Membrane-type matrix metalloproteinase-9 activity in placental tissue from patients with pre-existing and gestational diabetes mellitus

2000 ◽  
Vol 12 (6) ◽  
pp. 269 ◽  
Author(s):  
Carolina Pustovrh ◽  
Alicia Jawerbaum ◽  
Debora Sinner ◽  
Mario Pesaresi ◽  
Mario Baier ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Matrix Metalloproteinase ◽  
Placental Tissue ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Sod Activity ◽  
No Donors ◽  
Membrane Type ◽  
Metalloproteinase 9

The activity of matrix metalloproteinase (MMP)-9 was evaluated in placental tissue from healthy subjects (controls) and from patients with gestational and pre-existing diabetes mellitus (GDM and PDM, respectively). Compared with controls, MMP-9 activity was greater in placental tissue from patients with PDM and lower in placental tissue from patients with GDM. The modulatory role of nitric oxide (NO) and reactive oxygen species (ROS) on MMP-9 activity in placental tissue was evaluated. In healthy placenta, NO synthase inhibitors diminished MMP-9 activity, whereas NO donors enhanced it. The addition of xanthine/xanthine oxidase or hydrogen peroxide to placental incubates enhanced MMP-9 activity, while the addition of superoxide dismutase (SOD) diminished it. In placental tissue from patients with PDM, MMP-9 activity was stimulated by NO and by ROS. In placental tissue from patients with PDM, concentrations of nitrates/nitrites and thiobarbituric acid-reactive substances (TBARS) were enhanced, whereas SOD activity was decreased, suggesting that elevated concentrations of NO and ROS may be related to the enhanced MMP-9 concentrations found in these tissues. In placenta from GDM patients, in which a diminished concentration of MMP-9 were detected, nitrate/nitrite concentrations were increased, but placental MMP-9 activity did not change in the presence of either NO donors or inhibitors. The activity of MMP-9 in placental tissue from patients with GDM was stimulated by ROS donor systems and was inhibited by the addition of SOD; however, TBARS and SOD concentrations were unchanged in these tissues compared with controls. These findings demonstrate that placental MMP-9 activity is modulated by NO and ROS and that, in diabetic pathology, NO and ROS may determine changes in MMP-9 activity, which are probably involved in the structural and functional abnormalities of diabetic placental tissue.

Role of antioxidant defenses during estivation and anoxia exposure in the freshwater snail Biomphalaria tenagophila (Orbigny, 1835)

2003 ◽  
Vol 81 (7) ◽  
pp. 1239-1248 ◽  
Author(s):  
Marcus V.R Ferreira ◽  
Antonieta C.R Alencastro ◽  
Marcelo Hermes-Lima
Keyword(s):  
Thiobarbituric Acid ◽  
Freshwater Snail ◽  
Antioxidant Defenses ◽  
Oxygen Species ◽  
Thiobarbituric Acid Reactive Substances ◽  
Glutathione S Transferase ◽  
Sod Activity ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Gpx Activity

The effects of 24 h of exposure to underwater anoxia and 15 days of estivation (at 26–27°C) on the enzymatic antioxidant system of the hepatopancreas of the freshwater snail Biomphalaria tenagophila (Planorbidae) are described. The effect of 24 h of recovery was also investigated. Catalase activity dropped by 31% during 24 h of anoxia, and superoxide dismutase (SOD) activity was reduced by 43% during the 15 days of estivation. This is consistent with the overall decrease in metabolic rate during estivation or anoxia. Indeed, the heartbeat diminished by 28–36% during estivation (determination was possible for only 4 days) and by 66% after 24 h of anoxia. On the other hand, selenium-dependent glutathione peroxidase (Se-GPX) activity increased during anoxia (from 10 to 14 mU/mg protein) and estivation (by 14%). Glutathione S-transferase (GST) and glutathione reductase activities remained unchanged during estivation and anoxia. Glucose 6-phosphate dehydrogenase activity was unchanged during estivation and recovery. Recovery restored SOD activity. Catalase, Se-GPX, and GST activities during recovery were significantly lower than those of the respective controls. Lipid peroxidation, determined as the level of thiobarbituric acid-reactive substances, was unchanged in the hepatopancreas after 15 days of estivation and 26 h of recovery from estivation. It is possible that the increase in Se-GPX activity during anoxia and estivation, and the maintenance of GST activity, are relevant in minimizing the effects of reactive oxygen species that can be formed upon resumption of aerobic metabolism. Thus, B. tenagophila may have a biochemical strategy of preparation for oxidative stress such as that observed in several other species of anoxia/hypoxia-tolerant animals.

