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J Dent Res. 2000 Oct;79(10):1782-8.
Local injection of IFN-gamma reduces the number of myofibroblasts and the collagen content in palatal wounds.
Cornelissen AM, Maltha JC, Von den Hoff JW, Kuijpers-Jagtman AM.
Department of Orthodontics and Oral Biology, College of Dental Science, University of Nijmegen, The Netherlands. orthodonticent.kun.nl
Wound contraction and scar formation after cleft palate surgery impair maxillary growth and dentoalveolar development. Since myofibroblast numbers and scar formation are reduced by interferon-gamma (IFN-gamma) in the healing of dermal wounds, the hypothesis was tested that local administration of IFN-gamma reduces the numbers of myofibroblasts and the elevated amount of collagen during palatal mucoperiosteal wound healing. Standardized mucoperiosteal excision wounds were made in the palatal mucoperiosteum of young rats. Either IFN-gamma or vehicle alone (sham group) was repeatedly injected into the wound site between 4 and 29 days post-wounding. The results were compared with unmanipulated control wounds. Samples of wound tissue were prepared for biochemical and microscopic analysis. The hydroxyproline, sulfated glycosaminoglycan and DNA contents of the wound tissues were analyzed biochemically. The degree of re-epithelialization, tissue thickness, the numbers of myofibroblasts, and the amounts of elastin and collagen types I and III were evaluated on histological sections. Injection of vehicle alone affected almost all healing parameters, compared with the controls, and delayed the wound-healing process. IFN-gamma stimulated re-epithelialization and decreased the numbers of myofibroblasts when compared with vehicle-treated wounds. It also decreased the hydroxyproline and glycosaminoglycan contents of 60-day-old wound tissue, but the histological characteristics of scar tissue persisted. Therefore, IFN-gamma is able to reduce the numbers of myofibroblasts and the collagen content of scar tissue after palatal wound healing. It may be a promising pharmaceutical agent for the reduction of wound contraction and scarring after cleft palate surgery.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11077995&dopt=Abstract
J Dent Res. 2000 Oct;79(10):1789-93.
Role of MAP kinases p42erk-2/p44erk-1 in cementum-derived attachment-protein-mediated cell attachment.
Komaki M, Kang M, Narayanan AS.
Department of Pathology, University of Washington, Seattle 98195, USA.
Cementum-derived attachment protein (CAP) is a collagenous protein which promotes the attachment and spreading of periodontal cell types. We examined the role of the MEK/MAPK pathway in CAP-mediated fibroblast attachment. Human gingival fibroblasts were labeled with 35S-methionine, and the effect of MAP kinase pathway inhibitor PD98059 on attachment and spreading on CAP-coated dishes was examined. Effect on cell proliferation on CAP-coated plates was determined by [3H]-thymidine uptake. Attachment of human gingival fibroblasts to CAP-containing surfaces activated extracellular-signal-regulated kinases (ERK) ERK-2 and ERK-1. In the absence of serum, the ERKs were activated 15 min after attachment, reaching peak levels after 3 hours, and the activity was sustained for at least 12 hours. The enzyme levels were inhibited in cells treated with PD98059. The PD98059 did not significantly affect the kinetics of fibroblast attachment or the number of cells attaching to CAP-coated plates. However, cell spreading was retarded. DNA synthesis as indicated by [3H]-thymidine uptake was not significantly affected. In contrast to PD98059, attachment, spreading, and [3H]-thymidine uptake were inhibited by the protein tyrosine kinase inhibitor genestein. Our results indicate that the MEK/MAPK pathway participates in CAP-mediated fibroblast spreading, but cell attachment and proliferation do not appear to require ERK-2.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11077996&dopt=Abstract
Cell Mol Life Sci. 2000 Sep;57(10):1457-70.
Anti-interleukin-1 and anti-tumor necrosis factor-alpha synergistically inhibit adjuvant arthritis in Lewis rats.
Feige U, Hu YL, Gasser J, Campagnuolo G, Munyakazi L, Bolon B.
