Matrix metalloproteinases in peripheral vascular disease

Hobeika, Mark J.; Thompson, Robert W.; Muhs, Bart E.; Brooks, Peter C.; Gagne, Paul J.

doi:10.1016/j.jvs.2006.09.066

Cited by 95 publications

(86 citation statements)

References 100 publications

(121 reference statements)

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“…45 MMP-9 is incriminated as at least one of the intermediates whereby sustained inflammation can lead to injury of the arterial and venous vasculature. 34,35 The markedly increased inflammatory response observed in the venous wall along with the marked induction of MMP-9 in HO-1 Ϫ/Ϫ mice may thus set the stage for chronic venous injury and scarring.…”

Section: Discussionmentioning

confidence: 99%

“…33 MMP-9 is of considerable interest in the pathogenesis of vascular injury in general, 34,35 and in clot lysis as induced in this model, in particular. 4,7,36 In HO-1 Ϫ/Ϫ mice, MMP-9 was strikingly up-regulated following ligation of the IVC, as assessed by mRNA and protein expression, and by zymography ( Figure 11).…”

Section: Examination Of the Pathobiologic Significance Of Ho-1 Followmentioning

confidence: 99%

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Induction of Heme Oxygenase-1 is a Beneficial Response in a Murine Model of Venous Thrombosis

Tracz

Juncos

Grande

et al. 2008

The American Journal of Pathology

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؊/؊ mice exhibited increased nuclear factor B activation and markedly increased up-regulation of tissue factor, selectins, inflammatory cytokines, and matrix metalloproteinase-9, the latter incriminated in both clot lysis and vascular injury. We conclude that HO-1 deficiency impairs thrombus resolution and exaggerates the inflammatory response to thrombus formation. These findings offer insight into recent observations that polymorphisms in the HO-1 gene may increase the risk for recurrent venous thrombosis and dysfunction of hemodialysis arteriovenous fistulas, the latter caused, in part, by thrombosis.

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Section: Discussionmentioning

confidence: 99%

Section: Examination Of the Pathobiologic Significance Of Ho-1 Followmentioning

confidence: 99%

Induction of Heme Oxygenase-1 is a Beneficial Response in a Murine Model of Venous Thrombosis

Tracz

Juncos

Grande

et al. 2008

The American Journal of Pathology

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“…MMP activity has been implicated in the process of angiogenesis, as well as in a number of vascular pathologies including abdominal and cerebral aneurysms, vascular remodeling, the formation and thinning of atherosclerotic plaques, and arterial restenosis (15,20). A number of MMP subtypes (MMP-1, -2, -3, -7, -9, -12, -13, and -14) have been reported in vascular smooth muscle cells and macrophages (15).…”

Section: Discussionmentioning

confidence: 99%

Heparin-binding EGF-like growth factor mediates oxyhemoglobin-induced suppression of voltage-dependent potassium channels in rabbit cerebral artery myocytes

Koide¹,

Penar²,

Tranmer³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Koide M, Penar PL, Tranmer BI, Wellman GC. Heparinbinding EGF-like growth factor mediates oxyhemoglobin-induced suppression of voltage-dependent potassium channels in rabbit cerebral artery myocytes. Am J Physiol Heart Circ Physiol 293: H1750-H1759, 2007. First published June 8, 2007; doi:10.1152/ajpheart.00443.2007 can suppress voltage-dependent K ϩ channel (KV) currents through protein tyrosine kinase activation, which may contribute to cerebral vasospasm following subarachnoid hemorrhage. Here we have tested the hypothesis that shedding of heparin-binding EGF-like growth factor (HB-EGF) and the resulting activation of the tyrosine kinase EGF receptor (EGFR) underlie OxyHb-induced K V channel suppression in the cerebral vasculature. With the use of the conventional whole cell patch-clamp technique, two EGFR ligands, EGF and HB-EGF, were found to mimic OxyHb-induced KV suppression in rabbit cerebral artery myocytes. KV current suppression by OxyHb or EGF ligands was eliminated by a specific EGFR inhibitor, AG-1478, but was unaffected by PKC inhibition. that specifically interfere with HB-EGF signaling eliminated OxyHbinduced K V suppression, suggesting that HB-EGF is the EGFR ligand involved in this pathway. HB-EGF exists as a precursor protein that, when cleaved by matrix metalloproteases (MMPs), causes EGFR activation. MMP activation was detected in OxyHb-treated arteries by gelatin zymography. Furthermore, the MMP inhibitor (GM-6001) abolished OxyHb-induced KV current suppression. We also observed KV current suppression due to EGFR activation in human cerebral artery myocytes. In conclusion, these data demonstrate that OxyHb induces MMP activation, causing HB-EGF shedding and enhanced EGFR activity, ultimately leading to KV channel suppression. We propose that EGFR-mediated KV suppression contributes to vascular pathologies, such as cerebral vasospasm, and may play a more widespread role in the regulation of regional blood flow and peripheral resistance. vascular smooth muscle; growth factors; subarachnoid hemorrhage; tyrosine kinase VOLTAGE-DEPENDENT DELAYED rectifier K ϩ (K V ) channels play an important role in the maintenance of vascular smooth muscle membrane potential and the regulation of arterial diameter (13,35). A reduction in K V channel activity and/or a decrease in K V channel expression in vascular smooth muscle would promote membrane potential depolarization, increased Ca 2ϩ influx via voltage-dependent Ca 2ϩ channels, and vasoconstriction (27). Decreased K V currents have been linked to a number of endogenous and exogenous vasoconstrictors, and K V current suppression has been implicated in systemic and pulmonary hypertension, as well as cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) (22,24,42,49). A large body of evidence suggests that the blood component oxyhemoglobin (OxyHb) contributes to SAH-induced vasoconstriction (3), and our laboratory has recently reported that OxyHb suppresses K V currents in cerebral artery myocytes via a mechanism involving enhanced prote...

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“…[1][2][3][4] Matrix metalloproteinases (MMPs) are endopeptidases, belonging to the matrixin family that can degrade almost all the ECM components. 5 Although there is little doubt that MMPs are an important components in cancer invasion and metastasis, 6 they are also regarded as key regulatory molecules in degenerative processes and inflammation, 5,7 as playing roles also in physiopathological remodeling of the vascular wall 2,8 and as the pathogenesis of cardio-and cerebrovascular diseases. 9,10 Thus, MMPs have emerged as potential biomarkers of atherothrombotic risk and predictors of coronary and cerebrovascular disease recurrence.…”

mentioning

confidence: 99%

“…9,10 Thus, MMPs have emerged as potential biomarkers of atherothrombotic risk and predictors of coronary and cerebrovascular disease recurrence. 8 ATVB 2008;28:e15-e16.…”

mentioning

confidence: 99%

Serum or Plasma Samples?

Mannello

2008

ATVB

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Matrix metalloproteinases in peripheral vascular disease

Cited by 95 publications

References 100 publications

Induction of Heme Oxygenase-1 is a Beneficial Response in a Murine Model of Venous Thrombosis

Induction of Heme Oxygenase-1 is a Beneficial Response in a Murine Model of Venous Thrombosis

Heparin-binding EGF-like growth factor mediates oxyhemoglobin-induced suppression of voltage-dependent potassium channels in rabbit cerebral artery myocytes

Serum or Plasma Samples?

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