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Kidney Int. 2000 Nov;58(5):2028-43.
Endogenous hepatocyte growth factor ameliorates chronic renal injury by activating matrix degradation pathways.
Liu Y, Rajur K, Tolbert E, Dworkin LD.
Department of Medicine, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island, USA. liusx.upmc.edu
BACKGROUND: Hepatocyte growth factor (HGF) has been shown to promote tubule repair and renal regeneration following acute injury; however, whether HGF also modulates the development and progression of chronic renal diseases that are characterized by progressive tissue fibrosis is uncertain. To examine this question, this study investigated the functional consequence of blocking endogenous HGF signaling in vivo in a model of chronic renal disease. The effects of HGF on the processes of matrix synthesis and degradation in cultured renal epithelial cells were also examined. METHODS: The level of activity of the HGF/c-met axis was examined in rats following 5/6 nephrectomy at multiple time points. To determine the effects of HGF in modulating chronic renal injury, HGF action was blocked in remnant kidney rats using an anti-HGF antibody. The effects of HGF on extracellular matrix (ECM) synthesis and degradation were examined in renal epithelial cells by (35)S-methionine labeling, Western blotting, and zymographic analysis. RESULTS: An increase in renal and systemic production of HGF coupled with an increase in renal c-met was observed in rats with remnant kidneys. When HGF action was blocked by the administration of an anti-HGF antibody, rats experienced a rapid decrease in glomerular filtration rate and increased renal fibrosis. Kidney sections from the antibody-treated rats displayed a marked increase in ECM accumulation and in alpha-smooth muscle actin-positive cells in both the interstitium and tubular epithelium. In vitro studies revealed that HGF reduced net ECM accumulation by human proximal tubule cells (HKC), and this effect was abolished by incubating cells with an anti-HGF antibody. HGF did not alter the ECM synthetic rate in HKC cells. Rather, it markedly increased collagenase such as matrix metalloproteinase-9 (MMP-9) protein expression, as evidenced by Western blotting and zymographic analysis. HGF also decreased the expression of tissue inhibitors of matrix metalloproteinase-1 (TIMP-1) and TIMP-2, the endogenous inhibitors of MMPs. CONCLUSION: These results suggest that HGF is a potent antifibrogenic factor both in vitro and in vivo. Endogenous activation of HGF tends to preserve kidney structure and function in rats with chronic renal disease by activating matrix degradation pathways.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11044223&dopt=Abstract
Br J Cancer. 2000 Nov;83(10):1387-93.
Membrane-type 1 matrix metalloproteinase-mediated progelatinase A activation in non-tumorigenic and tumorigenic human keratinocytes.
Baumann P, Zigrino P, Mauch C, Breitkreutz D, Nischt R.
Department of Dermatology, University of Cologne, Koln, 50924, USA.
Elevated expression of type IV collagenases (MMP-2 and MMP-9) has been strongly correlated with tumour progression and metastasis in various tumours. Here, we analysed expression and activation of these MMPs in non-tumourigenic HaCaT cells and the malignant HaCaT variant II-4(rt). In monolayer cultures, both cell types secreted latent MMP-2 (proMMP-2) in comparable amounts, while MMP-9 production was clearly higher in II-4(rt)cells. Upon contact with fibrillar collagen type I the malignant II-4(rt)cells, but not the HaCaT cells, gained the capability to activate proMMP-2. This process is shown to be membrane-associated and mediated by MT1-MMP. Surprisingly, all membrane preparations from either HaCaT cells or II-4(rt)cells grown as monolayers, as well as within collagen gels, contained considerable amounts of active MT1-MMP. However, within collagen gels HaCaT cells showed significantly higher TIMP-2 levels compared to II-4(rt)cells. This indicates that TIMP-2 might play a central role for MT1-MMP-mediated gelatinolytic activity. Indeed, collagen type I-induced MT1-MMP-mediated proMMP-2 activation by II-4(rt)membranes could be completely abolished by an excess of TIMP-2. In conclusion, our data suggest that MT1-MMP-mediated proMMP-2 activation might be associated with malignant progression of epidermal tumour cells. 2000 Cancer Research Campaign.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11044366&dopt=Abstract
Biol Neonate. 2000 Oct;78(3):198-206.
High-dose inhaled nitric oxide and hyperoxia increases lung collagen accumulation in piglets.
Ekekezie II, Thibeault DW, Rezaeikhaligh MH, Mabry SM, Norberg M, Reddy GK, Youssef J, Truog WE.
Pediatrics, Children's Mercy Hospital, University of Missouri at Kansas City School of Medicine, Kansas City, MO 64108, USA.
