Contractile smooth muscle cell apoptosis early after saphenous vein grafting

Rodriguez, Evelio; Lambert, Erica H.; Magno, Michael G.; Mannion, John D.

doi:10.1016/s0003-4975(00)01768-9

Cited by 23 publications

(23 citation statements)

References 23 publications

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“…Matsushita and coworkers recently demonstrated that hypoxia induces endothelial apoptosis [17]. Mechanical stretch can induce vascular smooth muscle cell apoptosis, and apoptosis of smooth muscle cells occurs in experimental saphenous vein grafts [18,19]. This is in accordance with our study where we also found presence of apoptosis after venous bypass grafting in the mouse.…”

Section: Discussionsupporting

confidence: 92%

Rapamycin treatment is associated with an increased apoptosis rate in experimental vein grafts☆

Schachner

Oberhuber²,

Zou³

et al. 2005

European Journal of Cardio-Thoracic Surgery

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Section: Discussionsupporting

confidence: 92%

Rapamycin treatment is associated with an increased apoptosis rate in experimental vein grafts☆

Schachner

Oberhuber²,

Zou³

et al. 2005

European Journal of Cardio-Thoracic Surgery

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“…In animal models of vein PanX1 (200 μM), or carbenoxolone (CBX; 100 μM). ATP released were collected and concentration in the perfusates were measured (n = [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] grafting, nuclear condensation and membrane blebbing in medial SMCs were evident as early as 1 h post-grafting [53], and apoptosis peaked within 8 h of grafting [54]. Mechanical stretch associated both physiological or pathologic conditions is an inducer of cytokine production in difference tissues [55,56].…”

Section: Discussionmentioning

confidence: 99%

P2X7R antagonism after subfailure overstretch injury of blood vessels reverses vasomotor dysfunction and prevents apoptosis

Luo

Feldman

McCallister

et al. 2017

Purinergic Signalling

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Human saphenous vein (HSV) is harvested and prepared prior to implantation as an arterial bypass graft. Injury and the response to injury from surgical harvest and preparation trigger cascades of molecular events and contribute to graft remodeling and intimal hyperplasia. Apoptosis is an early response after implantation that contributes the development of neointimal lesions. Here, we showed that surgical harvest and preparation of HSV leads to vasomotor dysfunction, increased apoptosis and downregulation of the phosphorylation of the anti-apoptotic protein, Niban. A model of subfailure overstretch injury in rat aorta (RA) was used to demonstrate impaired vasomotor function, increased extracellular ATP (eATP) release, and increased apoptosis following pathological vascular injury. The subfailure overstretch injury was associated with activation of p38 MAPK stress pathway and decreases in the phosphorylation of the anti-apoptotic protein Niban. Treatment of RA after overstretch injury with antagonists to purinergic P2X7 receptor (P2X7R) antagonists or P2X7R/pannexin (PanX1) complex, but not PanX1 alone, restored vasomotor function. Inhibitors to P2X7R and PanX1 reduced stretch-induced eATP release. P2X7R/PanX1 antagonism led to decrease in p38 MAPK phosphorylation, restoration of Niban phosphorylation and increases in the phosphorylation of the anti-apoptotic protein Akt in RA and reduced TNFα-stimulated caspase 3/7 activity in cultured rat vascular smooth muscle cells. In conclusion, inhibition of P2X7R after overstretch injury restored vasomotor function and inhibited apoptosis. Treatment with P2X7R/PanX1 complex inhibitors after harvest and preparation injury of blood vessels used for bypass conduits may prevent the subsequent response to injury that lead to apoptosis and represents a novel therapeutic approach to prevent graft failure.

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“…93 Both processes are characterized by an increased cell proliferation in adventitia, apoptosis and necrosis of medial VSMCs, adventitial thickening, fibroblast-to-myofibroblast conversion, directional migration of activated adventitial cells to the neointima, and vascular remodeling. 11,12,[93][94][95][96][97][98] In the transplant there is a transient acute inflammation, platelet adhesion, and release of vasoactive substances, cytokines, and growth factors. 95 In an elegant work, Shi et al 94 demonstrated that, after porcine autologous vein-to-artery grafting, SM ␣-actin ϩ , BrdU ϩ pulse-labeled adventitial fibroblasts from adjacent tissue translocate from the interposed vein segment and, with time, migrate to the subendothelial space where numerous SM ␣-actin ϩ , BrdU ϩ -labeled myofibroblasts accumulate.…”

Section: Adventitia Response In Autologous Vein-to-artery Graft and Tamentioning

confidence: 99%

Contribution of Adventitial Fibroblasts to Neointima Formation and Vascular Remodeling

Sartore

Chiavegato

Faggin

et al. 2001

Circulation Research

460

379

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Abstract-The adventitial layer surrounding the blood vessels has long been exclusively considered a supporting tissue the main function of which is to provide adequate nourishment to the muscle layers of tunica media. Although functionally interconnected, the adventitial and medial layers are structurally interfaced at the external elastic lamina level, clearly distinguishable at the maturational phase of vascular morphogenesis. Over the last few years the "passive" role that the adventitia seemed to play in experimental and spontaneous vascular pathologies involving proliferation, migration, differentiation, and apoptosis of vascular smooth muscle cells (VSMCs) has been questioned. It has been demonstrated that fibroblasts from the adventitia display an important partnership with the resident medial VSMCs in terms of phenotypic conversion, proliferation, apoptotic, and migratory properties the result of which is neointima formation and vascular remodeling. This article is an attempt at reviewing the major themes and more recent findings dealing with the phenotypic conversion process that leads adventitial "passive" (static) fibroblasts to become "activated" (mobile) myofibroblasts. This event shows some facets in common with vascular morphogenesis, ie, the process of recruitment, incorporation, and phenotypic conversion of cells surrounding the primitive endothelial tube in the definitive vessel wall. We hypothesize that during the response to vascular injuries in the adult, "activation" of adventitial fibroblasts is, at least in part, reminiscent of a developmental program that also invests, although with distinct spatiotemporal features, medial VSMCs.

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Contractile smooth muscle cell apoptosis early after saphenous vein grafting

Cited by 23 publications

References 23 publications

Rapamycin treatment is associated with an increased apoptosis rate in experimental vein grafts☆

Rapamycin treatment is associated with an increased apoptosis rate in experimental vein grafts☆

P2X7R antagonism after subfailure overstretch injury of blood vessels reverses vasomotor dysfunction and prevents apoptosis

Contribution of Adventitial Fibroblasts to Neointima Formation and Vascular Remodeling

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