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Epidermal growth factor system regulates mucin production in airways.
Goblet-cell hyperplasia is a critical pathological feature in hypersecretory diseases of airways. However, the underlying mechanisms are unknown, and no effective therapy exists. Here we show that
IL-4 induces mucin gene expression and goblet cell metaplasia in vitro and in vivo.
TLDR
Results indicate that airway epithelial cells express IL- 4R constitutively and that IL-4 directly induces the differentiation of epithelium into mucous glycoconjugate-containing goblet cells.
Mitochondrial DNA damage and a hypoxic response are induced by CoCl(2) in rat neuronal PC12 cells.
TLDR
It is found that in the presence of hypoxia-mimicking concentrations of CoCl(2), mitochondrial but not nuclear DNA damage is induced in rat neuronal, PC12 cells, the first documentation of induction of mitochondrial DNA (mtDNA) damage under these conditions.
Minocycline reduces gingival collagenolytic activity during diabetes. Preliminary observations and a proposed new mechanism of action.
TLDR
The data suggests that tetracycline therapy inhibits tissue collagenolytic enzyme activity by a mechanism al least in part unrelated to its antibacterial efficacy, and this mechanism may provide a new therapeutic approach for suppressing excessive collagen resorption which occurs during periodontal disease and which can occur during other pathologic conditions.
Reactive oxygen species activate and tetracyclines inhibit rat osteoblast collagenase
TLDR
Data suggested that tetracyclines reduced available HOCI and thus prevented the hypochlorous acid conversion of the osteoblast proenzyme to active collagenase, which may have therapeutic potential in the treatment of periodontitis and other diseases by several mechanisms that inhibit pathologic collagen breakdown.
A matrix metalloproteinase inhibitor reduces bone-type collagen degradation fragments and specific collagenases in gingival crevicular fluid during adult periodontitis
TLDR
This is the first demonstration in human subjects of the simultaneous reduction of excessive MMP activity with concomitant reduction in levels of collagen degradation fragments, potentially applicable to a wide variety of human diseases characterized by excessive collagenase activity.
Doxycycline inhibits neutrophil (PMN)-type matrix metalloproteinases in human adult periodontitis gingiva.
TLDR
MMPS in inflamed gingival tissue of AP patients, like those in GCF, originate primarily from infiltrating PMNs rather than resident gingivals cells (fibroblasts and epithelial cells) or monocyte/macrophages, and that their pathologically-elevated tissue-degrading activities can be directly inhibited by pharmacologic levels of doxycycline.
A Non‐Antimicrobial Tetracycline Inhibits Gingival Matrix Metalloproteinases and Bone Loss in Porphyromonas gingivalis‐induced Periodontitis in Rats a
TLDR
The tetracycline antibiotics, which have long been used as adjuncts in periodontal therapy based on their antimicrobial effectiveness against a variety of suspected periodontopathic microorganisms, are now known to also inhibit pathologically excessive host-derived MMP activity during periodontals and other diseases, although the mechanisms of action are not yet well defined.
MOBILIZATION STUDIES IN COMPLEMENT-DEFICIENT MICE REVEAL THAT OPTIMAL AMD3100 MOBILIZATION OF HEMATOPOIETIC STEM CELLS DEPENDS ON COMPLEMENT CASCADE ACTIVATION BY AMD3100-STIMULATED GRANULOCYTES
TLDR
It is concluded that AMD3100-directed mobilization of HSPCs, similarly to G-CSF-induced mobilization, depends on activation of CC; however, in contrast to G -CSF,AMD3100 activates the distal steps of CC directly at the C5 level.
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