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111.
Periodontal ligament cells can potentially differentiate into osteoblast-like cells and influence the remodeling of periodontal tissues under mechanical strain conditions. In the present study, Gene chip technology was adopted to investigate the effect of the cyclic stretch on the expression of osteogenic-related genes in human periodontal ligament cells (HPDLCs). Cultured HPDLCs were subjected to 12% elongation cyclic stretch for 24 h using a Flexercell Strain Unit, and then GEArray Q series human osteogenesis gene expression profile chip with 96 spot array numbers was used to conduct parallel analyses on the change of the related gene expression in the osteogenic differentiation of HPDLCs stimulated by cyclic stretch. The results show that after the HPDLCs were stimulated by the cyclic stretch, the expression of 21 osteogenic-related genes was significantly upregulated, including 10 growth factor genes and their associated molecules, 10 extracellular matrix genes and their associated proteins, and 1 cell adhesion molecule. Two genes were significantly downregulated, including one growth factor gene and one cell adhesion molecule. Then the expressions of 10 candidate genes were validated using Real-time RT-PCR. These results indicate that cyclic stretch with 12% deformation can stimulate or inhibit some gene expression which was associated with the process of HPDLCs differentiation. 相似文献
112.
Redox-sensitive posttranslational modification emerged as important signaling mechanisms. Besides other posttranslational modifications nitroalkylation by nitrated fatty acids mediate favorable anti-inflammatory effects. This review gives an overview of the generation and the reactivity of nitrated fatty acids. Additionally, it provides insights into the so far described pathways regulated by nitrated fatty acids. This article is part of a Special Issue entitled Regulation of Cellular Processes by S-nitrosylation. 相似文献
113.
Expression and localization of extracellular matrix metalloproteinase inducer in giant cell tumor of bone 总被引:8,自引:0,他引:8
Matrix metalloproteinases (MMPs) are regarded as a significant regulator in tumor invasion and metastasis. Previous studies have shown that extracellular matrix metalloproteinase inducer (EMMPRIN) in tumor cells induces the synthesis of MMPs. EMMPRIN is abundantly present on the surface of tumor cells and stimulate adjacent stromal cells to synthesize MMPs to induce tumor progression. Giant cell tumor (GCT) of bone is a benign but locally aggressive primary neoplasm of bone. The spindle-shaped mononuclear stromal cells are considered to be the tumor components of GCT, which are capable of inducing osteoclast formation by recruiting the circulating monocyte and macrophage. In this study, we proposed that EMMPRIN is associated with the biological progression and aggressiveness of GCT. We have conducted semi-quantitative RT-PCR to determine the correlation of EMMPRIN expression with the clinical stage of GCT. We have also examined the cellular localization of EMMPRIN in GCT using in-situ hybridization (ISH) and Immunohistochemistry (IH). The results showed that EMMPRIN was present in GCT and its mRNA levels were associated with the clinical stage of GCT. Higher expression level of EMMPRIN was observed in GCT with advanced stage (stage III). There was a great significance (P < 0.05) of EMMPRIN expression between stage I & II and stage III GCTs. Both ISH and IH demonstrated that EMMPRIN is present at the multinuclear osteoclast-like giant cells of GCT, with strong immunostaining on the cell membrane. The stromal-like tumor cells were also positively stained but the intensity was weaker. Interestingly, the production of EMMPRIN in osteoclast-like cells of GCT seems to be regulated by stromal-like tumor cells. Receptor activator of NF-kappaB ligand (RANKL), which has been previously shown to be produced by the stromal-like tumor cells for the recruitment of osteoclast-like giant cells in GCT, enhanced the expression of EMMPRIN mRNA during the differentiation of macrophage-like RAW(264.7) cells into osteoclasts. In short, our studies suggest that EMMPRIN may be an important regulatory factor involved in the biological behaviors of GCT. 相似文献
114.
The temporomandibular joint (TMJ) is an important growth and articulation center in the craniofacial complex. In aging it develops spontaneous degenerative osteoarthritic (OA) lesions. Metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPS) play key roles in extracellular matrix remodeling and degradation. Gelatinase activities and immunohistochemical localization of MMP-2, -3, -8, -9, and -13 and TIMP-1 and -2 were examined in mandibular condyle cartilage of neonatal mice up to 18 months old. The most intense immunostaining for all enzymes and TIMPs and the peak of gelatinase activities were found in animals in the stages of early growth (1 week to 3 months) followed by a decrease during maturation and aging. However, clusters of positively immunoreactive chondrocytes were detected in cartilages of old animals displaying OA lesions. Positive safranin-O staining, indicative of sulfated proteoglycans (PGs), was prominent in the TMJ of newborn mice up to 3 months old followed by reduction during maturation and aging, except in regions displaying OA lesions. Temporal codistribution of PGs, MMPs, and TIMPs during skeletal maturation reflected an active growth phase, whereas their reduction coincided with the more quiescent articulating and maintenance phase in the joint cartilage. Osteoarthritic lesions were associated with both increased PG synthesis and MMP immunoreactivity, indicating limited repair activity during initial stages of osteoarthritis. 相似文献
115.