Department of Pharmacology/Pathology, Amgen, Thousand Oaks, California 91320-1789, USA. ufeigmgen.com
Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) play dominant roles in mediating the progression of many inflammatory joint diseases, including rheumatoid arthritis in humans, collagen-induced arthritis in mice and rats, and adjuvant arthritis in rats. Blockade of either cytokine partially controls these diseases. The present study investigated the value of combination anti-cytokine therapy in arthritis: the efficacy of IL-1 receptor antagonist (IL-1ra) and 30 kDa polyethylene glycol (PEG)-conjugated soluble TNF receptor type I (PEG sTNF-RI) given together was assessed in Lewis rats with adjuvant arthritis. Administration of either IL-1ra or PEG sTNF-RI partially alleviated joint inflammation, loss of bone mineral density, and loss of body weight. In contrast, combination of these anti-cytokine treatments exhibited a synergistic capacity to inhibit these changes, even when combining doses of IL-1ra and PEG sTNF-RI that did not affect lesion severity when used alone. Statistical analysis of these adjuvant arthritis data using the isobologram method proved that IL-1ra and PEG sTNF-RI were clearly synergistic in inhibiting inflammation, loss of bone mineral density, loss of body weight, and histopathologic parameters of inflammation and joint destruction. These results suggest that treating autoimmune arthritic diseases with combinations of anti-IL-1 and anti-TNF molecules will achieve superior efficacy compared to the use of a single class of anti-cytokine agent and may allow for dose reductions that could prove useful in minimizing potential side effects.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11078023&dopt=Abstract
Am J Otol. 2000 Nov;21(6):793-8.
Angiogenesis and angiogenic growth factors in middle ear cholesteatoma.
Sudhoff H, Dazert S, Gonzales AM, Borkowski G, Park SY, Baird A, Hildmann H, Ryan AF.
Department of Otorhinolaryngology, Head and Neck Surgery, St. Elisabeth Hospital, University of Bochum, Germany.
HYPOTHESIS: This study aimed to analyze the localization and distribution of vessels and of these angiogenic growth factors: basic fibroblast growth factor (FGF-2), transforming growth factor-alpha (TGF-alpha), transforming growth factor-beta1 (TGF-beta1), and vascular endothelial growth factor (VEGF) in middle ear cholesteatoma in comparison with normal middle ear mucosa and auditory meatal skin. BACKGROUND: Angiogenesis is particularly important in many normal and pathologic processes, including wound healing and inflammation. Because proliferating tissues require an enhanced blood supply, angiogenesis appears to be a prerequisite for the expansion of cholesteatoma. METHODS: The expression of FGF-2, TGF-alpha, TGF-beta1, and VEGF was studied by immunohistochemistry. The amount of vessels (collagen type IV staining) was determined by an automatic imaging analyzing system. RESULTS: The results showed an altered expression and distribution of VEGF, FGF-2, TGF-alpha, and TGF-beta1 in cholesteatoma in relation to middle ear mucosa and auditory meatal skin. The results were consistent with rapidly growing, activated keratinocytes and stromal cells. Vascularization within the perimatrix of cholesteatoma showed a 4.3-fold increase compared with middle ear mucosa and a twofold increase compared with ear canal skin. An increase of 3.2- to 4-fold in the number of vessels was observed. A close relationship was seen between the density of capillaries, degree of inflammation, and expression of the angiogenic factors investigated, and an increased number of microvessels in cholesteatoma tissue. CONCLUSIONS: Angiogenesis enables and supports the sustained migration of keratinocytes into the middle ear cavity. Therefore, it is a pivotal factor in the destructive behavior of middle ear cholesteatoma.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11078065&dopt=Abstract
Am J Otol. 2000 Nov;21(6):804-8.
Treatment with dexamethasone arrests the development of myringosclerosis after myringotomy.
Mattsson C, Stierna P, Hellstrom S.
Department of Otorhinolaryngology, Umea University Hospital, Sweden.
HYPOTHESIS: To attempt to inhibit the development of myringosclerosis by intraperitoneal injection of dexamethasone. BACKGROUND: The authors' earlier report showed that the development of myringosclerosis after myringotomy was associated with an inflammatory reaction. The present study was performed to secure evidence for this hypothesis. METHODS: Three groups of bilaterally myringotomized rats were treated at 12-hour intervals with intraperitoneal injection of dexamethasone, RU486 (a glucocorticoid receptor antagonist), and saline, respectively. At 6, 12, 24, and 48 hours after the myringotomy, 2 animals were anesthetized on each occasion and examined otomicroscopically. The animals were then killed, and the tympanic membranes were excised and prepared for light microscopic studies. RESULTS: Dexamethasone treatment retarded and diminished the development of sclerotic lesions markedly. Moreover, no inflammatory signs were seen in the flaccida specimens. When the RU486-treated animals were compared with the animals in the control group, there were no evident differences concerning the development of myringosclerosis or the extent of the inflammatory reaction. CONCLUSION: These findings confirm the earlier hypothesis that an inflammatory reaction in collagen tissue is involved in the mechanism that causes the development of myringosclerosis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11078067&dopt=Abstract
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