scholarly journals Protein expression of matrix metalloproteinase (MMP-1, -2, -3, -9 and -14) in Ewing family tumors and medulloblastomas of pediatric patients

2015 ◽  
Vol 01 (03) ◽  
pp. 181-187
Author(s):  
Fabio Motta ◽  
Rosane Queiroz ◽  
Carlos Scrideli ◽  
Luiz Tone ◽  
Elvis Mateo
Keyword(s):  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Pediatric Patients ◽  
Ewing Family Tumors

scholarly journals Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1549 ◽  
Author(s):  
Putcharawipa Maneesai ◽  
Sarawoot Bunbupha ◽  
Prapassorn Potue ◽  
Thewarid Berkban ◽  
Upa Kukongviriyapan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Wall Thickness ◽  
Tumor Necrosis ◽  
Left Ventricular ◽  
Cardiovascular Remodeling ◽  
Tgf Β1 ◽  
Necrosis Factor

Hesperidin is a major flavonoid isolated from citrus fruits that exhibits several biological activities. This study aims to evaluate the effect of hesperidin on cardiovascular remodeling induced by n-nitro l-arginine methyl ester (l-NAME) in rats. Male Sprague-Dawley rats were treated with l-NAME (40 mg/kg), l-NAME plus hesperidin (15 mg/kg), hesperidin (30 mg/kg), or captopril (2.5 mg/kg) for five weeks (n = 8/group). Hesperidin or captopril significantly prevented the development of hypertension in l-NAME rats. l-NAME-induced cardiac remodeling, i.e., increases in wall thickness, cross-sectional area (CSA), and fibrosis in the left ventricular and vascular remodeling, i.e., increases in wall thickness, CSA, vascular smooth muscle cells, and collagen deposition in the aorta were attenuated by hesperidin or captopril. These were associated with reduced oxidative stress markers, tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta 1 (TGF-β1), and enhancing plasma nitric oxide metabolite (NOx) in l-NAME treated groups. Furthermore, up-regulation of tumor necrosis factor receptor type 1 (TNF-R1) and TGF- β1 protein expression and the overexpression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) was suppressed in l-NAME rats treated with hesperidin or captopril. These data suggested that hesperidin had cardioprotective effects in l-NAME hypertensive rats. The possible mechanism may involve antioxidant and anti-inflammatory effects.

scholarly journals Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression

2018 ◽  
Author(s):  
Putcharawipa Maneesai ◽  
Sarawoot Bunbupha ◽  
Prapassorn Potue ◽  
Thewarid Berkban ◽  
Upa Kukongviriyapan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Wall Thickness ◽  
Tumor Necrosis ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Cardiovascular Remodeling ◽  
Necrosis Factor

Hesperidin is a major flavonoid isolated from citrus fruits that exhibits several biological activities. This study aims to evaluate the effect of hesperidin on cardiovascular remodeling induced by N-nitro L-arginine methyl ester (L-NAME) in rats.  Male Sprague-Dawley rats were treated with L-NAME (40 mg/kg); L-NAME plus hesperidin (15 mg/kg), or hesperidin (30 mg/kg), or captopril (2.5 mg/kg) for five weeks (n = 8/group). Hesperidin or captopril significantly prevented the development of hypertension in L-NAME rats.  Moreover, hesperidin or captopril alleviated L-NAME-induced cardiac remodeling; increases in wall thickness, cross sectional area (CSA) and fibrosis of left ventricular (LV), and vascular remodeling; increases in wall thickness, CSA, vascular smooth muscle cells and collagen deposition in the aorta. These were associated with reduced oxidative stress markers, tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta 1 (TGF-β1) and enhancing plasma nitric oxide metabolite (NOx) in L-NAME treated groups. Furthermore, up-regulation of tumor necrosis factor receptor type 1 (TNF-R1) and TGF-β1 protein expression and the over-expression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) were suppressed in L-NAME rats treated with hesperidin or captopril. These data suggested that hesperidin had cardioprotective effects in L-NAME hypertensive rats. The possible mechanism may involve its antioxidant and anti-inflammatory effects.

scholarly journals Lack of Association between Membrane-Type 1 Matrix Metalloproteinase Expression and Clinically Relevant Molecular or Morphologic Tumor Characteristics at the Leading Edge of Invasive Colorectal Carcinoma

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Annette Arndt ◽  
Klaus Kraft ◽  
Eva Wardelmann ◽  
Konrad Steinestel
Keyword(s):  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Growth Pattern ◽  
Leading Edge ◽  
Tumor Characteristics ◽  
Mutation Status ◽  
Membrane Type

Colorectal cancer (CRC) is one of the leading causes of death from cancer in the western world, but tumor biology and clinical course show great interindividual variation. Molecular and morphologic tumor characteristics, such asKRAS/BRAFmutation status, mismatch repair (MMR) protein expression, tumor growth pattern, and tumor cell budding, have been shown to be of key therapeutic and/or prognostic relevance in CRC. Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a membrane-anchored zinc-binding endopeptidase that is expressed at the leading edge of various invasive carcinomas and promotes tumor cell invasion through degradation of the extracellular matrix. The aim of this study was to investigate possible associations between MT1-MMP expression and molecular tumor characteristics as well as morphologic features of tumor aggressiveness in a consecutive series of 79 CRC tissue samples. However, although MT1-MMP was expressed in 41/79 samples (52%), there was no significant association between MT1-MMP expression andKRAS/BRAFmutation status, MMR protein expression, presence of lymphovascular invasion, tumor growth pattern, tumor-infiltrating lymphocytes, or tumor cell budding in our sample cohort (P>0.05). Thus, we conclude that although MT1-MMP may play a role in CRC invasion, it is not of key relevance to the current models of CRC invasion and aggressiveness.

