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Caspases01:24

Caspases

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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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Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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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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Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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Role of ER in the Secretory Pathway01:17

Role of ER in the Secretory Pathway

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Eukaryotic cells have a special pathway that enables communication between various intracellular membrane-bound compartments and also with the extracellular environment. This pathway is termed as the secretory pathway.
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Dendrobine suppresses endoplasmic reticulum stress-induced apoptosis through upregulating microRNA miR-381-3p to

Jing Meng1, Xiaoying Song1, Guoliang Yan2

  • 1Department of Geriatrics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

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This summary is machine-generated.

Dendrobine inhibits endothelial cell apoptosis in endoplasmic reticulum stress models by upregulating miR-381-3p, offering potential therapeutic benefits for atherosclerosis.

Keywords:
Dendrobineapoptosiscaspase-4endoplasmic reticulum stressmiR-381-3pproliferation

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Endothelial Cell Biology

Background:

  • Endothelial cell apoptosis is a key factor in atherosclerosis (AS).
  • Endoplasmic reticulum stress (ERS) contributes to endothelial dysfunction and AS.
  • Dendrobine has shown potential in reducing lipid levels and apoptosis.

Purpose of the Study:

  • To investigate the protective effects of dendrobine on endothelial cells under ERS.
  • To elucidate the molecular mechanisms underlying dendrobine's therapeutic action in AS.
  • To explore the role of miR-381-3p in dendrobine's anti-apoptotic effects.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were subjected to ERS using tunicamycin (TM).
  • Cells were pre-treated with dendrobine, and proliferation/apoptosis were assessed.
  • miR-381-3p expression, protein levels (GRP78, IRE1, caspase-4, CHOP, caspase-3), and target binding were analyzed.

Main Results:

  • TM-induced ERS led to decreased miR-381-3p expression and increased HUVEC apoptosis.
  • Dendrobine treatment promoted HUVEC proliferation and inhibited apoptosis.
  • Dendrobine upregulated miR-381-3p, reduced ERS markers, and caspase-4 activation, mitigating apoptosis.

Conclusions:

  • Dendrobine protects endothelial cells against ERS-induced apoptosis by upregulating miR-381-3p.
  • This protective effect is partially mediated by the inhibition of caspase-4.
  • Dendrobine demonstrates therapeutic potential for AS by targeting endothelial cell apoptosis.