Effect of high glucose concentrations on prostacyclin-stimulating factor mRNA expression in cultured aortic smooth muscle cells

Ono, Yasuhiro; Umeda, Fumio; Kunisaki, Makoto; Sekiguchi, Naotaka; Hashimoto, Toshihiko; Nawata, Hajime

doi:10.1007/s001250050881

Cited by 5 publications

(4 citation statements)

References 41 publications

(23 reference statements)

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“…PSF mRNA is readily detectable from total retina both in rats and neonatal mice. PSF mRNA and protein are expressed in numerous ocular cell types in vitro at levels comparable to those observed in AECs and SMCs (4,5,(7)(8)(9)(10)(11). We demonstrate that the constitutive expression in retinal microvascular pericytes is greater than threefold high- The ability of PSF in RPC-conditioned media to increase REC PGI2 production.…”

Section: Discussionmentioning

confidence: 60%

“…Total RNA samples were isolated from cells using acid guanidinium thiocyanate-phenol-chloroform-extraction method (25) and subjected to Northern blot analysis as described previously. Radioactive PSF and TGF-β cDNA probes (9,26) were generated using Amersham Multiprime labeling kits and 32 P-dCTP (NEN Life Science Products, Boston, Massachusetts, USA). Quantitation of Northern blots was performed using a computing PhosphorImager with ImageQuant software analysis (Molecular Dynamics, Sunnyvale, California, USA).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Retinal expression, regulation, and functional bioactivity of prostacyclin-stimulating factor

Hata¹,

Clermont²,

Yamauchi³

et al. 2000

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 60%

Section: Methodsmentioning

confidence: 99%

Retinal expression, regulation, and functional bioactivity of prostacyclin-stimulating factor

Hata¹,

Clermont²,

Yamauchi³

et al. 2000

J. Clin. Invest.

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“…Elevated glucose level has been reported to reduce prostacyclin synthesis, a vasoactive compound, in bovine aortic endothelial cells [93] . Prostacyclin-stimulating factor (which regulates prostacyclin synthesis) is greatly decreased in smooth muscle cells of diabetic rats and patients [94] and this may lead to decreased level of prostacyclin ultimately resulting in the development of diabetic angiopathy [95] . Redox mechanisms in the vascular system can induce profound endothelial cell dysfunction such as vascular permeability via stimulation of platelet activating factor production, abnormal coagulation via inhibitor of prostaglandin I 2 synthesis and cell lysis [96] , as well as contributing to diabetic macroangiopathy by enhancing gene expression of growth factors of the smooth muscle cells (such as the heparin-binding epidermal growth factor) [97] .…”

Section: Diabetes-associated Cardiovascular Complicationsmentioning

confidence: 99%

Free Radicals, Antioxidants and Diabetes: Embryopathy, Retinopathy, Neuropathy, Nephropathy and Cardiovascular Complications

et al. 2006

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The metabolic disturbances in the insulin-dependent diabetes mellitus or type 1 and noninsulin-dependent diabetes mellitus or type 2 are associated with a number of complications including cardiovascular diseases, nephropathy, neuropathy, retinopathy leading to blindness and embryopathy or congenital malformations. Maternal diabetes is associated with a high incidence of congenital malformations and fetal abortions. Heart and kidney anomalies, along with central nervous system defects are frequent manifestations of a maternal diabetic environment. Glycation products from excess glucose can chemically modify DNA causing mutations and complex DNA rearrangements. Therefore, DNA damage in fetal tissues as a result of maternal diabetes may reflect a level of genomic injury sufficient to affect embryonic development. The formation of advanced glycation end products can accelerate vascular occlusion by quenching the vasodilating agent nitric oxide. Interaction with high-affinity receptors located on monocytes and macrophages can enhance the production of free radicals and reactive oxygen/nitrogen species, the secretion of tumor necrosis factor-α, interleukin-1 and insulin-like growth factor 1 which can proliferate endothelial, mesangial and smooth muscle cells and hence contribute significantly to the pathogenesis of cardiovascular complications. Retinopathy is characterized by increased vascular permeability, by vascular closure, together with the growth of new blood vessels on the retina and posterior surface of the vitreous. Reactive oxygen species are involved in decreased retinal blood flow, increased vascular permeability and disruption of blood-retinal barrier. The involvement of oxidative stress in the pathology of diabetes from its associated cardiovascular dysfunctions, nephropathy, neuropathy, retinopathy (leading to blindness) and embryopathy or congenital malformations, suggests that potential management of diabetes could benefit from use of dietary biofactors in medicinal and food plants. There is therefore a requirement for research to focus on the molecular mechanisms of action of extracts and/or the biofactors flavonoids, proanthocyanidins, alkaloids, etc. derived from these plants.

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“…PKC inhibitors, however, could prevent glucose's rapid effect on VEGF expression in vascular smooth muscle cells. By contributing to vascular tone dysregulation, glucose reduces the expression of prostacyclin (PGI2)-stimulating factor by 66% through osmolarity and PKC regulation [155] and increases AT1 (angiotensin II) receptor expression 2.5 fold [156]. Plasminogen activator inhibitor-1 (PAI-1) mRNA is rapidly upregulated after 2 hours of exposure to 27.5 mM glucose; it peaks at 4 hours and decreases after 8 hours, reaching normal levels at 24 hours [157].…”

Section: Genes Regulated By Glucose In Other Vascular Cell Typesmentioning

confidence: 99%

Regulation of Vascular Genes by Glucose

Stenina¹

2005

CPD

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Endothelial dysfunction is an early sign of diabetic vascular disease. Due to their unique position at the border between blood and vascular tissue, endothelial cells (EC) are the first vascular cells to sensor humoral changes, and they are able to transmit the information about these changes to other vascular cell types by changing their gene expression profile and producing growth factors, cytokines, adhesion molecules, and other bioactive molecules. These signals alter vascular cell dynamics and interactions, vascular tone and result in inability of the vessel to maintain athrombogenic luminal surface and in alteration of vascular permeability. Although researchers have yet to uncover the precise mechanism(s) that leads to diabetic vascular disease, hyperglycemia has been identified as an independent risk factor for micro- and macrovascular complications. Elevated levels of glucose induce the expression of a variety of genes related to atherogenesis and angiogenesis regulation. However, most of our current knowledge about the molecular mechanisms used by glucose to regulate gene expression is based on studies that used cells with insulin-dependent glucose transport (hepatocytes, adipocytes). Such cells are significantly different than vascular cells, in which glucose uptake is mostly imparted by insulin-independent mechanisms. This review summarizes current information about the effects of hyperglycemia and elevated glucose in in vitro systems on vascular gene expression and molecular transcriptional and post-transcriptional mechanisms that may regulate the changes related to diabetic vascular complications.

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Effect of high glucose concentrations on prostacyclin-stimulating factor mRNA expression in cultured aortic smooth muscle cells

Cited by 5 publications

References 41 publications

Retinal expression, regulation, and functional bioactivity of prostacyclin-stimulating factor

Retinal expression, regulation, and functional bioactivity of prostacyclin-stimulating factor

Free Radicals, Antioxidants and Diabetes: Embryopathy, Retinopathy, Neuropathy, Nephropathy and Cardiovascular Complications

Regulation of Vascular Genes by Glucose

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