scholarly journals Angiotensin II induces extracellular matrix metalloproteinase inducer expression via an AT1R dependent pathway in aortic atherosclerotic plaque in apolipoprotein E knockout mice

2011 ◽  
Vol 13 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Li-xia Yang ◽  
Zhi-hua Yang ◽  
Rui-wei Guo ◽  
Jin-shan Ye ◽  
Hong Liu
Keyword(s):  
Extracellular Matrix ◽  
Angiotensin Ii ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Atherosclerotic Plaque ◽  
Knockout Mice ◽  
Ang Ii ◽  
Extracellular Matrix Metalloproteinase Inducer ◽  
Apolipoprotein E Knockout Mice ◽  
Apoe Knockout Mice

The pathogenesis of acute coronary syndrome is rupture of vulnerable plaque. Extracellular matrix metalloproteinase inducer (EMMPRIN) is reported to have a important role in the destabilization of atheroma. Objectives: this investigation examined the effect of angiotensin II (Ang II) on EMMPRIN expression in atherosclerotic plaques in ApoE knockout mice. Methods: ApoE knockout mice were fed a high fat diet to establish an atherosclerosis model then intervention was made with Ang II and valsartan. EMMPRIN gene and its protein expression were measured by real-time PCR immunohistochemistry, and Western blot. Results: EMMPRIN gene and protein expression intervened with Ang II were significantly increased; valsartan could inhibit the effect of Ang II. Conclusion: Ang II up-regulated EMMPRIN expression in atherosclerotic plaque via AT1R, and valsartan could inhibit the effect of Ang II.

Dynamic Changes in Matrix Metalloproteinase 9 and Tissue Inhibitor of Metalloproteinase 1 Levels During Wound Healing in Diabetic Rats

2009 ◽  
Vol 99 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Chuan Yang ◽  
Ping Zhu ◽  
Li Yan ◽  
Lihong Chen ◽  
Ren Meng ◽  
...  
Keyword(s):  
Wound Healing ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Messenger Rna ◽  
Diabetic Rats ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Control Group ◽  
Tissue Inhibitor ◽  
Dynamic Changes ◽  
Metalloproteinase 9

Background: We investigated the mechanism of delayed would healing caused by diabetes and measured the dynamic changes in matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) levels. We noted differences in the ratio of MMP-9 to TIMP-1 in the wounds of diabetic and nondiabetic rats.Methods: Forty-two Sprague-Dawley rats weighing 250 g were randomly assigned to either the control group or the streptozotocin-induced diabetes group. Then, full-thickness excision wounds were created on the middle of the back of each animal. Skin biopsy specimens were obtained on days 0, 3, 7, and 14 after incision. The content of collagen was quantified by Masson’s staining and the macrophage marker, and CD68 was detected by immunohistochemical analysis. Messenger RNA and protein expression of MMP-9 and TIMP-1 was measured by reverse transcriptase–polymerase chain reaction and Western blot, respectively.Results: Diabetic rats exhibited slower wound healing than control animals (P < .05). On days 3, 7, and 14 after incision, higher levels of MMP-9 messenger RNA and protein expression were detected in the diabetic group compared with the control group (P < .05), and expression of TIMP-1 messenger RNA and protein was significantly decreased. In addition, the ratio of MMP-9 to TIMP-1 was stable in controls, whereas there was a marked increase in the ratio in diabetic skin wounds.Conclusions: The balance between MMP-9 and its inhibitor, TIMP-1, is disturbed in diabetic skin tissue after injury, which may lead to histologic abnormality of diabetic skin and delayed wound healing. (J Am Podiatr Med Assoc 99(6): 489–496, 2009)

Ischemia-induced cleavage of cadherins in NRK cells requires MT1-MMP (MMP-14)

2006 ◽  
Vol 290 (1) ◽  
pp. F43-F51 ◽  
Author(s):  
Marisa D. Covington ◽  
Robert C. Burghardt ◽  
Alan R. Parrish
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Neutralizing Antibody ◽  
Proximal Tubules ◽  
High Morbidity ◽  
Chemical Inhibitors ◽  
Membrane Type

Ischemia is a leading cause of acute renal failure (ARF), a disease associated with high morbidity and mortality. Disruption of intercellular adhesion in the proximal tubules is linked to ARF, although the molecular mechanism(s) remains unclear. Our previous studies showed that ischemia is associated with cadherin cleavage and loss in NRK cells, putatively due to a matrix metalloproteinase (MMP) ( 7 ). In the current studies, a MMP required for E-cadherin cleavage and N-cadherin loss was identified. Chemical inhibitors against a number of soluble MMPs ( 1 , 2 , 3 , 8 , 9 ) failed to completely attenuate ischemia-induced cadherin loss. Under ischemic conditions, there was an increase in active membrane-type (MT)1-MMP but a decrease in MMP-2 protein expression. Plating cells on fibronectin protected against ischemia-induced loss of cadherins and, interestingly, no increase in active MT1-MMP levels was seen in ischemic cells on fibronectin-coated dishes. In addition, L cells stably expressing E- (LE) or N-cadherin (LN), but lacking MT1-MMP expression, were resistant to ischemia-induced cadherin loss. The role of MT1-MMP in ischemia-induced cadherin loss was confirmed by either blocking MT1-MMP activity with a neutralizing antibody or expression with shRNA constructs which protected full-length E- and N-cadherin during ischemia. Using shRNA constructs to suppress MT1-MMP expression, ischemia-induced disruption of cadherin function was ablated, and cell-cell contacts were preserved. These results demonstrate that ischemia induces increased expression of active MT1-MMP and subsequent disruption of cadherin/catenin complexes, implying that MT1-MMP plays a role in ischemia-induced ARF.

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