scholarly journals Oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes exposed to clomazone (in vitro)

2011 ◽  
Vol 4 (3) ◽  
pp. 149-153 ◽  
Author(s):  
Adriana Santi ◽  
Charlene Menezes ◽  
Marta Duarte ◽  
Jossiele Leitemperger ◽  
Thais Lópes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Acetylcholinesterase Activity ◽  
Human Erythrocytes ◽  
Thiobarbituric Acid Reactive Substances ◽  
Oxidative Stress Biomarkers ◽  
Sod Activity ◽  
Stress Biomarkers

Oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes exposed to clomazone (in vitro)The aim of this study was to investigate the effect of clomazone herbicide on oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes inin vitroconditions. The activity of catalase (CAT), superoxide dismutase (SOD) and acetylcholinesterase (AChE), as well as the levels of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) were measured in human erythrocytes exposed (in vitro) to clomazone at varying concentrations in the range of 0, 100, 250 and 500 μg/L for 1 h at 37°C. TBARS levels were significantly higher in erythrocytes incubated with clomazone at 100, 250 and 500 μg/L. However, erythrocyte CAT and AChE activities were decreased at all concentrations tested. SOD activity was increased only at 100 μg/L of clomazone. GSH levels did not change with clomazone exposure. These results clearly showed clomazone to induce oxidative stress and AChE inhibition in human erythrocytes (in vitro). We, thus, suggest a possible role of ROS on toxicity mechanism induced by clomazone in humans.

scholarly journals Matrix metalloproteinase 9, superoxide dismutase and lipid peroxidation in preterm newborns with perinatal hypoxia

2011 ◽  
Vol 10 (2) ◽  
pp. 26-29 ◽  
Author(s):  
Yu. V. Korenovsky ◽  
S. A. Elchaninova ◽  
N. I. Fadeyeva
Keyword(s):  
Superoxide Dismutase ◽  
Matrix Metalloproteinase ◽  
Thiobarbituric Acid ◽  
Matrix Metalloproteinase 9 ◽  
Oxygen Species ◽  
Perinatal Hypoxia ◽  
Thiobarbituric Acid Reactive Substances ◽  
Apgar Scores ◽  
Metalloproteinase 9 ◽  
Preterm Newborns

The perinatal hypoxia (PH) in preterm newborns is associated with elevated levels of matrix metalloproteinase 9 (MMP-9), superoxide dismutase (SOD) and thiobarbituric acid reactive substances in umbilical cord blood plasma. The severity of PH Apgar scores correlated with SOD (r = –0,40; p = 0,006) and MMP-9 (r = 0,36; p = 0,023). It is assumed that the SOD increase prevents the reactive oxygen species mediated activation of MMP-9, which destroy the collagen of the basement membrane of the bloodbrain barrier.

The role of matrix metalloproteinase 9 and its inhibitors in scarring processes following surgery for primary open-angle glaucoma

2019 ◽  
pp. 72-80
Author(s):  
Е.В. Маркелова ◽  
О.В. Овчинникова ◽  
А.С. Хохлова ◽  
Л.П. Догадова ◽  
А.В. Костюшко ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Postoperative Period ◽  
Open Angle Glaucoma ◽  
Matrix Metalloproteinase 9 ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Open Angle ◽  
Tissue Inhibitors ◽  
Surgery Outcome ◽  
Metalloproteinase 9

