β-Actin regulates platelet nitric oxide synthase 3 activity through interaction with heat shock protein 90

Ji, Yong; Ferracci, Géraldine; Warley, Alice; Ward, Malcolm; Leung, Kit‐Yi; Samsuddin, Salma; Lévêque, Christian; Queen, Lindsay; Reebye, Vikash; Pal, Pallavi; Gkaliagkousi, Εugenia; Seager, Michael; Ferro, Albert

doi:10.1073/pnas.0611416104

Cited by 41 publications

(30 citation statements)

References 37 publications

(35 reference statements)

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“…50,51 In platelets, Hsp90 has been shown to associate with NOS3 and to enhance its activity in response to insulin 31 and after binding to the globular form of ␤-actin. 26 In endothelial cells, NOSIP and NOSTRIN both inhibit, 52,53 and dynamin-2 and porin both augment, 54,55 NOS3 activity. However, at present nothing is known about the possible regulation of NOS3 in platelets by these proteins.…”

Section: The L-arginine-no Pathway In Plateletsmentioning

confidence: 99%

“…The formation of this ternary complex in turn gives rise to an increase in Hsp90 degradation, which acts as a negative feedback on NOS3 activation in platelets. 26 Catecholamines and adenosine stimulate platelet NO production, effects that are prevented by NOS inhibition. 27,28 This has been linked to the activation of PKA and subsequent phosphorylation of the Ser 1177 residue in NOS3.…”

Section: The L-arginine-no Pathway In Plateletsmentioning

confidence: 99%

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Platelet-Derived Nitric Oxide Signaling and Regulation

Gkaliagkousi

Ritter

Ferro

2007

Circulation Research

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134

103

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Abstract-Nitric oxide (NO) exerts important vasodilatory, antiplatelet, antioxidant, antiadhesive, and antiproliferative effects. Although endothelium derived NO has been shown to be of prime importance in cardio-and vasculoprotection, until recently little was known about the role of platelet-derived NO. New evidence suggests that NO synthesized by platelets regulates platelet functions, in particular suppressing platelet activation and intravascular thrombosis. Moreover, platelet NO biosynthesis may be decreased in patients with cardiovascular risk factors or with coronary heart disease, and this may contribute to arterial thrombotic disease in these patients. Here, we review the current state of knowledge as regards the role of platelet-derived NO, both in normal physiology and in cardiovascular disease states, and compare platelet NO signaling and regulation with that in endothelial cells. (Circ Res. 2007;101:654-662.)

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Section: The L-arginine-no Pathway In Plateletsmentioning

confidence: 99%

Section: The L-arginine-no Pathway In Plateletsmentioning

confidence: 99%

Platelet-Derived Nitric Oxide Signaling and Regulation

Gkaliagkousi

Ritter

Ferro

2007

Circulation Research

Self Cite

134

103

View full text Add to dashboard Cite

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“…It has been proposed that actin remodeling can spatially organize enzymes such as ERK and their substrates and thus regulate enzyme kinetics (41). In addition, binding of enzymes to actin can regulate enzyme activity, and this binding is dependent on the polymerization state of actin (24). G-actin can shuttle in and out of the nucleus, where it regulates chromatin structure and transcription (47).…”

Section: Discussionmentioning

confidence: 99%

Role of Porphyromonas gingivalis SerB in Gingival Epithelial Cell Cytoskeletal Remodeling and Cytokine Production

Hasegawa¹,

Tribble²,

Baker

et al. 2008

Infect Immun

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The SerB protein of Porphyromonas gingivalis is a HAD family serine phosphatase that plays a critical role in entry and survival of the organism in gingival epithelial cells. SerB is secreted by P. gingivalis upon contact with epithelial cells. Here it is shown by microarray analysis that SerB impacts the transcriptional profile of gingival epithelial cells, with pathways involving the actin cytoskeleton and cytokine production among those significantly overpopulated with differentially regulated genes. Consistent with the transcriptional profile, a SerB mutant of P. gingivalis exhibited defective remodeling of actin in epithelial cells. Interaction between gingival epithelial cells and isolated SerB protein resulted in actin rearrangement and an increase in the F/G actin ratio. SerB protein was also required for P. gingivalis to antagonize interleukin-8 accumulation following stimulation of epithelial cells with Fusobacterium nucleatum. SerB is thus capable of modulating host cell signal transduction that impacts the actin cytoskeleton and cytokine production.

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“…This process can delay the recruitment of neutrophils preventing the proper formation of the neutrophil wall, facilitating initial microbial colonization of the periodontium [61]. Other bacteria such as T. denticola are also able to manipulate the interleukin response of the host by yet not understood mechanism(s) [62].…”

Section: Host Defense Mechanismsmentioning

confidence: 99%

Impact of Dental Plaque Biofilms in Periodontal Disease: Management and Future Therapy

Lazăr¹,

Dițu²,

Curuţiu³

et al. 2017

Periodontitis - A Useful Reference

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Oral cavity represents an ideal environment for the microbial cell growth, persistence, and dental plaque establishment. The presence of different microniches leads to the occurrence of different biofilm communities, formed on teeth surface, above gingival crevice or at subgingival level, on tongue, mucosa and dental prosthetics too. The healthy state is regulated by host immune system and interactions between microbial community members, maintaining the predominance of "good" microorganisms. When the complexity and volume of biofilms from the gingival crevice increase, chronic pathological conditions such as gingivitis and periodontitis can occur, predisposing to a wide range of complications. Bacteria growing in biofilms exhibit a different behavior compared with their counterpart, respectively planktonic or free cells. There have been described numerous mechanisms of differences in antibiotic susceptibility of biofilm embedded cells. Resistance to antibiotics, mediated by genetic factors or, phenotypical, due to biofilm formation, called also tolerance, is the most important cause of therapy failure of biofilm-associated infections, including periodontitis; the mechanisms of tolerance are different, the metabolic low rate and cell's dormancy being the major ones. The recent progress in science and technology has made possible a wide range of novel approaches and advanced therapies, aiming the efficient management of periodontal disease.

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β-Actin regulates platelet nitric oxide synthase 3 activity through interaction with heat shock protein 90

Cited by 41 publications

References 37 publications

Platelet-Derived Nitric Oxide Signaling and Regulation

Platelet-Derived Nitric Oxide Signaling and Regulation

Role of Porphyromonas gingivalis SerB in Gingival Epithelial Cell Cytoskeletal Remodeling and Cytokine Production

Impact of Dental Plaque Biofilms in Periodontal Disease: Management and Future Therapy

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