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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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The Intrinsic Apoptotic Pathway01:31

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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The Extrinsic Apoptotic Pathway01:17

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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cCMP and cUMP in Apoptosis: Concepts and Methods.

Sabine Wolter1, Fanni Dittmar2, Roland Seifert2

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Handbook of Experimental Pharmacology
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Pyrimidine cyclic nucleotides, cyclic CMP (cCMP) and cyclic UMP (cUMP), act as novel second messengers influencing apoptosis. They trigger programmed cell death via intrinsic and ER stress pathways in certain cell types, but not in multidrug-resistant cells.

Keywords:
ApoptosisHEL cellsK-562 cellsPKA signalingS49 cellscCMPcUMP

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cyclic nucleotides like cAMP and cGMP are crucial second messengers regulating cellular processes including apoptosis.
  • Apoptosis, or programmed cell death, is a tightly controlled process involving specific protein families and distinct signaling pathways.
  • Emerging research identifies pyrimidine cyclic nucleotides, cCMP and cUMP, as potential new players in cellular signaling.

Purpose of the Study:

  • To investigate the role of pyrimidine cyclic nucleotides (cCMP and cUMP) as second messengers in apoptosis.
  • To elucidate the specific apoptotic pathways influenced by cCMP and cUMP.
  • To examine the differential effects of cCMP and cUMP on apoptosis in various cell models, including multidrug-resistant cells.

Main Methods:

  • Cell culture of S49 mouse lymphoma, human HEL, and human K-562 cells.
  • Induction of apoptosis using cCMP and cUMP.
  • Analysis of apoptosis signaling via intrinsic and ER stress pathways.
  • Assessment of PKA-independent signaling.
  • Evaluation of cellular responses in multidrug-resistant cell lines.

Main Results:

  • cCMP induced PKA-independent apoptosis through intrinsic and ER stress pathways in S49 mouse lymphoma cells.
  • cCMP and cUMP triggered apoptosis via the intrinsic pathway in human HEL cells.
  • cCMP and cUMP demonstrated no significant effect on apoptosis in multidrug-resistant human K-562 cells.

Conclusions:

  • Pyrimidine cyclic nucleotides cCMP and cUMP function as second messengers with the capacity to initiate apoptosis.
  • The apoptotic effects of cCMP and cUMP are pathway-specific and cell-type dependent, notably differing in multidrug-resistant cells.
  • Further research into cCMP and cUMP signaling pathways is warranted for understanding apoptosis regulation and potential therapeutic strategies.