Matrix metalloproteinases in tumor-host cell communication 总被引:11,自引:0,他引:11
The microenvironment or stroma immediately surrounding tumor cells consists of a three-dimensional extracellular matrix (ECM) and stromal cells such as fibroblasts and inflammatory cells. The matrix metalloproteinases (MMPs) constitute a family of over 24 members, which collectively are capable of degrading virtually the entire ECM. Strict regulation of MMP expression is critical in order to maintain proper ECM homeostasis, but in disease states such as cancer there is often a high level of MMP activity at the tumor-stroma interface. Several studies have documented the importance of MMP-mediated ECM destruction in the successful dissemination of several tumor types, but it has become increasingly clear that they are also involved in earlier stages of tumorigenesis. MMPs are implicated in a wide variety of roles that can assist tumor initiation, growth, migration, angiogenesis, the selection of apoptosis-resistant subpopulations, and in invasion and metastasis. Interestingly, the factors responsible for many of these effects are derived from the cell surfaces of the tumor or stromal cells or are embedded in the ECM. Therefore, the MMPs can no longer be thought of solely as ECM destructionists, but as part of an elegant communication system through which the tumor interacts with the stroma. 相似文献
116.
Ischemia injury alters endothelial cell properties of kidney cortex: stimulation of MMP-9 总被引:1,自引:0,他引:1
Although ischemia is the leading cause of acute renal failure in human, there is little information on the remodeling the kidney endothelium matrix during ischemic injury. In this study, we investigated the activity and expression of MMP-2 and MMP-9, in an isolated endothelial fraction following an acute in vivo reversible ischemia induced in rats by vascular clamping. Ischemia increased serum creatinine levels 1.4-fold, hallmark of acute renal failure. Isolation of the endothelial cell fraction was performed by affinity chromatography using an anti-PECAM-1 antibody. The isolated fraction was assessed by Western blotting analysis of endothelial cell markers. The positively selected fractions were enriched in the endothelial markers eNOS and PECAM-1 by 128-fold and 44-fold, respectively. Gelatin zymography showed that ischemia strongly stimulated proteolytic activity of proMMP-2 (1.8-fold), proMMP-9 (3-fold) and MMP-9 (4-fold) in the endothelial fractions. Western blot analysis indicated that TIMP-2 protein level increased by 3.2-fold in the endothelial fractions during ischemia. Surprisingly, TIMP-1 was absent from the endothelial preparations but was easily detected in the non-endothelial cells. Levels of the endocytic receptor LRP were increased by 2-fold during ischemia in the endothelial fractions. Occludin, a known in vivo MMP-9 substrate, was partly degraded in the endothelial fractions during ischemia, suggesting that the MMP-9 which was upregulated during ischemia was functional. These data suggest that ischemia in kidney could lead to the degradation of the vascular basement membrane and to increased permeability. This suggests new therapeutic approaches for ischemic pathologies by targeting MMP-9 and its regulators. 相似文献
117.
MMPs and TIMPs--an historical perspective 总被引:5,自引:0,他引:5
Woessner JF 《Molecular biotechnology》2002,22(1):33-49
There are currently 25 known vertebrate matrix metalloproteinases (MMPs) and 4 tissue inhibitors of metalloproteinases (TIMPs).
This article reviews these proteases from an historical perspective in terms of who discovered each protein, when the sequence
was established, when action on protein substrates was demonstrated, and what names have been used. A similar approach is
taken for the TIMPS, and their multiple functions in addition to protease inhibition are emphasized. MMPs from invertebrates,
plants, and bacteria are also discussed. This review is an outgrowth and update of a chapter by the same name originally published
in Matrix Metalloproteinase Protocols, pp. 1–23, edited by I. M. Clark and published by Humana Press in 2001. 相似文献
118.