Оперативное вмешательство - один из основных методов лечения глаукомы. Однако развитие избыточного рубцевания созданных путей оттока определяет результат хирургического лечения в отдаленные сроки. Процессы рубцевания на данный момент недостаточно изучены. Цель исследования - оценка роли матриксной металлопротеиназы-9, ее ингибиторов в процессах рубцевания у больных с первичной открытоугольной глаукомой после оперативного лечения. Методика. Для выявления возможных маркеров избыточного рубцевания методом твердофазного иммуноферментного анализа определяли содержание матриксных металлопротеиназ-9, тканевых ингибиторов металлопротеиназ 2 и -3 в слезной жидкости у 37 пациентов с активной стадией первичной остроугольной глаукомы в динамике послеоперационного периода. Средний возраст пациентов составил 52,8 лет. В зависимости от исхода оперативного вмешательства все пациенты были разделены на 2 группы - с благоприятным исходом (без избыточного рубцевания) и с неблагоприятным исходом (с избыточным рубцеванием) на месте сформированных дополнительных путей оттока внутриглазной жидкости в послеоперационном периоде. Группа контроля включала 20 человек в возрасте от 50 до 66 лет без сопутствующей офтальмологической и соматической патологии в стадии обострения. Результаты. В динамике показано изменение концентрации матриксной металлопротеиназы-9 и ее ингибиторов в послеоперационном периоде. Анализ данных свидетельствует об обратной зависимости уровня матриксной металлопротеиназы-9 и тканевых ингибиторов металлопротеиназы 2 и 3 типов с исходом операции - чем выше концентрация металлопротеиназы-9 и ниже концентрация тканевых ингибиторов металлопротеиназ 2, -3 в слезной жидкости, тем выше вероятность неблагоприятного исхода в виде рубцевания сформированных дополнительных путей оттока внутриглазной жидкости в послеоперационном периоде. Заключение. Мониторинг уровня металлопротеиназ и их тканевых ингибиторов после проведения хирургического лечения пациентов с первичной открытоугольной глаукомой позволяет прогнозировать раннее рубцевание, дает возможность разработки новых методов лечения как в раннем, так и в позднем послеоперационном периоде. Surgery is one of the major treatments for glaucoma; however excessive scarring of created outflow patways affects the long-term outcome. At the present time, scarring processes are not sufficiently studied. Aim. To evaluate the role of matrix metalloproteinase 9 and its inhibitors in scarring after surgical treatment of open-angle glaucoma. Methods. Concentrations of matrix metalloproteinase 9 and tissue inhibitors of metalloproteinases 2 and 3 were measured in tear fluid of 37 patients (mean age, 52.8) with active primary open-angle glaucoma in dynamics during the postoperative period to identify possible markers of excessive scarring. Based on the surgery outcome, all patients were divided into two groups, with a favorable outcome (without excessive scarring) and an unfavorable outcome (with excessive scarring) in the created additional outflow pathways for the intraocular fluid in the postoperative period. The control group included 20 subjects aged 50-66 without eye disease or somatic disease at exacerbation stage. Results. Analysis of changes in concentrations of matrix metalloproteinase 9 and its inhibitors in the postoperative period showed their inverse relationship with the surgery outcome. The higher was the metalloproteinase 9 level and the lower the level of tissue inhibitors of metalloproteinases 2 and 3 the higher was the probability of unfavorable outcome evident as excessive scarring of the formed additional pathways for tear fluid outflow in the postoperative period. Conclusion. Postoperative monitoring of metalloproteinases and their tissue inhibitors allows to predict early scarring and to develop new treatments both in early and late postoperative periods.

scholarly journals Lens Lipid Peroxides and Glutathione Concentrations in Diabetic Cataract

1997 ◽  
Vol 34 (2) ◽  
pp. 190-192 ◽  
Author(s):  
D Özmen ◽  
I Mutaf ◽  
B Özmen ◽  
J Mentes ◽  
O Bayindir
Keyword(s):  
G Protein ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Diabetic Cataract ◽  
Free Radical Damage ◽  
Significant Difference ◽  
Radical Damage

