Serum monocyte chemoattractant protein-1 levels in rat models of intimal hyperplasia

Yamamura, Mitsuhiro; Miyamoto, Takashi; Yao, Hideki

doi:10.1055/s-0031-1276344

Cited by 6 publications

(7 citation statements)

References 6 publications

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“…20 We found that MCP-1 mRNA expression was similar in the vein grafts and FA anastomoses at the early time points, but increased significantly in the vein grafts on day 1 (P Ͻ 0.05), just before the establishment of IH. We speculate that there might be a direct correlation between Mo/Mf infiltration and the development of IH in vein grafts, not seen in FA anastomoses.…”

Section: Mcp-1 Mrna Expressionmentioning

confidence: 61%

Monocyte Chemoattractant Protein-1 Expression in Intimal Hyperplasia of Vein Grafts in a Rat Model

2002

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Section: Mcp-1 Mrna Expressionmentioning

confidence: 61%

Monocyte Chemoattractant Protein-1 Expression in Intimal Hyperplasia of Vein Grafts in a Rat Model

2002

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“…Similarly, late up-regulation of MCP-1 has been demonstrated in vein graft neointimal stenotic lesions. 51,66,68 Inhibition or deficiencies in MCP-1 and its receptor CCR2 have been correlated to a 30 and 60% reduction in lesion formation, respectively. 29,47 In 2002, Roque et al, demonstrated a decrease in neointimal hyperplasia and SMC proliferation following the inhibition of CCR2, and suggested MCP-1 may directly or indirectly influence SMC migration and proliferation.…”

Section: Discussionmentioning

confidence: 99%

Realistic Temporal Variations of Shear Stress Modulate MMP-2 and MCP-1 Expression in Arteriovenous Vascular Access

et al. 2009

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Venous neointimal hyperplasia (VNH) lesions are prone to localized development within the vascular access junction (VAJ) and efferent vein of arteriovenous (AV) fistulae and grafts. The creation of VAJ dramatically alters the local venous hemodynamics with high pulsatile flow velocities enter the vein resulting in blood-flow separation, recirculation and flow reversal. This study conducted a computational hemodynamic investigation of an idealized AV graft and realistic AV fistula which demonstrated a complex hemodynamic environment within the VAJ, producing elevated wall shear stress (WSS) magnitudes and significant spatial and temporal WSS gradients in the VAJ. These hemodynamic patterns and non-physiological WSSs are postulated to initiate VNH development at the transcriptional level. Human umbilical vein endothelial cells (HU-VEC) were exposed to elevated temporal WSS waveforms obtained from the aforementioned computational analysis, using a cone-and-plate bioreactor. Using real-time RT-PCR, early induction of MMP-2 and delayed transcriptional upregulation of MCP-1 was observed following EC exposure to VAJ high wall shear forces. These results indicate that MMP-2 and MCP-1 may be induced by high WSS present in the VAJ, suggesting a link between elevated WSS magnitudes and temporal gradients, extracellular matrix decomposition, smooth muscle cell migration and proliferation, and the subsequent VNH development in AV VAJs.

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“…In 1999, Ross (3) stated that "atherosclerosis is an inflammatory disease". Similar to atherosclerosis, postoperative intimal hyperplasia is now also thought to be an inflammatory disease (4,5). Endothelial injury is a crucial factor in these diseases.…”

Section: Discussionmentioning

confidence: 99%

Edaravone suppresses endothelial cell injury in vein grafts of a rat model

Yamamura

Mitsuno²,

Tanaka³

et al. 2008

Int J Angiol

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Serum monocyte chemoattractant protein-1 levels in rat models of intimal hyperplasia

Cited by 6 publications

References 6 publications

Monocyte Chemoattractant Protein-1 Expression in Intimal Hyperplasia of Vein Grafts in a Rat Model

Monocyte Chemoattractant Protein-1 Expression in Intimal Hyperplasia of Vein Grafts in a Rat Model

Realistic Temporal Variations of Shear Stress Modulate MMP-2 and MCP-1 Expression in Arteriovenous Vascular Access

Edaravone suppresses endothelial cell injury in vein grafts of a rat model

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