Increased matrix metalloproteinase 9 activity and mRNA expression in lung ischemia-reperfusion injury

Yano, Motoki; Omoto, Yoko; Yamakawa, Yosuke; Nakashima, Yoshiaki; Kiriyama, Masanobu; Saito, Yushi; Fujii, Yoshitaka

doi:10.1016/s1053-2498(01)00250-9

Cited by 59 publications

(43 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…PMN-vascular wall interactions may play a pathological role in different situations, including ischemia/reperfusion injury 26 or blood stasis-induced varicose vein development. 27 A role for PMNs in plaque rupture 28 and aneurysm development has also been suggested.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Potentiation of Natriuretic Peptide Limits Polymorphonuclear Neutrophil-Vascular Cell Interactions

Mtairag

Houard

Rais

et al. 2002

ATVB

View full text Add to dashboard Cite

Objective-Activated polymorphonuclear neutrophils (PMNs) are the main source of circulating neutral endopeptidase (NEP). We tested the hypothesis that NEP inhibition could potentiate the effect of atrial natriuretic peptide (ANP) on PMN-vascular cell interactions in vitro. Methods and Results-ANP alone and its potentiation by retrothiorphan, the NEP inhibitor, significantly inhibited superoxide, lysozyme, and matrix metalloproteinase (MMP)-9 release by N-formyl-Met-Leu-Phe-stimulated PMNs. Activated PMNs degraded exogenous ANP, which was prevented by NEP inhibition. Hypoxia significantly increased the adhesion of PMNs to endothelial cells and their subsequent MMP-9 release by 60% and 150%, respectively (PϽ0.01). ANP and its potentiation by retrothiorphan limited PMN adhesion to hypoxic endothelial cells and thus decreased their MMP-9 release (PϽ0.01). Smooth muscle cells (SMCs) incubated with conditioned medium of N-formyl-Met-Leu-Phe-stimulated PMNs exhibited morphological and biochemical changes characteristic of apoptosis (terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling positivity, nuclear condensation/fragmentation, poly ADP-ribose polymerase cleavage, and DNA laddering). SMC detachment and subsequent apoptosis could be related to leukocyte elastase-induced pericellular proteolysis, inasmuch as both events are inhibited by elastase inhibitors. ANP and its potentiation by retrothiorphan were able to limit elastase release, fibronectin degradation, and SMC apoptosis. with the use of leukotriene B4 as a trigger. In contrast, Matsumura et al 8 showed that ANP and its potentiation by NEP inhibition increased intracellular cGMP, which limited protease release by PMNs.Therefore, we hypothesized that the potentiation of ANP by NEP inhibition could limit PMN-vascular cell interactions by acting predominantly on PMNs. For this purpose, we have developed an in vitro approach testing the ability of ANP potentiation by NEP inhibition (1) to inhibit PMN protease release, (2) to limit PMN-endothelial cell interactions in hypoxic conditions, and (3) to limit the pericellular proteolysis induced by activated PMN secretions. Methods Cell CulturesHuman umbilical vein endothelial cells (HUVECs) were harvested and cultured as described. 12 Human smooth muscle cells (SMCs) were obtained from venous wall explants after removal of the adventitia and were cultured. 13

show abstract

Section: Discussionmentioning

confidence: 99%

Pharmacological Potentiation of Natriuretic Peptide Limits Polymorphonuclear Neutrophil-Vascular Cell Interactions

Mtairag

Houard

Rais

et al. 2002

ATVB

View full text Add to dashboard Cite

show abstract

“…Possible triggers of ALI in mice are mechanical ventilation, pulmonary ischaemia/reperfusion (I/R), LPS, live bacteria, hyperoxia, bleomycin, oleic acid, caecal ligation and puncture, and acid aspiration. Increased MMP expression is observed in lung injury induced by LPS, oleic acid and I/R [163][164][165]. Ilomastat attenuated lung inflammation and injury caused by I/R or oleic acid, which was reflected in a decrease in leukocyte influx [65].…”

Section: Acute Lung Injurymentioning

confidence: 96%

A therapeutic role for matrix metalloproteinase inhibitors in lung diseases?

Vandenbroucke¹,

Dejonckheere²,

Libert³

2011

European Respiratory Journal

111

105

View full text Add to dashboard Cite

Disruption of the balance between matrix metalloproteinases (MMPs) and their endogenous inhibitors is considered a key event in the development of pulmonary diseases such as chronic obstructive pulmonary disease, asthma, interstitial lung diseases and lung cancer. This imbalance often results in elevated net MMP activity, making MMP inhibition an attractive therapeutic strategy. Although promising results have been obtained, the lack of selective MMP inhibitors, together with limited knowledge regarding the exact functions of a particular MMP, hampers clinical application. This review discusses the involvement of different MMPs in lung disorders and future opportunities and limitations of therapeutic MMP inhibition.

show abstract

“…A growing body of evidence suggests that BOS is mediated by the coordinated infiltration and effector functions of alloreactive T cells (4,5). In this regard, it has become clear that novel immune mediator molecules such as matrix metalloproteinases (MMP), in particular MMP-2 and MMP-9, may also play an important role in the pathogenesis of BOS (6)(7)(8)(9). Currently, conventional immunosuppressive protocols are the only available treatment for BOS.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Obliterative Airway Disease Development in Murine Tracheal Allografts by Matrix Metalloproteinase-9 Deficiency

Fernández

Campbell

Liu

et al. 2005

American Journal of Transplantation

View full text Add to dashboard Cite

This study was designed to define the roles of matrix metalloproteinase (MMP)-2 and MMP-9 in obliterative airway disease (OAD) in heterotopic murine tracheal allografts, considered a suitable animal model for chronic lung allograft rejection. BALB/c tracheal allografts were transplanted into MMP-2-deficient (−/−) and MMP-9−/− mice. Also, wild-type recipients were treated with doxycycline, a nonspecific MMP inhibitor. After 10, 20 and 30 days, allografts were analyzed for OAD development, intragraft levels of MMP-2 and MMP-9 and the frequency and cytokine/chemokine production profile of alloreactive T cells. Allografts transplanted into wild-type mice developed OAD lesions within 30 days. These allografts revealed significant upregulation of both MMP-2 and MMP-9. Allografts transplanted into MMP-9−/− and doxycycline-treated recipients did not develop OAD. In contrast, allografts transplanted into MMP-2−/− mice developed OAD lesions with normal kinetics. Interestingly, MMP-9−/− recipients showed an enhanced T cell alloreactivity associated with an abnormal profile of cytokine/chemokine production. The enhanced T cell alloreactivity in MMP-9−/− mice was mediated by enhanced dendritic cell stimulatory capacity as well as enhanced T cell responsive capacity. These results suggest that MMP-9 plays an important role in the pathogenesis of OAD and may represent a target for the therapeutic intervention of chronic lung allograft rejection.

show abstract

Increased matrix metalloproteinase 9 activity and mRNA expression in lung ischemia-reperfusion injury

Cited by 59 publications

References 26 publications

Pharmacological Potentiation of Natriuretic Peptide Limits Polymorphonuclear Neutrophil-Vascular Cell Interactions

Pharmacological Potentiation of Natriuretic Peptide Limits Polymorphonuclear Neutrophil-Vascular Cell Interactions

A therapeutic role for matrix metalloproteinase inhibitors in lung diseases?

Inhibition of Obliterative Airway Disease Development in Murine Tracheal Allografts by Matrix Metalloproteinase-9 Deficiency

Contact Info

Product

Resources

About