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10.1038/cddis.2016.186 http://scihub22266oqcxt.onion/10.1038/cddis.2016.186 C5108337!5108337!27362801     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2016 ; 7 (6): e2283- Nephropedia Template TP {{tp|p=27362801|t=2016. Extracellular DNA traps released by acute promyelocytic leukemia cells through autophagy |pdf=|usr=}}{{27362801}} gab.com Text Extracellular DNA traps released by acute promyelocytic leukemia cells through autophagy JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=27362801 #FOAvip Acute promyelocytic leukemia (APL) cells exhibit disrupted regulation of cell death and differentiation, and therefore the fate of these leukemic cells is unclear. Here, we provide the first evidence that a small percentage of APL cells undergo a novel cell death pathway by releasing extracellular DNA traps (ETs) in untreated patients. Both APL and NB4 cells stimulated with APL serum had nuclear budding of vesicles filled with chromatin that leaked to the extracellular space when nuclear and cell membranes ruptured. Using immunofluorescence, we found that NB4 cells undergoing ETosis extruded lattice-like structures with a DNA?histone backbone. During all-trans retinoic acid (ATRA)-induced cell differentiation, a subset of NB4 cells underwent ETosis at days 1 and 3 of treatment. The levels of tumor necrosis factor-? (TNF-?) and interleukin-6 (IL-6) were significantly elevated at 3 days, and combined treatment with TNF-? and IL-6 stimulated NB4 cells to release ETs. Furthermore, inhibition of autophagy by pharmacological inhibitors or by small interfering RNA against Atg7 attenuated LC3 autophagy formation and significantly decreased ET generation. Our results identify a previously unrecognized mechanism for death in promyelocytes and suggest that ATRA may accelerate ET release through increased cytokines and autophagosome formation. Targeting this cellular death pathway in addition to conventional chemotherapy may provide new therapeutic modalities for APL. Twit Text FOAVip Extracellular DNA traps released by acute promyelocytic leukemia cells through autophagy ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=27362801 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27362801 #FOAvip English Wikipedia <ref>{{Cite pmid|27362801}}</ref> Extracellular DNA traps released by acute promyelocytic leukemia cells through autophagy #MMPMID27362801 Ma R; Li T; Cao M; Si Y; Wu X; Zhao L; Yao Z; Zhang Y; Fang S; Deng R; Novakovic VA; Bi Y; Kou J; Yu B; Yang S; Wang J; Zhou J; Shi J Cell Death Dis 2016[Jun]; 7 (6): e2283- PMID27362801show ga Acute promyelocytic leukemia (APL) cells exhibit disrupted regulation of cell death and differentiation, and therefore the fate of these leukemic cells is unclear. Here, we provide the first evidence that a small percentage of APL cells undergo a novel cell death pathway by releasing extracellular DNA traps (ETs) in untreated patients. Both APL and NB4 cells stimulated with APL serum had nuclear budding of vesicles filled with chromatin that leaked to the extracellular space when nuclear and cell membranes ruptured. Using immunofluorescence, we found that NB4 cells undergoing ETosis extruded lattice-like structures with a DNA?histone backbone. During all-trans retinoic acid (ATRA)-induced cell differentiation, a subset of NB4 cells underwent ETosis at days 1 and 3 of treatment. The levels of tumor necrosis factor-? (TNF-?) and interleukin-6 (IL-6) were significantly elevated at 3 days, and combined treatment with TNF-? and IL-6 stimulated NB4 cells to release ETs. Furthermore, inhibition of autophagy by pharmacological inhibitors or by small interfering RNA against Atg7 attenuated LC3 autophagy formation and significantly decreased ET generation. Our results identify a previously unrecognized mechanism for death in promyelocytes and suggest that ATRA may accelerate ET release through increased cytokines and autophagosome formation. Targeting this cellular death pathway in addition to conventional chemotherapy may provide new therapeutic modalities for APL. äExtracellular DNA traps released by acute promyelocytic leukemia cells(epmc).pdf DeepDyve Pubget Overpricing