Nitric oxide (NO), a pro-oxidant gas, is used with hyperoxia (O(2)) to treat neonatal pulmonary hypertension and recently bronchopulmonary dysplasia, but great concerns remain regarding NO's potential toxicity. Based on reports that exposure to oxidant gases results in pulmonary extracellular matrix injury associated with elevated lavage fluid levels of extracellular matrix components, we hypothesized that inhaled NO with or without hyperoxia will have the same effect. We measured alveolar septal width, lung collagen content, lavage fluid hydroxyproline, hyaluronan and laminin levels in neonatal piglets after 5 days' exposure to room air (RA), RA + 50 ppm NO (RA + NO), O(2) (FiO(2) > 0.96) or O(2) + NO. Matrix metalloproteinase (MMP) activity and MMP-2 mRNA were also measured. In recovery experiments, we measured lung collagen content in piglets exposed to RA + NO or O(2) + NO and then allowed to recover for 3 days. The results show that lung collagen increased 4-fold in the RA + NO piglets, the O(2) and O(2) + NO groups had only a 2-fold elevation relative to RA controls. Unlike the RA + NO piglets, the O(2) and O(2) + NO groups had more than 20-fold elevation in lung lavage fluid hydroxyproline compared to the RA group. O(2) and O(2) + NO also had increased lung MMP activity, extravascular water, and lavage fluid proteins. MMP-2 mRNA levels were unchanged. After 3 days' recovery in room air, the RA + NO groups' lung collagen had declined from 4-fold to 2-fold above the RA group values. The O(2) + NO group did not decline. Alveolar septal width increased significantly only in the O(2) and O(2) + NO groups. We conclude that 5 days' exposure to NO does not result in pulmonary matrix degradation but instead significantly increases lung collagen content. This effect appears potentially reversible. In contrast, hyperoxia exposure with or without NO results in pulmonary matrix degradation and increased lung collagen content. The observation that NO increased lung collagen content represents a new finding and suggests NO could potentially induce pulmonary fibrosis. 2000 S. Karger AG, Basel.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11044769&dopt=Abstract
Di Yi Jun Yi Da Xue Xue Bao. 2002 Nov;22(11):996-9.
[Improvement upon construction of tissue-engineered allogeneic cartilage molded with polyglycolic acid as the scaffold]
[Article in Chinese]
Sun AK, Pei GX, Zhou GP, Chen WX.
Department of Orthopedics and Traumatology, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China.
OBJECTIVE: To improve the method for constructing allogeneic molded cartilage by means of tissue engineering techniques. METHODS: The chondrocytes from the rib and articular cartilage of infant rabbits were harvested by type II collagenase digestion, followed by in vitro cell culture for 3 to 4 passages. The chondrocytes were then prepared into cell suspension and seeded onto C -and O -shaped pre-molded polyglycolic acid (PGA) scaffolds form chondrocyte-PGA composites, which were subsequently cultured in vitro for 7 to 10 d before implanted subcutaneously into adult rabbits. Improvement was made upon conventional shaping and implantation procedures. Morphological observation and cartilage regeneration assessment were conducted at different time points following the implantation, in comparison with the observation by conventional shaping and implantation methods. RESULTS: During in vitro cell culture, the rate of viable chondrocytes in the final cell suspension was (92+/-2)% after well-controlled prolongation of digestion trypsin, similar to the viable cell rate (93+/-2) % by traditional procedures (P>0.05). Gross observation found milk-white, newly generated cartilage which had good flexibility 4 weeks after implantation, and after 8 weeks and later, the cartilage took on the color of porcelain-white. Histological examination showed a few inflammatory cells around the newly generated immature cartilage 4 weeks after implantation, and the inflammation abated when the newly generated cartilage acquired similar histological properties to that of the original cartilage 8 weeks postoperatively and later. After 16 weeks, no blood vessel or capillaries were visible within the new cartilage. CONCLUSION: The chondrocyte viability is not affected when the cells are treated with well-controlled prolonged digestion with trypsin during in vitro cell culture. Improved PGA scaffolds shaping and the implantation procedure facilitate the regeneration of the cartilage after the implantation of the composites.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12433628&dopt=Abstract
Hum Gene Ther. 2000 Oct 10;11(15):2143-58.
Tissue repair with a therapeutic transcription factor.
Bryant M, Drew GM, Houston P, Hissey P, Campbell CJ, Braddock M.
Wound Healing and Tissue Regeneration Program, Endothelial Gene Expression Group, Vascular Diseases Unit, Glaxo-Wellcome Medicines Research Centre, Stevenage, Hertfordshire, SG1 2NY, UK.
The healing of tissue involves a wide range of molecular, cellular, and physiological events that are coordinated in a temporally specific manner. The cellular transcription factor early growth response factor 1 (Egr-1) is expressed minutes after acute injury and serves to stimulate the production of a class of growth factors whose role is to promote tissue repair. We have studied the effects of Egr-1 expression at the site of dermal wounding in rodents. We find that Egr-1 promotes angiogenesis in vitro and in vivo, increases collagen production, and accelerates wound closure. These results show that Egr-1 gene therapy accelerates the normal healing process and raises the potential use of this therapeutic transcription factor for any aspect of tissue repair.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11044915&dopt=Abstract
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