Expansion and evolution of cell death programmes

Degterev, Alexei; Yuan, Junying

doi:10.1038/nrm2393

Cited by 477 publications

(409 citation statements)

References 141 publications

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“…We tested the expression of apoptosis-regulating genes Traf2, Traf6, Parp1, Atf6, Ask1, Ask2, Dapk1, and Apaf1 in siBrg1 NCCs (21)(22)(23)(24)(25)(26)(27)(28). Of these genes, only Ask1 (apoptosis signal-regulating kinase 1) exhibited increased expression (a 1.65-fold increase; P < 0.03) in siBrg1NCCs; the other genes showed no significant changes (Fig.…”

Section: Resultsmentioning

confidence: 99%

Brg1 governs distinct pathways to direct multiple aspects of mammalian neural crest cell development

Xiong²,

Shang³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Development of the cerebral vessels, pharyngeal arch arteries (PAAs). and cardiac outflow tract (OFT) requires multipotent neural crest cells (NCCs) that migrate from the neural tube to target tissue destinations. Little is known about how mammalian NCC development is orchestrated by gene programming at the chromatin level, however. Here we show that Brahma-related gene 1 (Brg1), an ATPase subunit of the Brg1/Brahma-associated factor (BAF) chromatin-remodeling complex, is required in NCCs to direct cardiovascular development. Mouse embryos lacking Brg1 in NCCs display immature cerebral vessels, aberrant PAA patterning, and shortened OFT. Brg1 suppresses an apoptosis factor, Apoptosis signal-regulating kinase 1 (Ask1), and a cell cycle inhibitor, p21 cip1 , to inhibit apoptosis and promote proliferation of NCCs, thereby maintaining a multipotent cell reservoir at the neural crest. Brg1 also supports Myosin heavy chain 11 (Myh11) expression to allow NCCs to develop into mature vascular smooth muscle cells of cerebral vessels. Within NCCs, Brg1 partners with chromatin remodeler Chromodomain-helicase-DNAbinding protein 7 (Chd7) on the PlexinA2 promoter to activate PlexinA2, which encodes a receptor for semaphorin to guide NCCs into the OFT. Our findings reveal an important role for Brg1 and its downstream pathways in the survival, differentiation, and migration of the multipotent NCCs critical for mammalian cardiovascular development.N eural crest cells (NCCs) originate from the neural crest of the dorsal neural tube and migrate to many regions of the embryo, where they differentiate into a variety of local cells, including cardiovascular tissues (1). NCCs that emigrate from the neural crest of rhombomere 6-8 to pharyngeal arches and the heart are essential for the patterning of pharyngeal arch arteries (PAAs) and the cardiac outflow tract (OFT) (2, 3). These NCCs also differentiate into vascular smooth muscle cells (SMCs) of PAAs and the muscular septum of the aorta and pulmonary trunk (4, 5). In contrast, NCCs from the cephalic neural tube migrate to the face and forebrain to form craniofacial bones, as well as SMCs of facial and forebrain vessels (6). Thus, NCCs are critical for the formation of cardiac OFT and vascular supplies of large areas of the body.Disruption of NCC development, either directly or indirectly, results in many forms of human birth defects with cardiovascular malformations, including Alagille, Carpenter, Ivemark, Leopard, Williams, DiGeorge, and CHARGE syndromes (7). These syndromes involve defects in PAAs or cardiac OFT, such as coarctation of the aorta, interrupted aortic arch, pulmonary artery stenosis, double-outlet right ventricle, tetralogy of Fallot, or persistent truncus arteriosus. During PAA and OFT development, NCCs are regulated by numerous transcription factors, including Pax3, Pbx1/2/3, Tbx1/2/3/20, Msx1/2, Hand2, AP2a, Cited2, Pitx2, Sox4, Foxc1/c2/d3/h1, Fog2, Gata3/4/6, and Notch/NICD (8). Such extensive involvement of transcription factors indicates the importance of gene pr...

