Collagen type IV-specific tripeptides for selective adhesion of endothelial and smooth muscle cells

2012 ◽  
Vol 109 (7) ◽  
pp. 1808-1816 ◽  
Author(s):  
Kei Kanie ◽  
Yuji Narita ◽  
Yingzi Zhao ◽  
Fumiaki Kuwabara ◽  
Makoto Satake ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type Iv ◽  
Type Iv

scholarly journals Cyclic Mechanical Stretch Induced Smooth Muscle Cell Changes in Cerebral Aneurysm Progress by Reducing Collagen Type IV and Collagen Type VI Levels

2018 ◽  
Vol 45 (3) ◽  
pp. 1051-1060 ◽  
Author(s):  
Peixi Liu ◽  
Yaying Song ◽  
Yingjie Zhou ◽  
Yingjun Liu ◽  
Tianming Qiu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Collagen Type ◽  
Cerebral Aneurysms ◽  
Muscle Cells ◽  
Mechanical Stretch ◽  
Collagen Type Iv ◽  
Type Iv

Background/Aims: Cerebral aneurysm growth is characterized by continuous structural weakness of local smooth muscle cells, though the mechanism is unclear. In this study, we examine protein changes in cerebral aneurysm and human brain vascular smooth muscle cells after cyclic mechanical stretch. We further explore the relationship between the smooth muscle cell changes and reductions in the levels of collagen types IV and VI. Methods: Saccular cerebral aneurysms (n=10) were collected, and temporal artery samples were used as controls. Quantitative proteomics were analyzed and histopathological changes were examined. Smooth muscle cells were cultured in a flexible silicone chamber and subjected to 15% cyclic mechanical stretch. The effect of stretch on the cell viability, function, gene and protein expression were further studied for the understanding the molecular mechanism of aneurysm development. Results: Proteomics analysis revealed 92 proteins with increased expression and 88 proteins with decreased expression compared to the controls (p<0.05). KEGG pathway analysis showed that the change in focal adhesion and extracellular matrix-receptor interaction, suggesting the involvement of collagen type IV and VI. The aneurysm tissue exhibited fewer smooth muscle cells and lower levels of collagen type IV and VI. Human brain vascular smooth muscle cell culture showed spindle-like cells and obvious smooth muscle cell layer. Cell proteomics analysis showed that decreased expression of 118 proteins and increased expression of 32 proteins in smooth muscle cells after cyclic mechanical stretch. KEGG pathway analysis indicated that focal adhesion and ECM-receptor interaction were involved. After cyclic mechanical stretch, collagen type IV and IV expression were decreased. Moreover, the stretch induced MMP-1 and MMP-3 expression elevation. Conclusion: We demonstrated that collagen type IV and VI were decreased in cerebral aneurysms and continuous cyclic mechanical stretch induced smooth muscle cell changes. Smooth muscle cell protection provides an additional therapeutic option to prevent the growth of cerebral aneurysms.

Stereotactic Radiosurgery of the Rete Mirabile in Swine: A Longitudinal Study of Histopathological Changes

Neurosurgery ◽  
2006 ◽  
Vol 58 (3) ◽  
pp. 551-558 ◽  
Author(s):  
Reza Jahan ◽  
Timothy D. Solberg ◽  
Daniel Lee ◽  
Paul Medin ◽  
Satoshi Tateshima ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Stereotactic Radiosurgery ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type Iv ◽  
Histopathological Changes ◽  
Rete Mirabile ◽  
Type Iv

