Shear Stress Induction of C-type Natriuretic Peptide (CNP) in Endothelial Cells is Independent of NO Autocrine Signaling

Zhang, Zhaohui; Xiao, Zeshuai; Diamond, Scott L.

doi:10.1114/1.203

Cited by 30 publications

(23 citation statements)

References 39 publications

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“…It has been proposed that CNP in the mammalian vasculature maintains a substantial cytoprotective, anti-mitogenic, antiatherogenic and vasorelaxant influence on the blood vessel wall, and that loss of endothelial-derived CNP may be an important contributor to the pathogenesis of inflammatory cardiovascular diseases such as atherosclerosis and restenosis (Ahluwalia et al, 2004). Other vascular stressors such as shear stress (blood flow) and stretch (blood pressure) have also been shown to augment vascular CNP production in mammals (Itoh and Nakao, 1999;Okahara et al, 1995;Zhang et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Endogenous vascular synthesis of B-type and C-type natriuretic peptides in the rainbow trout

Johnson

Hoagland

Olson

2011

Journal of Experimental Biology

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SUMMARYIn mammals, natriuretic peptides (NPs) lower blood pressure, reduce blood volume and broadly inhibit cardiovascular remodeling. NPs are often referred to as cardiac hormones, though they also have integral roles in regulating vascular tone, endothelial remodeling and inhibiting vascular smooth muscle cell hypertrophy. Two NPs [atrial (ANP) and C-type (CNP)] have been identified as endogenous constituents in the vasculature of mammals, though such a phenomenon has not previously been described in fishes. Here we describe the endogenous production of B-type NP (BNP) and CNP in multiple blood vessels of the rainbow trout. Western blot analysis showed pro-BNP and pro-CNP production in the efferent branchial artery, celiacomesenteric artery, ventral aorta and anterior cardinal vein. The detection of pro-BNP and pro-CNP was also supported by MALDI-TOF mass spectrometry analysis of NP-enriched tissue extracts. Although vascular pro-peptide levels of BNP and CNP were quantitatively quite comparable to those found in reference tissues (the atrium for BNP and brain for CNP), mRNA levels of these NPs in the vasculature were greatly reduced as determined by quantitative PCR. When the evolutionarily conserved vascular NP (CNP) was infused into un-anesthetized trout, it reduced central venous pressure and mean circulatory filling pressure. CNP also decreased cardiac output via a reduction in preload. The presence of endogenous NP production in the trout vasculature and potent in vivo hypotensive effects further support the numerous functional similarities between teleost and mammalian NP systems. Supplementary material available online at

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Section: Discussionmentioning

confidence: 99%

Endogenous vascular synthesis of B-type and C-type natriuretic peptides in the rainbow trout

Johnson

Hoagland

Olson

2011

Journal of Experimental Biology

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“…Blockade of flow up-regulated KLF-2 expression significantly reduced the expression of several flow-regulated genes, including CNP, suggesting that KLF-2 could potentially mediate the flow-mediated increases in CNP production in vivo that have been described [16,104]. Whether KLF-2 bears any affinity to KLF-9 in binding to a tandem GC-box in preference to a single GC-box has yet to be determined.…”

Section: Putative Transcription Factorsmentioning

confidence: 99%

“…These include an up-regulation of CNP transcription by shear stress [16,104], and an increase in mRNA levels in human cells by the bioactive lipid, lysophosphatidylcholine, in a process independent of intracellular calcium flux [53]. Similarly, the observed suppression of endothelial CNP by vascular endothelial growth factor (VEGF) might be specific to those cells, such as endothelial cells, that express VEGF receptors in high concentration [26].…”