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Section: Resultsmentioning

confidence: 99%

Brg1 governs distinct pathways to direct multiple aspects of mammalian neural crest cell development

Xiong²,

Shang³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…10 Necrotic death is associated with diverse pathological conditions, including myocardial infarction, cerebral ischemia, acute organ failure and infection. 16 The in vitro and in vivo models of TRAIL-induced necroptosis described in this work may be the basis to identify new modulators or inhibitors. These drugs would be particularly useful in the treatment of degenerative diseases where necrotic pathways are involved.…”

Section: Discussionmentioning

confidence: 96%

“…14 Nonetheless, some specific molecular mechanisms have been pointed out in PARP-1 (poly (ADP-ribose) polymerase-1)-mediated necrotic cell death induced by DNA-damaging agents, called parthanatos, 15 and in RIPK1-dependent programmed necrosis induced by TNF-like cytokines. 16 Recently, RIPK3, another RIP family kinase, has been identified as an essential mediator for TNF-, FasL-and TRAIL-mediated necroptosis. [17][18][19] This emerging necrotic pathway in vitro has been shown to be relevant in vivo in vaccinia virus infection 17 and ceruleininduced pancreatitis.…”

Section: Tumor Necrosis Factor (Tnf)-related Apoptosis Inducing Liganmentioning

confidence: 99%

TRAIL induces necroptosis involving RIPK1/RIPK3-dependent PARP-1 activation

et al. 2012

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Although TRAIL (tumor necrosis factor (TNF)-related apoptosis inducing ligand) is a well-known apoptosis inducer, we have previously demonstrated that acidic extracellular pH (pHe) switches TRAIL-induced apoptosis to regulated necrosis (or necroptosis) in human HT29 colon and HepG2 liver cancer cells. Here, we investigated the role of RIPK1 (receptor interacting protein kinase 1), RIPK3 and PARP-1 (poly (ADP-ribose) polymerase-1) in TRAIL-induced necroptosis in vitro and in concanavalin A (Con A)-induced murine hepatitis. Pretreatment of HT29 or HepG2 with pharmacological inhibitors of RIPK1 or PARP-1 (Nec-1 or PJ-34, respectively), or transient transfection with siRNAs against RIPK1 or RIPK3, inhibited both TRAILinduced necroptosis and PARP-1-dependent intracellular ATP depletion demonstrating that RIPK1 and RIPK3 were involved upstream of PARP-1 activation and ATP depletion. In the mouse model of Con A-induced hepatitis, where death of mouse hepatocytes is dependent on TRAIL and NKT (Natural Killer T) cells, PARP-1 activity was positively correlated with liver injury and hepatitis was prevented both by Nec-1 or PJ-34. These data provide new insights into TRAIL-induced necroptosis with PARP-1 being active effector downstream of RIPK1/RIPK3 initiators and suggest that pharmacological inhibitors of RIPKs and PARP-1 could be new treatment options for immune-mediated hepatitis.

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“…Apoptosis is morphologically defined by nuclear shrinkage and fragmentation (Kerr et al, 1972), whereas necrosis is defined by early permeabilization of the plasma membrane (Golstein and Kroemer, 2007;Degterev and Yuan, 2008). By definition, ACD is characterized by massive sequestration of portions of the cytoplasm within autophagosomes, giving the cell a characteristic vacuolated aspect (Shintani and Klionsky, 2004;Tsujimoto and Shimizu, 2005).…”

Section: Introductionmentioning

confidence: 99%

Association and dissociation of autophagy, apoptosis and necrosis by systematic chemical study

et al. 2011

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To address the question of whether established or experimental anticancer chemotherapeutics can exert their cytotoxic effects by autophagy, we performed a highcontent screen on a set of cytotoxic agents. We simultaneously determined parameters of autophagy, apoptosis and necrosis on cells exposed to B1400 compounds. Many agents induced a 'pure' autophagic, apoptotic or necrotic phenotype, whereas less than 100 simultaneously induced autophagy, apoptosis and necrosis. A systematic analysis of the autophagic flux induced by the most potent 80 inducers of GFP-LC3 puncta among the NCI panel agents showed that 59 among them truly induced autophagy. The remaining 21 compounds were potent inducers of apoptosis or necrosis, yet failed to stimulate an autophagic flux, which were characterized as microtubule inhibitors. Knockdown of ATG7 was efficient in preventing GFP-LC3 puncta, yet failed to attenuate cell death by the agents that induce GFP-LC3 puncta. Thus there is not a single compound that would induce cell death by autophagy in our screening, underscoring the idea that cell death is rarely, if ever, executed by autophagy in human cells.

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Expansion and evolution of cell death programmes

Cited by 477 publications

References 141 publications

Brg1 governs distinct pathways to direct multiple aspects of mammalian neural crest cell development

Brg1 governs distinct pathways to direct multiple aspects of mammalian neural crest cell development

TRAIL induces necroptosis involving RIPK1/RIPK3-dependent PARP-1 activation

Association and dissociation of autophagy, apoptosis and necrosis by systematic chemical study

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