Abstract OBJECTIVE: Stereotactic radiosurgery is an established, effective treatment for brain arteriovenous malformations. The mechanisms of vessel occlusion in arteriovenous malformations has not been extensively evaluated. To better understand these mechanisms, we report histopathological changes in the swine rete mirabile after stereotactic radiosurgery. METHODS: Thirty-five swine were used, 15 as nonradiated controls and 20 as radiated. Two in the control group and five in the radiated group were sacrificed before the study endpoint. Tissue was obtained from 13 nonradiated (4 at 3 mo, 5 at 6 mo, 4 at 9 mo) and 15 radiated swine (2 at 3 mo, 3 at 6 mo, 10 at 9 mo) for histological, immunohistochemical, and morphometric analysis. RESULTS: Radiated vessels showed increasing intimal hyperplasia over the follow-up period. Histometrical analysis confirmed this with evidence of progressive luminal narrowing over the follow-up period. Immunohistochemical analysis showed intimal cells to be proliferating smooth muscle cells with surrounding extracellular collagen Type IV. Adventitial fibrosis composed of collagen Type IV was also seen with smooth muscle cells interspersed within the collagen matrix. The nonradiated animals showed no intimal hyperplasia or change in the appearance or size of the vessels over the same follow-up period. Adventitial fibrosis was minimal in the nonradiated animals. CONCLUSION: The vessels show an intimal response to radiation with progressive occlusion caused by migrating, proliferating smooth muscle cells, a likely source of the extracellular collagen in the intima. Cytokine mediated pathways likely produce these morphological changes. Future studies will be directed toward elucidating these underlying molecular mechanisms.

An Arteriovenous Malformation Model for Stereotactic Radiosurgery Research

Neurosurgery ◽  
2007 ◽  
Vol 61 (1) ◽  
pp. 152-159 ◽  
Author(s):  
Reza Jahan ◽  
Timothy D. Solberg ◽  
Daniel Lee ◽  
Paul Medin ◽  
Satoshi Tateshima ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Arteriovenous Malformation ◽  
Smooth Muscle Cells ◽  
Stereotactic Radiosurgery ◽  
Intimal Hyperplasia ◽  
Morphological Changes ◽  
Muscle Cells ◽  
Collagen Type Iv ◽  
Internal Elastic Lamina ◽  
Type Iv

Abstract OBJECTIVE To introduce the utilization of a swine arteriovenous malformation (AVM) model for stereotactic radiosurgery research and to describe the morphological changes in the vessels after radiation. METHODS The model was created in six animals by creation of a right-sided carotid-jugular fistula. Pre- and postsurgical hemodynamic evaluation was performed. The left rete was radiated in four animals; two animals were not radiated. All animals were sacrificed 4 months after surgery, and the bilateral retia were obtained at autopsy. RESULTS There were no procedure-related complications. A pressure gradient of 20 mmHg across the nidus was obtained after surgery. The peak velocity in the arterial feeder increased from 18.5 to 83 cm/s. Microscopic examination of the control animals showed intimal hyperplasia and disrupted internal elastic lamina, similar to human AVMs. The radiated retia showed more prominent intimal hyperplasia. This was confirmed by histometric studies showing greater luminal occlusion in radiated specimens. Adventitial fibrosis was prominent in the radiated retia and was absent in the control animals. Immunohistochemical studies showed proliferating smooth muscle cells in the intima. The adventitial fibrosis consisted of smooth muscle cells surrounded by collagen Type IV extracellular matrix. CONCLUSION The nidus component and high-flow vasculopathy make this an attractive model for stereotactic radiosurgery research. Histology of the radiated models is similar to those described in radiated human AVMs. Further studies of the model are warranted to gain a better understanding of the cellular and molecular events in AVM vessels after stereotactic radiosurgery.

scholarly journals Perlecan regulates Oct-1 gene expression in vascular smooth muscle cells.

