The effect of growth factors, cytokines, and extracellular matrix proteins on fibronectin production in human vascular smooth muscle cells

Kaiura, Terry L.; Itoh, Hiroyuki; Kubaska, Stephen M.; McCaffrey, Timothy A.; Liu, Bo; Kent, K. Craig

doi:10.1067/mva.2000.103692

Cited by 27 publications

(11 citation statements)

References 33 publications

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“…15 Several growth factors associated with vascular injury, specifically TGF-b and EGF, stimulate VSMCs to secrete fibronectin (Fn), a potent chemoattractant, through which they may indirectly induce VSMC migration. 7…”

Section: Other Growth Factorsmentioning

confidence: 99%

“…[1][2][3]6 When in the intima, VSMCs proliferate and are the major producer of ECM proteinsthe predominant component of developed lesions of intimal hyperplasia and atherosclerosis. 2,7 Migration of VSMCs from the media to the intima is an essential part of both pathologic processes, which make the study of this phenomenon important for understanding the development of vascular lesions. Cell migration involves a dominant plasma membrane leading lamellae, or leading edge, protruding in contact with an extracellular substrate, and binding by way of integrin transmembrane receptors to form focal complexes and secure focal adhesions (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vascular Smooth Muscle Cell Migration: Current Research and Clinical Implications

Willis¹,

Pierre-Paul²,

Sumpio

et al. 2004

Vasc Endovascular Surg

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Atherosclerosis and intimal hyperplasia are major causes of morbidity and mortality. These processes develop secondary to endothelial injury due to multiple stimuli, including smoking, diabetes mellitus, hypertension, and hyperlipidemia. Once this injury occurs, an essential element in the development of both these processes is vascular smooth muscle cell (VSMC) migration. Understanding the mechanisms involved in VSMC migration and ultimately the development of strategies by which this process can be inhibited, has been a major focus of research. The authors present a review of the extracellular proteins (growth factors, extracellular matrix components, and cell surface receptors) and intracellular signaling pathways involved in VSMC migration, as well as potential therapeutic approaches to inhibit this process.

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Section: Other Growth Factorsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vascular Smooth Muscle Cell Migration: Current Research and Clinical Implications

Willis¹,

Pierre-Paul²,

Sumpio

et al. 2004

Vasc Endovascular Surg

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“…Detected spectral shifts and high expression of the 405 nm blue signature (most likely overshadowing diminished 388 and 427 nm peaks), could therefore be correlated with a change of a molecular content of the human fibrinogen complex/fibrin. In particular, the appearance of human fibronectin-1, which is known to be produced by the hSMC cells 37 , was not present in the initial CFC matrix, but was later observed in the 4 weeks cell-free gel as shown in the mass-spectrometry data (Fig. 5).…”

Section: Resultsmentioning

confidence: 90%

Quantitative intrinsic auto-cathodoluminescence can resolve spectral signatures of tissue-isolated collagen extracellular matrix

Zieliński¹,

Vardar

Vythilingam

et al. 2019

Commun Biol

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By analyzing isolated collagen gel samples, we demonstrated in situ detection of spectrally deconvoluted auto-cathodoluminescence signatures of specific molecular content with precise spatial localization over a maximum field of view of 300 µm. Correlation of the secondary electron and the hyperspectral images proved ~40 nm resolution in the optical channel, obtained due to a short carrier diffusion length, suppressed by fibril dimensions and poor electrical conductivity specific to their organic composition. By correlating spectrally analyzed auto-cathodoluminescence with mass spectroscopy data, we differentiated spectral signatures of two extracellular matrices, namely human fibrin complex and rat tail collagen isolate, and uncovered differences in protein distributions of isolated extracellular matrix networks of heterogeneous populations. Furthermore, we demonstrated that cathodoluminescence can monitor the progress of a human cell-mediated remodeling process, where human collagenous matrix was deposited within a rat collagenous matrix. The revealed change of the heterogeneous biological composition was confirmed by mass spectroscopy.

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“…This result suggests that upregulation of these eight atherosclerosis-or injury-related genes in differentiating NCSCs was not solely due to the action of TGF on fully differentiated SMCs, and that most of the upregulation is likely related to the differentiation process itself. Syndecan-2 [38] Calcitonin receptor activity modifying protein-2 (isolated twice) [39] OX-2 [40] Fibronectin I [41] ABC-1 cholesterol transporter [42] *Tumor necrosis factor stimulated gene (TSG)-6 *Tenascin C (isolated twice) *Nicastrin *Cathepsin K *Oxidized LDL receptor-1 (LOX-1) *Macrophage chemotactic factor/Monocyte chemoattractant protein-(MCP-1) *MDM2 *Cyclin G1 *Vimentin * Denotes genes that are known to be upregulated in injury or atherosclerosis; references for these are given in Table 3.…”

Section: Effect Of Tgf-β1 On Gene Expression In Rat Aortic Smcsmentioning

confidence: 99%

A set of genes activated in differentiating smooth muscle is also activated in smooth muscle from injured arteries or atherosclerotic lesions

Moon

Ray

Leach

et al. 2002

Gene Function & Disease

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stimulated differentiation of purified rat neural crest stem cells (NCSCs) into smooth MI, USA muscle cells (SMCs) in culture, then subtracted NCSC sequences from SMC sequences to make a cDNA library specific for differentiating smooth muscle cells. Sequence analysis of the library shows that a large subset of clones is strongly associated with smooth muscle biology, confirming the overall success of the differentiation and subtraction procedures. Of this subset of clones, more than half encode proteins that have previously been shown to be upregulated in atherosclerotic or injured vascular smooth muscle as compared to normal vascular smooth muscle. Thus, a set of genes activated in differentiating smooth muscle of the neural crest lineage is also activated in atherosclerotic or injured vascular smooth muscle.

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The effect of growth factors, cytokines, and extracellular matrix proteins on fibronectin production in human vascular smooth muscle cells

Abstract: Cytokines, growth factors, and matrix proteins have varying quantitative effects on ECM protein production by human vascular SMCs. Knowledge of the factors that influence ECM protein production may allow for the design of specific inhibitors that can prevent intimal hyperplasia.

Cited by 27 publications

References 33 publications

Vascular Smooth Muscle Cell Migration: Current Research and Clinical Implications

Vascular Smooth Muscle Cell Migration: Current Research and Clinical Implications

Quantitative intrinsic auto-cathodoluminescence can resolve spectral signatures of tissue-isolated collagen extracellular matrix

A set of genes activated in differentiating smooth muscle is also activated in smooth muscle from injured arteries or atherosclerotic lesions

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