This study aims to explore the role of reactive oxygen radicals in the genesis of diabetic cataract. Lipid peroxide (LPO) concentrations in senile ( n = 30) and diabetic ( n = 14) cataractous lenses, were determined as thiobarbituric acid-reactive substances (TBARS) by a method modified from Satoh and Yagi, and reduced glutathione (GSH) concentrations were measured according to Beutler. Lens LPO levels (mean, SD; nmol TBARS/g protein) were significantly higher in diabetics (107·54, 18·12) than senile cataractous subjects (53·54, 15·48) ( P < 0·0001). Lens GSH levels (mean, SD; nmol/g protein) showed no significant difference between diabetics (4·29, 2·05) and senile cataractous subjects (4·68, 3·12). These results suggest that free radical damage is more effective in the genesis of diabetic cataract than in senile cataract.

scholarly journals Piezo1 mediates angiogenesis through activation of MT1-MMP signaling

2019 ◽  
Vol 316 (1) ◽  
pp. C92-C103 ◽  
Author(s):  
Hojin Kang ◽  
Zhigang Hong ◽  
Ming Zhong ◽  
Jennifer Klomp ◽  
Kayla J. Bayless ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Sprouting Angiogenesis ◽  
Sphingosine 1 Phosphate ◽  
Wall Shear ◽  
Membrane Type

Angiogenesis is initiated in response to a variety of external cues, including mechanical and biochemical stimuli; however, the underlying signaling mechanisms remain unclear. Here, we investigated the proangiogenic role of the endothelial mechanosensor Piezo1. Genetic deletion and pharmacological inhibition of Piezo1 reduced endothelial sprouting and lumen formation induced by wall shear stress and proangiogenic mediator sphingosine 1-phosphate, whereas Piezo1 activation by selective Piezo1 activator Yoda1 enhanced sprouting angiogenesis. Similarly to wall shear stress, sphingosine 1-phosphate functioned by activating the Ca2+ gating function of Piezo1, which in turn signaled the activation of the matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase during sprouting angiogenesis. Studies in mice in which Piezo1 was conditionally deleted in endothelial cells demonstrated the requisite role of sphingosine 1-phosphate-dependent activation of Piezo1 in mediating angiogenesis in vivo. These results taken together suggest that both mechanical and biochemical stimuli trigger Piezo1-mediated Ca2+ influx and thereby activate matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase and synergistically facilitate sprouting angiogenesis.

scholarly journals SKIP Downregulation Increases TGF-β1-Induced Matrix Metalloproteinase-9 Production in Transformed Keratinocytes

Scientifica ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Jelena Kocić ◽  
Victor Villar ◽  
Aleksandra Krstić ◽  
Juan F. Santibanez
Keyword(s):  
Matrix Metalloproteinase ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Regulatory Protein ◽  
Mek Inhibitor ◽  
Matrix Metalloproteinase 9 ◽  
Transformed Cells ◽  
Interacting Protein ◽  
Metalloproteinase 9

Transforming growth factor-beta (TGF-β1) is a potent inductor of matrix metalloproteinase-9 (MMP-9) in transformed cells. Recently, Ski-interacting protein (SKIP) has been described as a regulator of TGF-β1 signal transduction, but its role in the induction of cell malignance by TGF-β1 has not been fully elucidated so far. In the present study, we analyzed the role of SKIP on TGF-β1-induced MMP-9 production. Mouse transformed keratinocytes (PDV) were stably transfected with SKIP antisense construct. We observed that SKIP depletion provoked an enhancement in the expression of MMP-9 in response to TGF-β1 treatment. The downregulation of SKIP produced an enhancement in TGF-β1-activated ERK1,2 MAP kinase as well as increased transactivation of downstream Elk1 transcription factor. The increased MMP-9 production in response to TGF-β1 was dependent of MAPK activation as PD98059, an MEK inhibitor, reduced MMP-9 expression in SKIP antisense transfected cells. Thus, we propose SKIP as a regulatory protein in TGF-β1-induced MMP-9 expression acting by controlling ERK1,2 signaling in transformed cells.

Sign in / Sign up

Export Citation Format

Share Document