1997 ◽  
Vol 8 (6) ◽  
pp. 999-1011 ◽  
Author(s):  
M C Weiser ◽  
N A Grieshaber ◽  
P E Schwartz ◽  
R A Majack
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Type Iv Collagen ◽  
Muscle Cells ◽  
Mrna Levels ◽  
Type Iv

Vascular smooth muscle cells (SMCs) are very quiescent in the mature vessel and exhibit a remarkable phenotype-dependent diversity in gene expression that may reflect the growth responsiveness of these cells under a variety of normal and pathological conditions. In this report, we describe the expression pattern of Oct-1, a member of a family of transcription factors involved in cell growth processes, in cultured and in in vivo SMCs. Oct-1 mRNA was undetectable in the contractile-state in vivo SMCs; was induced upon disruption of in vivo SMC-extracellular matrix interactions; and was constitutively expressed by cultured SMCs. Oct-1 transcripts were repressed when cultured SMCs were plated on Engelbreth-Holm-Swarm tumor-derived basement membranes (EHS-BM) but were rapidly induced after disruption of SMC-EHS-BM contacts; reexpression was regulated at the transcriptional level. To identify the EHS-BM component involved in the active repression of Oct-1 mRNA expression, SMCs were plated on laminin, type IV collagen, fibronectin, or perlecan matrices. Oct-1 mRNA levels were readily detectable when SMCs were cultured on matrices composed of laminin, type IV collagen, or fibronectin but were repressed when SMCs were cultured on perlecan matrices. Finally, the Oct-1-suppressing activity of EHS-BM was sensitive to heparinase digestion but not to chondroitinase ABC or hyaluronidase digestion, suggesting that the heparan sulfate side chains of perlecan play a biologically important role in negatively regulating the expression of Oct-1 transcripts.

scholarly journals Maximal migration of human smooth muscle cells on fibronectin and type IV collagen occurs at an intermediate attachment strength

1993 ◽  
Vol 122 (3) ◽  
pp. 729-737 ◽  
Author(s):  
PA DiMilla ◽  
JA Stone ◽  
JA Quinn ◽  
SM Albelda ◽  
DA Lauffenburger
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Cells ◽  
Type Iv Collagen ◽  
Muscle Cells ◽  
Migration Speed ◽  
Initial Attachment ◽  
Type Iv ◽  
Attachment Strength

Although a biphasic dependence of cell migration speed on cell-substratum adhesiveness has been predicted theoretically, experimental data directly demonstrating a relationship between these two phenomena have been lacking. To determine whether an optimal strength of cell-substratum adhesive interactions exists for cell migration, we measured quantitatively both the initial attachment strength and migration speed of human smooth muscle cells (HSMCs) on a range of surface concentrations of fibronectin (Fn) and type IV collagen (CnIV). Initial attachment strength was measured in order to characterize short time-scale cell-substratum interactions, which may be representative of dynamic interactions involved in cell migration. The critical fluid shear stress for cell detachment, determined in a radial-flow detachment assay, increased linearly with the surface concentrations of adsorbed Fn and CnIV. The detachment stress required for cells on Fn, 3.6 +/- 0.2 x 10(-3) mu dynes/absorbed molecule, was much greater than that on CnIV, 5.0 +/- 1.4 x 10(-5) mu dynes/absorbed molecule. Time-lapse videomicroscopy of individual cell movement paths showed that the migration behavior of HSMCs on these substrates varied with the absorbed concentration of each matrix protein, exhibiting biphasic dependence. Cell speed reached a maximum at intermediate concentrations of both proteins, with optimal concentrations for migration at 1 x 10(3) molecules/micron2 and 1 x 10(4) molecules/micron2 on Fn and CnIV, respectively. These optimal protein concentrations represent optimal initial attachment strengths corresponding to detachment shear stresses of 3.8 mu dyne/micron2 on Fn and 1.5 mu dyne/micron2 on CnIV. Thus, while the optimal absorbed protein concentrations for migration on Fn and CnIV differed by an order of magnitude, the optimal initial attachment strengths for migration on these two proteins were very similar. Further, the same minimum strength of initial attachment, corresponding to a detachment shear stress of approximately 1 mu dyne/micron2, was required for movement on either protein. These results suggest that initial cell-substratum attachment strength is a central variable governing cell migration speed, able to correlate observations of motility on substrata differing in adhesiveness. They also demonstrate that migration speed depends in biphasic manner on attachment strength, with maximal migration at an intermediate level of cell-substratum adhesiveness.

