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Investigating the role of Bax/Bak as a driver of inflammation in aging

ABSTRACT: Investigating the role of Bax/Bak as a driver of inflammation in aging

PROVIDER: PRJNA985583 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24968065_1.fastq.gz	Fastqsanger.gz
	SRR24968065_2.fastq.gz	Fastqsanger.gz
	SRR24968066_1.fastq.gz	Fastqsanger.gz
	SRR24968066_2.fastq.gz	Fastqsanger.gz
	SRR24968067_1.fastq.gz	Fastqsanger.gz

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Investigating the role of Bax/Bak as a driver of inflammation in aging

Project description:Senescent cells drive age-related tissue dysfunction partially via the induction of a chronic senescence-associated secretory phenotype (SASP). Mitochondria are major regulators of the SASP; however, the underlying mechanisms have not been elucidated. Mitochondria are often essential for apoptosis, a cell fate distinct from cellular senescence. During apoptosis, widespread mitochondrial outer membrane permeabilization (MOMP) commits a cell to die. Here, we find that MOMP occurring in a subset of mitochondria is a feature of cellular senescence. This process, called minority MOMP (miMOMP), depends on the formation of BAX and BAK macropores leading to the release of mitochondrial DNA (mtDNA) into the cytosol, which in turn activates the cGAS-STING pathway, a major regulator of the SASP. Importantly, we found that inhibition of MOMP in vivo decreases inflammatory markers and improves healthspan in aged mice. Our results reveal, unexpectedly, that apoptosis and senescence are regulated by similar mitochondrial-dependent mechanisms, and that sub-lethal mitochondrial apoptotic stress is a major driver of the SASP. We also provide proof-of-concept that inhibition of miMOMP-induced inflammation may be a new therapeutic avenue to improve healthspan.

2023-08-16 | GSE235225 | GEO

Wild type mouse embryonic fibroblasts (MEF) vs Bax/BAK double knock out MEF treated with and without Nocodazole

Project description:MEF WT, MEF DKO(Bax/Bak), MEF DKO(Bax/Bak) expressing rabbit Serca2a, MEF DKO(Bax/Bak) expressing Bak at the endoplasmic reticulum both control and treated with Noco 100 nM for 48h

2023-06-12 | E-MTAB-10997 | biostudies-arrayexpress

VDAC2 promotes BAX apoptotic activity

Project description:Intrinsic apoptosis is critical for normal physiology including the prevention of tumor formation. BAX and BAK, which are essential for mediating this process and for the cytotoxic action of many anti-cancer drugs, are thought to be regulated through similar mechanisms and act redundantly to drive apoptosis. Here we have established the various mitochondrial complexes that contain VDAC1, VDAC2, VDAC3 and BAX or BAK.

2018-10-29 | PXD011195 | Pride

Stromal inflammation is a targetable driver of hematopoietic aging [Microarray analysis]

Project description:Stromal inflammation is a targetable driver of hematopoietic aging [Microarray analysis]

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Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death

Project description:Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death

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Stromal inflammation is a targetable driver of hematopoietic aging [droplet-based scRNAseq]

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Transcription profiling of mouse Bax null versus NGF-Bax double null animals

Project description:We report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its receptor TrkA in neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain derived neurotrophic factor (BDNF) and neurotrophin-4 (NT4), which, through the receptor p75, can kill neighboring neurons with low retrograde NGFâ??TrkA signaling whereas neurons with high NGFâ??TrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects. Experiment Overall Design: This experiment examine gene expression differences in superior cervical ganglia fro P0 bax null versus NGF-Bax double null animals. The Bax genotype was used in order to prevent the neuronal cell death normally observed in the NGF null animal.

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Expression data from BAX/BAK double knockout mouse embryonic fibroblast at baseline and following exposure to genotoxic stress.

Project description:The BCL-2 family proteins are central regulators of apoptosis. However, cells doubly deficient for BAX and BAK or overexpressing BCL-2 still succumb to oxidative stress upon DNA damage or loss of matrix attachment. Our studies indicate a central role for the transcription factor deltaNp63alpha (referred to as p63 from this point forward) in this form of non-apoptotic cell death. We used microarrays to investigate gene expression in apoptosis-incompetent cells expressing a control vector or p63, at baseline and following exposure to genotoxic stress, to further elucidate molecular mechanisms regulating this type of non-apoptotic death and the role of p63 in this context.

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Stromal inflammation is a targetable driver of blood aging [droplet-based scRNAseq - Batch 2]

Project description:Stromal inflammation is a targetable driver of blood aging [droplet-based scRNAseq - Batch 2]

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