Interplay between caspase, Yes-associated protein, and mechanics: A possible switch between life and death?

Kabigting, Jessica Evangeline Tan; Toyama, Yusuke

doi:10.1016/j.ceb.2020.10.010

Cited by 8 publications

(7 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Caspase-9, as the upstream regulator of caspase-3, plays a key role in cell apoptosis together with caspase-3. 47 Our results showed that Cd exposure decreased Bcl-2 mRNA level and elevated the mRNA levels of Bax, caspase-3, and caspase-9. Meanwhile, the protein level of Bcl-2 was decreased, and the protein levels of Bax, cleaved caspase-3, caspase-9, and cleaved caspase-9 were increased.…”

Section: Western Blotting Analysissupporting

confidence: 49%

See 1 more Smart Citation

Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death via PI3K/AKT/PTEN signaling

Feng

Yang

et al. 2022

Environmental Toxicology

View full text Add to dashboard Cite

Cadmium (Cd) is an environmental pollutant that has an enormous influence on agricultural production, but selenium (Se) can alleviate its toxicity. The present study aimed to illustrate the effects of Se on Cd-induced heart injury. All 40 rabbits were randomly divided into four groups: control group, Se [0.5 mg kg À1 Ábody weight (BW)] group, Cd (1 mg kg À1 ÁBW) group, and Se + Cd group. After 30 days of feeding, morphological changes, the levels of oxidative stress and myocardial enzyme, the content of cardiac troponin T, programmed cell death (pyroptosis, autophagy and apoptosis), and PI3K/AKT/PTEN transduction capacity were observed. The results showed that Cd destroyed the physiological balance of trace elements and caused myocardial damage, increased the cardiac oxidative damage and led to programmed cell death.Coadministration of Se prominently ameliorated histological lesions and improved cardiac function of hearts in Cd-induced rabbits. Furthermore, Se exerted detoxification and oxidation resistance, maintained trace element homeostasis, and alleviated the changes of mRNA and protein levels of pyroptosis-, autophagy-and apoptosiscontrolling factors and PI3K/AKT/PTEN signal molecules caused by Cd. In conclusion, Se might protect against Cd-induced pyroptosis, autophagy and apoptosis by interfering with PI3K/AKT/PTEN signaling in heart.

show abstract

Section: Western Blotting Analysissupporting

confidence: 49%

“…Caspase‐3 is the most important executor of apoptosis in the caspase cascade reaction. Caspase‐9, as the upstream regulator of caspase‐3, plays a key role in cell apoptosis together with caspase‐3 47 . Our results showed that Cd exposure decreased Bcl‐2 mRNA level and elevated the mRNA levels of Bax, caspase‐3, and caspase‐9.…”

Section: Discussionmentioning

confidence: 57%

Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death via PI3K/AKT/PTEN signaling

Feng

Yang

et al. 2022

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…The proteomics analysis revealed that the changes are likely to be associated particularly with non‐canonical roles of caspase‐9. These novel functions included impact on proteins participating in metabolism which would thus support the novel insight into caspases as a switch between life and death [34]. Additionally, inhibition of caspase‐9 modified levels of proteins having roles in cell collagen metabolic processes which would further explain the micromass morphology after caspase‐9 inhibition.…”

Section: Discussionmentioning

confidence: 95%

“…Increasing body of recent studies provides evidence about yet unexpected contribution of the apoptotic caspases to proliferation and differentiation of cells [15,33]. Recently, caspases were even assigned as a key switch between life and death [34].…”

Section: Discussionmentioning

confidence: 99%

DiaPASEF proteotype analysis indicates changes in cell growth and metabolic switch induced by caspase‐9 inhibition in chondrogenic cells

et al. 2023

View full text Add to dashboard Cite

Caspase-9 is the major apical caspase responsible for triggering the intrinsic apoptotic pathway. Our previous study indicated that specific inhibition of caspase-9 caused microscopically evident alterations in appearance of the primary chondrogenic cultures which cannot be explained by decrease in apoptosis. To describe a complex molecular background of this effect, proteomics analysis of control and caspase-9 inhibitor-treated chondrogenic cultures were performed. Proteins were extracted, identified and quantified using LC-MS in both data dependent and data independent acquisition (DIA) mode. While directDIA analysis of diaPASEF data obtained using timsTOF Pro LC-MS system revealed 7849 protein groups (Q-value <0.01), a parallel analysis of iTRAQ-2DLC-MS3 and conventional DIA-MS data identified only 5146 and 4098 protein groups, respectively, showing diaPASEF a superior method for the study.The detailed analysis of diaPASEF data disclosed 236/551 significantly down-/upregulated protein groups after caspase-9 inhibition, respectively (|log2FC|>0.58, Q value <0.05). Classification of downregulated proteins revealed changes in extracellular matrix organization, collagen metabolism, and muscle system processes. Moreover, deregulations suggest a switch from glycolytic to lipid based metabolism in the inhibited cells. No essential changes were found in the proteins involved in apoptosis. The data indicate new non-apoptotic participation of caspases in chondrocyte homeostasis with potential applications in cartilage pathophysiology.

show abstract

“…The mitochondrial pathway can be divided into three parts, increased mitochondrial outer membrane permeabilization (MOMP), (Kalkavan & Green, 2018), apoptosome formation (Dorstyn et al, 2018), and caspase protein execution (Kabigting & Toyama, 2020). MOMP is regulated by B-cell lymphoma 2 (BCL-2) family proteins (Kalkavan & Green, 2018).…”

Section: Apoptosis Suppression By Aktmentioning

confidence: 99%

Multiple forms of cell death: A focus on the PI3K/AKT pathway

Xu,

Li,

Kang

et al. 2023

Journal Cellular Physiology

View full text Add to dashboard Cite

Cell death is a natural biological process that occurs in living organisms. Since 1963, extensive research has shed light on the occurrence, progress, and final outcome of cell death. According to different cell phenotypes, it is classified into different types, including apoptosis, pyroptosis, necroptosis, autophagy, ferroptosis, cuproptosis, and so on. However, regardless of the form of cell death, what we ultimately expect is the disappearance of abnormal cells, such as tumor cells, while normal cells survive. As a result, it is vital to investigate the details of cell death, including death triggers, potent regulators, and executioners. Although significant progress has been made in understanding molecular pathways of cell death, many aspects remain unclear because of the complex regulatory networks in cells. Among them, the phosphoinositide‐3‐kinase (PI3K)/protein kinase B(AKT) pathway is discovered to be a crucial regulator of the cell death process. AKT, as a proto‐oncogene, has become a major focus of attention in the medical community due to its role in regulating a multiplicity of cellular functions counting metabolism, immunity, proliferation, survival, transcription, and protein synthesis. Here, we explored the connection between the PI3K/AKT pathway and cell death, aiming to enhance our comprehension of the mechanism underlying this process. Such knowledge may pave the way for the subsequent development of more effective disease treatments, such as finding suitable targets for drug intervention.

show abstract

Interplay between caspase, Yes-associated protein, and mechanics: A possible switch between life and death?

Cited by 8 publications

References 47 publications

Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death via PI3K/AKT/PTEN signaling

Selenium protects against cadmium‐induced cardiac injury by attenuating programmed cell death via PI3K/AKT/PTEN signaling

DiaPASEF proteotype analysis indicates changes in cell growth and metabolic switch induced by caspase‐9 inhibition in chondrogenic cells

Multiple forms of cell death: A focus on the PI3K/AKT pathway

Contact Info

Product

Resources

About