated reactive oxygen species levels, inhibited ascorbate-glutathione cycle enzymes and relative gene expression of its enzymes and thus, causing lipid and protein oxidation. These results correlate with reduced nitric oxide synthase-like and _L-cysteine desulfhydrase activity along with endogenous NO and H₂S. While, L-NAME or PAG augmented As(V) toxicity, and addition of SNP or NaHS effectively reversed their respective effects. Furthermore, SNP under PAG or NaHS under L-NAME were able to pacify As(V) stress, implicating that endogenous NO and H₂S efficiently ameliorate As(V) toxicity but without their shared signaling in rice seedlings.

01 Sep 2024·Translational Andrology and Urology

NOSTRIN is involved in benign prostatic hyperplasia via inhibition of proliferation, oxidative stress, and inflammation in prostate epithelial cells

Article

Author: Li, Shoubin ; Xu, Qingle ; Guo, Liuxiong ; Liu, Junjiang ; Gao, Bo ; Yu, Chunhong ; Xiao, Helong ; Sun, Zhanxin

BackgroundBenign prostatic hyperplasia (BPH) is a common disease among older men characterized by non-malignant proliferation of epithelial cells and inflammation. Nitric oxide synthase traffic inducer (NOSTRIN) is a pleiotropic regulator of endothelial cell function and signaling and exerts anti-inflammatory, anti-proliferation, and modulating nuclear factor-kappa B (NF-κB) signaling effects. Its expression and function in BPH tissues and prostate epithelial cells are unknown. The study aims to investigate the expression and functions of NOSTRIN in BPH, and its possible molecular mechanism.MethodsThe BPH model was constructed in male Institute of Cancer Research (ICR) mice using 5 mg/kg/day testosterone propionate (TP) for 30 days, and the model was evaluated by detecting prostate index, prostate epithelial thickness, and prostate-specific antigen (PSA) expression. Dihydrotestosterone (DHT, 10 nM)-induced in vitro model of human prostate epithelial cells (RWPE-1) was established. We generated lentivirus-harboring human NOSTRIN. The mRNA expression was detected by real-time quantitative polymerase chain reaction (PCR) assay; the protein expression or localization was detected by western blot assay, immunohistochemistry, or immunofluorescence staining. Cell proliferation was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and 5-ethynyl-2'-deoxyuridine (EdU) staining. Reactive oxygen species (ROS) production was observed by dihydroethidium staining. Nitric oxide (NO) and malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were detected using commercial kits. Enzyme-linked immunosorbent assay (ELISA) was used to determine levels of interleukin 1 beta (IL1B), interleukin 6 (IL6), interferon gamma (IFNG), and tumor necrosis factor (TNF).ResultsNOSTRIN expression was significantly inhibited in the TP-induced ICR mouse BPH model and DHT-induced model of RWPE-1 proliferation. Protein expression of the BPH-related and proliferation markers PSA and proliferating cell nuclear antigen (PCNA) was suppressed in NOSTRIN-overexpressing RWPE-1 cells exposed to DHT. NOSTRIN overexpression notably inhibited the RWPE-1 cell proliferation in vitro, as evidenced by MTT and EdU staining. NOSTRIN overexpression significantly decreased the expression of cell cycle-related proteins cyclin dependent kinase 4 (CDK4) and cyclin D1 (CCND1) in vitro. The production of ROS, NO, and lipid peroxidation products MDA was inhibited by NOSTRIN overexpression in vitro, while the SOD activity was increased. NOSTRIN overexpression reduced the mRNA expression of inflammatory mediator nitric oxide synthase 2 (NOS2) and inhibited the mRNA expression and secretion of pro-inflammatory cytokines IL1B, IL6, IFNG, and TNF in vitro. The mechanistic studies revealed an increased phosphorylation of NF-κB p65 in vivo and in vitro. Remarkably, NOSTRIN overexpression notably inhibited the protein expression of phospho-NF-κB p65 in vitro.ConclusionsNOSTRIN is involved in BPH by inhibiting proliferation, oxidative stress, and inflammation in prostate epithelial cells. These functions may act through the inhibition of NF-κB signaling.

01 Sep 2024·Digestive and Liver Disease

NOSTRIN is an emerging positive regulator of decompensated cirrhotic patients with portal hypertension

Article

Author: Vairappan, Balasubramaniyan ; Ts, Ravikumar ; Pottakkat, Biju ; Ram, Amit Kumar ; Mohan, Pazhanivel ; TS, Ravikumar

BACKGROUND AND AIMSDecreased nitric oxide (NO) bioavailability in a cirrhotic liver contributes to high intrahepatic vascular resistance (IHVR) and portal hypertension (PHT). Nostrin is an inhibitory protein of NO synthesising enzyme endothelial NO synthase (eNOS), shown to increase in cirrhosis with PHT, however, the precise molecular mechanism is poorly documented. This study aimed to elucidate the role of Nostrin and associated derangement in hepatic NO generation in cirrhotic liver. Further, we investigate whether Nostrin could be a biomarker in the progression of cirrhosis.METHODSThis study was conducted on sixty healthy subjects and 120 cirrhotic patients. In addition, liver tissue samples were collected from cirrhotic patients for the analysis of Nostrin, eNOS and inflammatory markers.RESULTSWhen compared to healthy controls, systemic levels of Nostrin and cGMP were elevated in compensated cirrhosis. In decompensated cirrhosis, further robust increases in Nostrin and cGMP were noted. Furthermore, Nostrin expression was considerably higher whilst reduced eNOS activity and hepatic cGMP levels in cirrhotic liver compared to control liver.CONCLUSIONSIn cirrhotic patients, a robust increase in hepatic Nostrin expression may reduce eNOS activity and associated local NO generation. Furthermore, Blood Nostrin concentration was higher and parallel to disease severity and could be a key diagnostic and prognostic biomarker in cirrhotic patients with PHT.

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