Glucosaminylmuramyl dipeptide (GMDP) modulates endothelial cell activities in vitro but has no effect on angiogenesis in vivo

Li, C G; Kumar, Shant; Ledger, Philip W.; Ponting, J; Carette, M. J. M.; Allan, Ernest

doi:10.1007/s000110050200

Cited by 7 publications

(4 citation statements)

References 15 publications

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“…To accomplish this, the CAM assay was used for the present study because it is a well-accepted model in vascular research. [20][21][22][23] EMD was analyzed for its effect on the production of blood vessels in the CAM. Because amelogenin is the predominant component of EMD, rh-amelogenin was also analyzed for its effect on the production of blood vessels in the CAM.…”

Section: Discussionmentioning

confidence: 99%

In Vivo Angiogenic Activity of Enamel Matrix Derivative

Kauvar

Thoma

Carnes

et al. 2010

Journal of Periodontology

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EMD stimulates angiogenesis in the CAM model. As a heterogeneous mixture of extracellular matrix components, EMD may have multiple biologic functions, but it is likely that at least part of the explanation for its observed positive clinical effects may be the stimulation of angiogenesis. The fact that vascularity was also increased by recombinant human amelogenin raises the possibility that this 28.9-kDa protein may be the source of the angiogenic activity because it is the predominant protein of the EMD mixture. These results, taken together with results from previously reported in vitro studies, suggest that EMD may increase angiogenesis directly and/or indirectly at the wound-healing site.

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Section: Discussionmentioning

confidence: 99%

In Vivo Angiogenic Activity of Enamel Matrix Derivative

Kauvar

Thoma

Carnes

et al. 2010

Journal of Periodontology

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“…Cell survival was quantified in the colorimetric MTT assay, which measures mitochondrial activity in viable cells 12) on the basis of conversion of MTT to formazan crystals by mitochondrial enzymes. Transfected and untransfected cells were seeded in 96-multiwell plates at 3ϫ10 4 cells/well in 200 ml of medium containing 10% FBS.…”

Section: Determination Of Cell Viability In the Mtt Assaymentioning

confidence: 99%

Establishment of a Cell-Based Assay to Screen Regulators of the Hypoxia-Inducible Factor-1-Dependent Vascular Endothelial Growth Factor Promoter

Zhu

Jia

et al. 2008

Biological & Pharmaceutical Bulletin

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“…Cell cycle distribution was evaluated by propidium iodide staining of nuclei and flow cytometric analysis (Li et al, 1997). 1×10 6 cells were fixed with 2 ml cold 70% (v/v) ethanol in PBS, immediately mixed and slowly agitated for 15 minutes at room temperature.…”

Section: Cell Cycle Analysismentioning

confidence: 99%

CD105 prevents apoptosis in hypoxic endothelial cells

Issa

Kumar

et al. 2003

Journal of Cell Science

153

116

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CD105, a marker of endothelial cells, is abundantly expressed in tissues undergoing angiogenesis and is a receptor for transforming growth factorβ. The pivotal role of CD105 in the vascular system was demonstrated by the severe vascular defects that occur in CD105-knockout mice,but the exact mechanisms for CD105 regulation of vascular development have not been fully elucidated. In light of the function of CD105 and the importance of hypoxia in neovascularisation, we speculated that CD105 is involved in hypoxia-initiated angiogenesis. Using tissue-cultured human microvascular endothelial cells, we have investigated the effects of hypoxic stress on CD105 gene expression. Hypoxia induced a significant increase in membrane-bound and secreted CD105 protein levels. CD105 mRNA and promoter activity were also markedly elevated, the latter returning to the basal level after 16 hours of hypoxic stress. Hypoxia induced cell cycle arrest at the G0/G1 phases and massive cell apoptosis after 24 hours through a reduction in the Bcl-2 to Bax ratio, downregulation of Bcl-XL and Mcl-1, and upregulation of caspase-3 and caspase-8. The consequence of CD105 upregulation was revealed using an antisense approach and a TUNEL assay. Suppression of CD105 increased cell apoptosis under hypoxic stress in the absence of TGFβ1. Furthermore,hypoxia and TGFβ1 synergistically induced apoptosis in the CD105-deficient cells but not in the control cells. We conclude that hypoxia is a potent stimulus for CD105 gene expression in vascular endothelial cells,which in turn attenuates cell apoptosis and thus contributes to angiogenesis.

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Glucosaminylmuramyl dipeptide (GMDP) modulates endothelial cell activities in vitro but has no effect on angiogenesis in vivo

Abstract: GMDP can modulate endothelial cell activity without the induction of angiogenesis in vivo which may have implications for its use as a therapeutic agent.

Cited by 7 publications

References 15 publications

In Vivo Angiogenic Activity of Enamel Matrix Derivative

In Vivo Angiogenic Activity of Enamel Matrix Derivative

Establishment of a Cell-Based Assay to Screen Regulators of the Hypoxia-Inducible Factor-1-Dependent Vascular Endothelial Growth Factor Promoter

CD105 prevents apoptosis in hypoxic endothelial cells

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