Mahmood Rasool Arif Malik Muhammad Abdul Basit Ashraf Mahwish Arooj Asia Kiran Sulayman Waquar Ujala Ayyaz Ayesha Zahid Ahmad Zaheer Abdul Jabbar Maryam Zain Amir Raza Asim Mehmood Tahira Batool Qaisrani Zeenat Mirza Mohammed Hussein Al-Qahtani Sajjad Karim Absarul Haque 《Saudi Journal of Biological Sciences》2018,25(8):1724-1728
Background
Cancer patients when treated with different chemotherapeutic drugs often develop mild to severe sight threatening diseases during or after chemotherapy. The mechanism involved in the pathogenesis of ocular toxicities is poorly understood. Oxidative stress, inflammation and MMPs (angiogenic factor) are involved in the progression of chemotherapy related ocular disorders.Materials and methods
The concentration of oxidative stress markers such as MDA, NO and levels of different antioxidant molecules such as SOD, CAT, GSH, GPx, GPr, VIT A, VIT E and VIT C present in the serum of chemotherapy treated patients (n?=?50) and in normal persons (n?=?20) were estimated by the direct spectrophotometric method while the concentration of TNF-α and MMP-9 activity were determined using human TNF-α and MMP-9 ELISA kits.Results
The concentration of SOD and CAT (0.356?±?0.05?μg/dl and 1.26?±?0.01?μmol/mol of protein) was significantly lower as compared to that (1.09?±?0.03?μg/dl and 3.99?±?0.04?μmol/mol of protein) in controls. The levels of GPx (0.06?±?0.01?mmol/dl) in the cancer patients were much lower than those in the controls (0.78?±?0.06?mmol/dl). Lower level of GSH (0.96?±?0.003?μg/dl) in serum of the diseased group was observed as compared to healthy group (7.26?±?1.40?μg/dl). The level of Vit A, Vit C and Vit E was lower in systemic circulation of cancer patients (109.99?±?6.35?μg/ml, 1.26?±?0.36?μg/ml and 1.29?±?0.191?μg/ml) as compared to control subjects (166.35?±?14.26?μg/ml, 3.25?±?0.099?μg/ml and 6.354?±?2.26?μg/ml) respectively. The concentration of nitric oxide was significantly higher in the cancer patients (45.26?±?6.35?ng/ml) than that in the normal subjects (16.35?±?3.26?ng/ml). The higher concentration of MDA (8.65?±?3.26?nmol/ml) was observed in the patients than normal ones (1.254?±?0.065?nmol/ml). The quantity of TNF-α was significantly higher in chemotherapy treated patients (32.68?±?4.33?pg/ml) as compared to the control group (20.979?±?1.98?pg/ml). Significantly higher concentration of MMP-9 (40.26?±?3.26?ng/ml) was observed in the cancer patients than the controls (7.256?±?1.95?ng/ml).Conclusion
Lower levels of antioxidant enzymes and non-enzymatic small molecules and higher levels of oxidative stress and inflammatory clinical parameters such as NO, MDA, TNF-α and MMP-9 may be involved in the pathogenesis of systemic chemotherapy related ocular complications such as cataract, glaucoma, blepharitis, retinitis pigmentosa, macular degeneration, pterygium and retinal degeneration. 相似文献119.
Polarity is critical for development and tissue-specific function. However, the acquisition and maintenance of tissue polarity is context dependent. Thus, cell and tissue polarity depend on cell adhesion which is regulated by the cytoskeleton and influenced by the biochemical composition of the extracellular microenvironment and modified by biomechanical cues within the tissue. These biomechanical cues include fluid flow induced shear stresses, cell-density and confinement-mediated compression, and cellular actomyosin tension intrinsic to the tissue or induced in response to morphogens or extracellular matrix stiffness. Here, we discuss how extracellular matrix stiffness and fluid flow influence cell–cell and cell–extracellular matrix adhesion and alter cytoskeletal organization to modulate cell and tissue polarity. We describe model systems that when combined with state of the art molecular screens and high-resolution imaging can be used to investigate how force modulates cell and tissue polarity. 相似文献
120.
Transendothelial migration of monocytes followed by their differentiation into macrophages involves interaction of monocytes
with subendothelial matrix. The influence of extracellular matrix on monocyte–macrophage differentiation was studied using
an in vitro model system with human PBMC maintained on different matrix protein substrata. Upregulation of macrophage specific marker
activities such as endocytosis of modified proteins, changes in expression of cell surface antigen, and production of matrix
metalloproteinases was studied. Cells maintained on Fibronectin (Fn) showed significantly higher rate of endocytosis and production
of MMP2 and MMP9 when compared to other matrix protein substrata. Immunoblot analysis, ELISA, and zymography showed that Fn-dependent
upregulation of MMPs was blocked by antibodies to α5β1 integrin indicating that the Fn effect was mediated by integrins. The Fn effect on mo–mΦ was blocked by genistein and herbimycin.
As monocytes differentiate to macrophages there was an increase in the rate of production of Fn. These results indicate the
influence of the microenvironment of the cell, particularly Fn, on mo–mΦ differentiation and integrin-mediated downstream
signaling through focal adhesion kinase and Src type tyrosine kinase is involved in this. 相似文献