scholarly journals Collagen degradation and platelet-derived growth factor stimulate the migration of vascular smooth muscle cells

2000 ◽  
Vol 113 (11) ◽  
pp. 2055-2064
Author(s):  
E. Stringa ◽  
V. Knauper ◽  
G. Murphy ◽  
J. Gavrilovic
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type I ◽  
Type I

Cell migration is a key event in many biological processes and depends on signals from both extracellular matrix and soluble motogenic factors. During atherosclerotic plaque development, vascular smooth muscle cells migrate from the tunica media to the intima through a basement membrane and interstitial collagenous matrix and proliferate to form a neointima. Matrix metalloproteinases have previously been implicated in neointimal formation and in this study smooth muscle cell adhesion and migration on degraded collagen have been evaluated. Vascular smooth muscle cells adhered to native intact collagen type I and to its first degradation by-product, 3/4 fragment (generated by collagenase-3 cleavage), unwound at 35 degrees C to mimic physiological conditions. PDGF-BB pre-treatment induced a fourfold stimulation of smooth muscle cell motility on the collagen 3/4 fragment whereas no increase in smooth muscle cell motility on collagen type I was observed. Cell migration on collagen type I was mediated by alpha2 integrin, whereas PDGF-BB-stimulated migration on the 3/4 collagen fragment was dependent on alphavbeta3 integrin. alphavbeta3 integrin was organised in clusters concentrated at the leading and trailing edges of the cells and was only expressed when cells were exposed to the 3/4 collagen fragment. Tyrphostin A9, an inhibitor of PDGF receptor-beta tyrosine kinase activity, resulted in complete abolition of migration of PDGF-BB treated cells on collagen type I and 3/4 fragment. These results strongly support the hypothesis that the cellular migratory response to soluble motogens can be regulated by proteolytic modification of the extracellular matrix.

A Novel In-Vitro System for the Simultaneous Exposure of Bladder Smooth Muscle Cells to Mechanical Strain and Sustained Hydrostatic Pressure

2002 ◽  
Vol 124 (2) ◽  
pp. 208-213 ◽  
Author(s):  
Karen M. Haberstroh ◽  
Martin Kaefer ◽  
Natacha DePaola ◽  
Sarah A. Frommer ◽  
Rena Bizios
Keyword(s):  
Smooth Muscle ◽  
Hydrostatic Pressure ◽  
Smooth Muscle Cells ◽  
Collagen Type ◽  
Mechanical Strain ◽  
Muscle Cells ◽  
Collagen Type Iii ◽  
Bladder Smooth Muscle ◽  
Simultaneous Exposure

The novel hydrostrain system was designed in an effort to establish and maintain conditions that simulate the in-vivo mechanical environment of the bladder. In this laboratory system, ovine bladder smooth muscle cells on flexible, 10-cm-dia silastic membranes were exposed simultaneously to hydrostatic pressure (40 cm H2O, a pressure level currently associated with bladder pathologies) and mechanical strains (up to 25 percent) under standard cell culture conditions for 7 h. Under these conditions, Heparin Binding-Epidermal Growth Factor and Collagen Type III mRNA expression were significantly increased (p<0.01 and 0.1, respectively); however, no changes were observed in Collagen Type I mRNA expression. Decreases in the Collagen Type I:Type III ratio following simultaneous exposure of bladder smooth muscle cells to pathological levels of hydrostatic pressure and mechanical strain in vitro are in agreement with clinically observed increases in Collagen Type III with concomitant decreased human bladder compliance. The results of the present study, therefore, provide cellular/molecular level information relevant to bladder pathology that could have significant implications in the field of clinical urology.

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