Role of protein kinase C- or RhoA-induced Ca2+ sensitization in stretch-induced myogenic tone

Yeon, Dong Soo

doi:10.1016/s0008-6363(01)00496-5

Cited by 69 publications

(70 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PKCε has also been suggested to mediate Ca 2+ sensitization (14) although there are some reports against it (39,40). The present study did not directly explore the possible involvement of PKCε in the pressure-induced Ca 2+ sensitization.…”

Section: +mentioning

confidence: 75%

Distinct Roles of Protein Kinase C Isoforms in Myogenic Constriction of Rat Posterior Cerebral Arteries

Kashihara¹,

Nakayama²,

Ishikawa³

2008

J Pharmacol Sci

View full text Add to dashboard Cite

Abstract. The involvement of protein kinase C (PKC) in myogenic constriction at physiological intraluminal pressure was investigated in rat posterior cerebral arteries. ] i elevation gradually declined in the presence of rottlerin, and it was nearly abolished by ruthenium red. Immunohistochemical analysis showed positive staining for PKCα, γ, δ, and ε, but not PKCβ, in smooth muscle cells of rat posterior cerebral arteries. These results suggest distinct roles of PKC isoforms in myogenic constriction: conventional PKC mediates Ca 2+ sensitization, whereas PKCδ mediates sustained [Ca 2+ ] i elevation via the activation of cation channels, resulting in sustained constriction.

show abstract

Section: +mentioning

confidence: 75%

Distinct Roles of Protein Kinase C Isoforms in Myogenic Constriction of Rat Posterior Cerebral Arteries

Kashihara¹,

Nakayama²,

Ishikawa³

2008

J Pharmacol Sci

View full text Add to dashboard Cite

show abstract

“…68,69 Experiments to determine the relative importance of PA SMC versus other cell types in the observed cytoprotective effects of NEP are being developed. In addition, we are expanding the current observations made in mice to the study of relevant human disease states.…”

Section: Discussionmentioning

confidence: 99%

Neprilysin Null Mice Develop Exaggerated Pulmonary Vascular Remodeling in Response to Chronic Hypoxia

Dempsey

Wick

Karoor³

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

Neprilysin is a transmembrane metalloendopeptidase that degrades neuropeptides that are important for both growth and contraction. In addition to promoting carcinogenesis, decreased levels of neprilysin increases inflammation and neuroendocrine cell hyperplasia, which may predispose to vascular remodeling. Early pharmacological studies showed a decrease in chronic hypoxic pulmonary hypertension with neprilysin inhibition. We used a genetic approach to test the alternate hypothesis that neprilysin depletion increases chronic hypoxic pulmonary hypertension. Loss of neprilysin had no effect on baseline airway or alveolar wall architecture, vessel density, cardiac function, hematocrit, or other relevant peptidases. Only lung neuroendocrine cell hyperplasia and a subtle neuropeptide imbalance were found. After chronic hypoxia, neprilysin-null mice exhibited exaggerated pulmonary hypertension and striking increases in muscularization of distal vessels. Subtle thickening of proximal media/adventitia not typically seen in mice was also detected. In contrast, adaptive right ventricular hypertrophy was less than anticipated. Hypoxic wild-type pulmonary vessels displayed close temporal and spatial relationships between decreased neprilysin and increased cell growth. Smooth muscle cells from neprilysin-null pulmonary arteries had increased proliferation compared with controls, which was decreased by neprilysin replacement. These data suggest that neprilysin may be protective against chronic hypoxic pulmonary hypertension in the lung, at least in part by attenuating the growth of smooth muscle cells. Lung-targeted strategies to increase neprilysin levels could have therapeutic benefits in the treatment of this disorder. Chronic hypoxic pulmonary hypertension (PHTN) is a major clinical problem, complicating most lung and heart disorders. 1,2 In large animal models of chronic hypoxic PHTN that closely resemble human disease, the earliest pulmonary artery (PA) smooth muscle cell (SMC) proliferative changes occur at the medial/adventitial border. 3 Growth and migration of SMC and myofibroblasts in distal vessels is also a prominent feature. 4,5 These structural changes, together with derangements in vascular tone, are major contributors to the severity of chronic hypoxic PHTN. [1][2][3][4][5][6] However, mechanisms that regulate susceptibility to, and severity of, chronic hypoxic PHTN and vascular remodeling remain poorly understood. Currently available treatments for chronic hypoxic PHTN are also inadequate.

show abstract

“…It was also demonstrated that exposure of mouse cortical brain slices to hypoosmosis stimulated ROS production, which was absent in brain slices from p47phox knockout animals, suggesting that PKC-induced p47phox phosphorylation had a pivotal role in osmotic stress-induced Nox activation in astrocytes (Reinehr et al, 2007). It is noteworthy that several lines of study have demonstrated that PKC activation can be observed after exposing cells to a variety of stress stimuli (for example, cytotoxic chemicals, physical stretch, osmotic shock, hypoxia, and inflammatory cytokines) (Kugiyama et al, 1992;Rzymkiewicz et al, 1996;Goldberg et al, 1997;Liu and Huang, 1997;Schanne et al, 1997;Wyatt et al, 1997;Deng and Poretz, 2002;Motley et al, 2002;Suzuma et al, 2002;Yeon et al, 2002;Liu et al, 2003), and PKC may be viewed as a stress sensor in some circumstances (Barnett et al, 2007). If PKC is indeed involved in Nox activation in acute stress responses, the specific roles of different PKC isoforms need to be defined.…”

Section: B Protein Kinase C-mediated Phosphorylationmentioning

confidence: 99%

NADPH Oxidase-Mediated Redox Signaling: Roles in Cellular Stress Response, Stress Tolerance, and Tissue Repair

2011

View full text Add to dashboard Cite

Role of protein kinase C- or RhoA-induced Ca2+ sensitization in stretch-induced myogenic tone

Cited by 69 publications

References 30 publications

Distinct Roles of Protein Kinase C Isoforms in Myogenic Constriction of Rat Posterior Cerebral Arteries

Distinct Roles of Protein Kinase C Isoforms in Myogenic Constriction of Rat Posterior Cerebral Arteries

Neprilysin Null Mice Develop Exaggerated Pulmonary Vascular Remodeling in Response to Chronic Hypoxia

NADPH Oxidase-Mediated Redox Signaling: Roles in Cellular Stress Response, Stress Tolerance, and Tissue Repair

Contact Info

Product

Resources

About