Section: Cnp Regulation In the Cardiovascular Systemmentioning

confidence: 99%

Regulation of C-type natriuretic peptide expression

2011

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a b s t r a c t C-type natriuretic peptide (CNP) is a member of the small family of natriuretic peptides that also includes atrial natriuretic peptide (ANP) and brain, or B-type natriuretic peptide (BNP). Unlike them, it performs its major functions in an autocrine or paracrine manner. Those functions, mediated through binding to the membrane guanylyl cyclase natriuretic peptide receptor B (NPR-B), or by signaling through the non-enzyme natriuretic peptide receptor C (NPR-C), include the regulation of endochondral ossification, reproduction, nervous system development, and the maintenance of cardiovascular health. To date, the regulation of CNP gene expression has not received the attention that has been paid to regulation of the ANP and BNP genes. CNP expression in vitro is regulated by TGF-␤ and receptor tyrosine kinase growth factors in a cell/tissue-specific and sometimes species-specific manner. Expression of CNP in vivo is altered in diseased organs and tissues, including atherosclerotic vessels, and the myocardium of failing hearts. Analysis of the human CNP gene has led to the identification of a number of regulatory sites in the proximal promoter, including a GC-rich region approximately 50 base pairs downstream of the Tata box, and shown to be a binding site for several putative regulatory proteins, including transforming growth factor clone 22 domain 1 (TSC22D1) and a serine threonine kinase (STK16). The purpose of this review is to summarize the current literature on the regulation of CNP expression, emphasizing in particular the putative regulatory elements in the CNP gene and the potential DNA-binding proteins that associate with them.Published by Elsevier Inc.

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“…The addition of flow to a static system also inherently adds fluid shear stress. The addition of fluid shear stress augments mass and heat transport 5,6,17 and modulates cellular activity, [14][15][16]18,19 but the exact mechanisms through which it functions are incompletely known. The physiochemical factors that govern gene transfer for retroviral methods have been extensively considered.…”

Section: Introductionmentioning

confidence: 99%

“…Parallel plate flow is also desirable because it is well described, both theoretically and experimentally. [1][2][3][4][14][15][16] This work seeks to characterize the addition of convection to static transfection protocols in terms of modulating the amount of plasmid that reaches the cellular surface and, consequently, the amount available for uptake and successful incorporation into the cell. The addition of flow to a static system also inherently adds fluid shear stress.…”

Section: Introductionmentioning

confidence: 99%

Convective flow increases lipoplex delivery rate to in vitro cellular monolayers

Harris

Giorgio

2005

Gene Ther

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The mass transport characteristics of cationic, nonviral liposome-DNA plasmid complexes (lipoplexes) were evaluated over a range of fluid shear stresses. The typical case of stagnant flow transfection was expanded to include controlled fluid convection provided by constant flow through a parallel plate flow chamber. Equations describing the transport of lipoplex by sedimentation and convection were derived from theory and solved numerically. Instantaneous lipoplex delivery rate and total lipoplex surface delivery during a 72-h transfection were estimated for two shear stress levels and for static conditions. Theory predicted that lipoplex is delivered to the cell surface more than 12-to 19-fold faster through the addition of convection, at least for physiologic shear stresses of 2.3-9.7 dyn/cm 2 , respectively. These calculations were tested experimentally using a cell line (ECV-304) transfected with fluorescently labeled plasmid DNA formulated into a lipoplex. Transfections were conducted during cellular exposure to the same known, uniform levels of fluid shear stress presumed in theoretical calculations. Lipoplex delivery was increased by more than nine-fold at 2.3 dyn/cm 2 compared to the static case as assessed by flow cytometric measurement. Lipoplex delivery was modestly reduced at the highest fluid shear stress, to six-fold of the static case, consistent with the disruption of lipoplex-cell binding mediated by hydrodynamic forces. The complicated relationship between fluid convection and lipoplex delivery has important implications for nonviral gene therapy. Gene Therapy (2005) 12, 512-520.

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Shear Stress Induction of C-type Natriuretic Peptide (CNP) in Endothelial Cells is Independent of NO Autocrine Signaling

Cited by 30 publications

References 39 publications

Endogenous vascular synthesis of B-type and C-type natriuretic peptides in the rainbow trout

Endogenous vascular synthesis of B-type and C-type natriuretic peptides in the rainbow trout

Regulation of C-type natriuretic peptide expression

Convective flow increases lipoplex delivery rate to in vitro cellular monolayers

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