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Related Concept Videos

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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Chronic stress has been linked to both the onset and progression of serious health conditions, including Type 2 diabetes and cancer. Type 2 diabetes, a widespread chronic illness, is closely associated with obesity and insulin resistance, both of which often worsen under stress. Studies indicate that men experiencing high levels of chronic stress face a 45% higher risk of developing diabetes compared to those with minimal stress. Stress triggers physiological responses that elevate blood...
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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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Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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Regulating islet stress responses through CD47 activation.

Atharva Kale1,2, Mahmoud Azar1,3, Vanessa Cheng1

  • 1Kidney Injury Group, Centre for Transplant and Renal Research, Westmead Institute for Medical Research, Westmead, NSW, Australia.

Diabetologia
|March 26, 2025
PubMed
Summary
This summary is machine-generated.

Targeting CD47, a cell surface protein, shows promise for protecting beta cells from stress and dysfunction in diabetes. Modulating CD47 signaling improved cell survival and insulin secretion, offering a potential therapeutic strategy for diabetes treatment.

Keywords:
CD47Diabetes mellitusER stressHypoxiaIslet transplantationIsletsThrombospondin-1

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Immunology

Background:

  • Diabetes mellitus is a major global health challenge characterized by progressive beta cell loss.
  • Islet transplantation is a treatment for type 1 diabetes, but limited islet survival hinders its widespread use.
  • The molecular mechanisms driving beta cell dysfunction and death are not fully understood, necessitating new therapeutic targets.

Purpose of the Study:

  • To investigate the role of CD47, a cell surface protein, in beta cell function and survival under metabolic stress.
  • To determine if modulating CD47 expression or signaling could offer cytoprotective effects for beta cells.
  • To explore CD47 signaling as a potential therapeutic target for diabetes and islet transplantation.

Main Methods:

  • Utilized primary murine islets, human islets, and MIN6 cells with genetic or pharmacological disruption of CD47 signaling.
  • Induced metabolic stress using hypoxia, hyperglycemia, or thapsigargin to assess beta cell responses.
  • Examined CD47 and thrombospondin-1 (TSP1) expression in human pancreases from donors with and without diabetes.

Main Results:

  • CD47 and TSP1 expression were upregulated by exogenous stressors in beta cells.
  • Limiting CD47 signaling improved markers of beta cell senescence, apoptosis, and endoplasmic reticulum stress.
  • Reduced CD47 signaling maintained insulin secretory function and enhanced markers of self-renewal and autophagy.

Conclusions:

  • CD47 plays a critical role in regulating islet dysfunction and beta cell responses to stress.
  • Upregulated CD47 signaling is associated with beta cell damage in diabetes and impaired islet transplant function.
  • Inhibiting CD47 activation represents a potential therapeutic strategy to improve islet function in diabetes.