Protein kinase C-δ (PKC-δ) and PKC-α mediate Ca2+-dependent increases in CNP mRNA in human vascular cells

Mendonça, Maria C.; Koles, Nancy L.; Sellitti, Donald F.

doi:10.1016/j.vph.2012.05.002

Cited by 5 publications

(5 citation statements)

References 24 publications

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“…And the results showed that treatment with rottlerin, a specific inhibitor of PKC-δ, and Gö 6976, a specific inhibitor of PKC-α, lead to a decrease of PDGF-stimulated CNP mRNA expression. In addition, gene silencing by PKC-δ siRNA exhibited the similar results in HAoSMCs (Mendonca, Koles, & Sellitti, 2012). The present evidence may contribute to a consensus that PKC signaling pathway can be triggered in response to PDGF.…”

Section: Pkc Signaling Pathwaysupporting

confidence: 79%

Roles of platelet‐derived growth factor in vascular calcification

Ouyang

Zhang

Chen

et al. 2017

Journal Cellular Physiology

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Vascular calcification (VC) is prevalent in aging, and patients with hypertension, chronic kidney disease (CKD), or diabetes. VC is regarded as an active and complex process that involves multiple mechanisms responsible for calcium deposition in vessel wall. In light of the complicated pathogenesis of VC, effective therapy for ameliorating VC is limited. Thus, it is urgent to explore the potential mechanisms and find new targets for the therapy of VC. Platelet-derived growth factor (PDGF), a potent mitogen, and chemoattractant have been found to disturb the vascular homeostasis by inducing inflammation, oxidative stress, and phenotype transition, all of which accelerate the process of VC. The aim of current review is to present a review about the roles of PDGF in affecting VC and to establish a potential target for treating VC.

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Section: Pkc Signaling Pathwaysupporting

confidence: 79%

Roles of platelet‐derived growth factor in vascular calcification

Ouyang

Zhang

Chen

et al. 2017

Journal Cellular Physiology

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“…Protein kinase C (PKC) signaling also mediates the effects of LH in oocyte maturation (Morris and Richards, 1993;Shimamoto et al, 1993;Morris and Richards, 1995;Kawashima et al, 2014). Although PKC has been reported to regulate BNP and CNP signaling in cell lines (Hanford and Glembotski, 1996;Mendonca et al, 2006;Chu et al, 2008;Mendonca et al, 2009;Mendonca et al, 2012), further study is required to establish if and how PKC interacts with EGF signaling downstream of LH to regulate natriuretic peptide signaling within the ovarian follicle.…”

Section: Discussionmentioning

confidence: 99%

Epidermal growth factor‐network signaling mediates luteinizing hormone regulation of BNP and CNP and their receptor NPR2 during porcine oocyte meiotic resumption

Zhang

Chen

Yang

et al. 2014

Molecular Reproduction Devel

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The epidermal growth factor (EGF) network, induced by luteinizing hormone (LH), plays an essential role during the regulation of oocyte maturation, cumulus expansion, and ovulation. Binding of brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) to natriuretic receptor 2 (NPR2) generates cyclic guanosine monophosphate (cGMP), a key inhibitor that sustains porcine oocyte meiotic arrest. This correlation suggests that LH interacts with natriuretic-peptide signaling, possibly via the EGF network, to promote porcine meiotic resumption. In testing this hypothesis, we found that the majority of porcine oocytes remain arrested in the germinal-vesicle stage after 44 hr of co-culturing cumulus-oocyte complexes with 10(7) granulosa cells, which secreted active BNP and CNP; these natriuretic peptides associate with NPR2 on cumulus cells, thereby inhibiting porcine oocyte maturation. This inhibitory effect of BNP and CNP was relieved by EGF-like growth factors, whose expression naturally increases in granulosa cells 18 hr after human chorionic gonadotropin injection. LH and the EGF-like peptide amphiregulin (AREG) decreased BNP and CNP production in granulosa cells and down-regulated NPR2 expression in cumulus cells, which together decreased oocyte cGMP to levels that permit meiotic resumption. The effects of AREG on the gene expression of natriuretic-peptide signaling components and on oocyte maturation were completely blocked by the EGF receptor kinase inhibitor AG1478; the effect of LH, however, was only partially reversed by AG1478. Based on these results, LH regulates natriuretic-peptide signaling, although other pathways also cooperate with the EGF network to induce porcine oocyte maturation.

