Increased Gene and Protein Expression of the Novel eNOS Regulatory Protein NOSTRIN and a Variant in Alcoholic Hepatitis

Mookerjee, Rajeshwar P.; Wiesenthal, Anja; Icking, Ann; Hodges, Stephen; Davies, Nathan; Schilling, Kirstin; Sen, Sambit; Williams, Roger; Novelli, Marco; Müller‐Esterl, Werner; Jalan, Rajiv

doi:10.1053/j.gastro.2006.12.035

Cited by 48 publications

(52 citation statements)

References 31 publications

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“…4A). The development of ammoniainduced ROS production was further quantitatively measured as described previously, [34] and confirmed that primary hHSCs treated with ammonia produced significant ROS (Fig. 4B).…”

Section: Hyperammonemia Induces Ros Production In Hhscsupporting

confidence: 81%

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Ammonia produces pathological changes in human hepatic stellate cells and is a target for therapy of portal hypertension

Jalan

Chiara

Vairappan

et al. 2016

Journal of Hepatology

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Section: Hyperammonemia Induces Ros Production In Hhscsupporting

confidence: 81%

“…7C). eNOS protein expression was significantly increased in BDL rats compared to sham animals (as we previously described [34]) and this remained statistically unchanged after OP therapy (Fig. 7C).…”

Section: In Vivo Study Ii: Treatment With Op Improves Portal Pressuresupporting

confidence: 78%

Ammonia produces pathological changes in human hepatic stellate cells and is a target for therapy of portal hypertension

Jalan

Chiara

Vairappan

et al. 2016

Journal of Hepatology

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“…NO is one of the essential regulators of intrahepatic vascular tone and decreased production of NO results in portal hypertension (Iwakiri et al, 2008;Sanyal et al, 2008). NOS inhibitors such as caveolin-1 (Shah et al, 1999), ADMA (Mookerjee et al, 2007b), and NOSTRIN (Mookerjee et al, 2007c) play roles in the occurrence of portal hypertension. Severity of portal hypertension is correlated with levels of ADMA (Mookerjee et al, 2007b).…”

Section: Discussionmentioning

confidence: 99%

The restorative effect of ascorbic acid on liver injury inducedby asymmetric dimethylarginine

Okuyucu¹,

Şalış²,

Alıcı³

et al. 2016

Turk J Biol

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“…32,38 Additional antibodies were monoclonal eNOS and monoclonal peNOS Ser 1179 antibody (BD Bioscience, Heidelberg, Germany), polyclonal rabbit anti-M3R antibody (Santa Cruz Biotechnology, Heidelberg, Germany), polyclonal goat anti-platelet endothelial cell adhesion molecule-1 antibody (BD Bioscience, Heidelberg, Germany), polyclonal anti-caveolin-1 antibody (Santa Cruz Biotechnology, Heidelberg, Germany), monoclonal mouse anti-GAPDH antibody (Abcam, Cambridge, United Kingdom), monoclonal anti-extracellular signal-regulated protein kinases 1 and 2 (ERK1/2; Cell Signaling Technology, Leiden, The Netherlands), monoclonal mouse anti-maltose-binding protein (NEB, Ipswich, MA), and polyclonal rabbit anti-green fluorescent protein antibody (Clontech, Saint-Germain-en-Laye, France).…”

Section: Antibodiesmentioning

confidence: 99%

The F-BAR Protein NOSTRIN Dictates the Localization of the Muscarinic M3 Receptor and Regulates Cardiovascular Function

Kovačević

Müller

Kojonazarov

et al. 2015

Circulation Research

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Rationale: Endothelial dysfunction is an early event in cardiovascular disease and characterized by reduced production of nitric oxide (NO). The F-BAR protein NO synthase traffic inducer (NOSTRIN) is an interaction partner of endothelial NO synthase and modulates its subcellular localization, but the role of NOSTRIN in pathophysiology in vivo is unclear. Objective: We analyzed the consequences of deleting the NOSTRIN gene in endothelial cells on NO production and cardiovascular function in vivo using NOSTRIN knockout mice. Methods and Results: The levels of NO and cGMP were significantly reduced in mice with endothelial cell–specific deletion of the NOSTRIN gene resulting in diastolic heart dysfunction. In addition, systemic blood pressure was increased, and myograph measurements indicated an impaired acetylcholine-induced relaxation of isolated aortic rings and resistance arteries. We found that the muscarinic acetylcholine receptor subtype M3 (M3R) interacted directly with NOSTRIN, and the latter was necessary for correct localization of the M3R at the plasma membrane in murine aorta. In the absence of NOSTRIN, the acetylcholine-induced increase in intracellular Ca 2+ in primary endothelial cells was abolished. Moreover, the activating phosphorylation and Golgi translocation of endothelial NO synthase in response to the M3R agonist carbachol were diminished. Conclusions: NOSTRIN is crucial for the localization and function of the M3R and NO production. The loss of NOSTRIN in mice leads to endothelial dysfunction, increased blood pressure, and diastolic heart failure.

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Increased Gene and Protein Expression of the Novel eNOS Regulatory Protein NOSTRIN and a Variant in Alcoholic Hepatitis

Cited by 48 publications

References 31 publications

Ammonia produces pathological changes in human hepatic stellate cells and is a target for therapy of portal hypertension

Ammonia produces pathological changes in human hepatic stellate cells and is a target for therapy of portal hypertension

The restorative effect of ascorbic acid on liver injury inducedby asymmetric dimethylarginine

The F-BAR Protein NOSTRIN Dictates the Localization of the Muscarinic M3 Receptor and Regulates Cardiovascular Function

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