Example sentences for: antiapoptotic

How can you use “antiapoptotic” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Progression of granulation tissue to neodermis requires a decrease in cellularity through apoptosis of endothelial cells, fibroblasts and myofibroblasts [ 28 29 ] . Keloid fibroblasts demonstrate aberrant apoptotic behavior [ 30 31 ] although studies have given variable results [ 5 9 11 30 31 32 33 34 35 ] . Our initial data for serum-starvation-induced apoptosis in monolayer cultures of dermal fibroblasts demonstrated delayed apoptosis of keloid fibroblasts and a negative correlation with α-SMA expression [ 36 ] . Similar correlations were observed in rat lung fibroblasts, where TGFβ1 increased α-SMA content while acting as an antiapoptotic agent [ 37 38 ] . It should be noted however, that many of the myofibroblasts were still able to undergo apoptosis consistent with in vivo data on palatal wound healing [ 39 ] . Thus, TGFβ1 can promote both α-SMA expression in the initial stages of wound healing and apoptosis in later stages of wound healing.

  • In contrast, TGF-β1 protects L929 cells from TNF cytotoxicity by upregulating the expression of antiapoptotic TIAF1, TIF2 and a novel matrix protein [ 11 12 13 14 ] . TGF-β1 blocks PH-20-increased TNF susceptibility [ 15 ] . Likewise, PH-20 inhibits TGF-β1-induced TNF-resistance [ 15 ] . TGF-β1 suppresses PH-20-mediated ERK activation [ 16 ] ; however, the ERK activation is not related with PH-20-increased TNF susceptibility in L929 cells [ 15 ] . Whether the proapoptotic p53 and WOX1 block the function of antiapoptotic TIAF1 and TIF2 is not known.

  • TGF-β family proteins, including β1,β2 and β3, induce TNF-resistance and suppress the PH-20 effect of increasing TNF cytotoxicity in murine L929 fibroblasts [ 8 11 ] . TGF-β1 induces a novel extracellular matrix protein that prevents TNF-mediated cell death and blocks the activation of extracellular signal-regulated kinase (ERK; also known as p42/44 mitogen-activated protein kinase, p42/44 MAPK) in L929 cells [ 8 12 ] . Additionally, TGF-β1 induces the expression of TIAF1 (TGF-β-induced antiapoptotic factor) [ 13 ] and TIF2 (TGF-β-induced factor 2) [ 14 ] that inhibit TNF cytotoxicity.

  • IκBα is a physiological inhibitor of NF-κB activation; IκBα complexes with NF-κB and prevents its translocation to the nucleus [ 10 24 ] . NF-κB activation is believed to induce antiapoptotic proteins to block cell death [ 8 ] . However, in several studies activated NF-κB cannot protect cells from apoptosis [ 8 ] . Also, NF-κB appears to be essential in the p53-mediated apoptosis in tested cell lines [ 25 ] .

  • Injured adult DRG neurons do not die after axonal injury [ 15 ] as a result of the upregulation of cell survival factors such as the small heat shock protein HSP27 [ 16 ] . We now find several genes that could have a survival-promoting role, including the peripheral benzodiazepine receptor, whose agonists are potent antiapoptotic compounds [ 17 ] , GADD45A, which maintains genomic stability and appears to be anti-apoptotic in neurons after ischemic damage [ 18 ] , metallothionein 1L, which is a free radical scavenger [ 19 ] , GTP cyclohydrolase 1, which is obligatory for the actions of NGF on PC12 cells [ 20 ] , and IES-JE (MCP-1) which attracts macrophages, which in turn have been reported to have a role in neuronal survival [ 21 ] .


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