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“…In human VSMCs, PKC activation stimulates secretion of C-type natriuretic peptide (CNP), a known endogenous vasodilator [344, 345]. PMA increases CNP expression via PKCα- and PKCδ-mediated pathways, and PDGF increases CNP in SMCs via a PKCδ-dependent pathway [346]. PKC also regulates the activity of endothelial NO synthase, and in turn NO production and vasodilation [321].…”

Section: Protein Kinase Cmentioning

confidence: 99%

Evolving mechanisms of vascular smooth muscle contraction highlight key targets in vascular disease

Liu

Khalil

2018

Biochemical Pharmacology

116

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Vascular smooth muscle (VSM) plays an important role in the regulation of vascular function. Identifying the mechanisms of VSM contraction has been a major research goal in order to determine the causes of vascular dysfunction and exaggerated vasoconstriction in vascular disease. Major discoveries over several decades have helped to better understand the mechanisms of VSM contraction. Ca has been established as a major regulator of VSM contraction, and its sources, cytosolic levels, homeostatic mechanisms and subcellular distribution have been defined. Biochemical studies have also suggested that stimulation of Gq protein-coupled membrane receptors activates phospholipase C and promotes the hydrolysis of membrane phospholipids into inositol 1,4,5-trisphosphate (IP) and diacylglycerol (DAG). IP stimulates initial Ca release from the sarcoplasmic reticulum, and is buttressed by Ca influx through voltage-dependent, receptor-operated, transient receptor potential and store-operated channels. In order to prevent large increases in cytosolic Ca concentration ([Ca]), Ca removal mechanisms promote Ca extrusion via the plasmalemmal Ca pump and Na/Ca exchanger, and Ca uptake by the sarcoplasmic reticulum and mitochondria, and the coordinated activities of these Ca handling mechanisms help to create subplasmalemmal Ca domains. Threshold increases in [Ca] form a Ca-calmodulin complex, which activates myosin light chain (MLC) kinase, and causes MLC phosphorylation, actin-myosin interaction, and VSM contraction. Dissociations in the relationships between [Ca], MLC phosphorylation, and force have suggested additional Ca sensitization mechanisms. DAG activates protein kinase C (PKC) isoforms, which directly or indirectly via mitogen-activated protein kinase phosphorylate the actin-binding proteins calponin and caldesmon and thereby enhance the myofilaments force sensitivity to Ca. PKC-mediated phosphorylation of PKC-potentiated phosphatase inhibitor protein-17 (CPI-17), and RhoA-mediated activation of Rho-kinase (ROCK) inhibit MLC phosphatase and in turn increase MLC phosphorylation and VSM contraction. Abnormalities in the Ca handling mechanisms and PKC and ROCK activity have been associated with vascular dysfunction in multiple vascular disorders. Modulators of [Ca], PKC and ROCK activity could be useful in mitigating the increased vasoconstriction associated with vascular disease.

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Protein kinase C-δ (PKC-δ) and PKC-α mediate Ca2+-dependent increases in CNP mRNA in human vascular cells

Cited by 5 publications

References 24 publications

Roles of platelet‐derived growth factor in vascular calcification

Roles of platelet‐derived growth factor in vascular calcification

Epidermal growth factor‐network signaling mediates luteinizing hormone regulation of BNP and CNP and their receptor NPR2 during porcine oocyte meiotic resumption

Evolving mechanisms of vascular smooth muscle contraction highlight key targets in vascular disease

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