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A link between endoplasmic reticulum stress-induced β-cell apoptosis and the group VIA Ca2+-independent phospholipase A2 (iPLA2β).

Publication ,  Journal Article
Lei, X; Zhang, S; Emani, B; Barbour, SE; Ramanadham, S
Published in: Diabetes Obes Metab
October 2010

Endoplasmic reticulum (ER) stress is becoming recognized as an important contributing factor in various diseases, including diabetes mellitus. Prolonged ER stress can cause β-cell apoptosis; however, the underlying mechanism(s) that contribute to this process are not well understood. Early reports suggested that arachidonic acid metabolites and a Ca(2+)-independent phospholipase A(2) (iPLA(2)) activity play a role in β-cell apoptosis. The PLA(2) family of enzymes catalyse the hydrolysis of the sn-2 substituent (i.e. arachidonic acid) of membrane phospholipids. In light of our findings that the pancreatic islet β-cells are enriched in arachidonate-containing phospholipids and express the group VIA iPLA(2)β, we considered the possibility that iPLA(2)β participates in ER stress-induced β-cell apoptosis. Our work revealed a novel mechanism, involving ceramide generation and triggering of mitochondrial abnormalities, by which iPLA(2)β participates in the β-cell apoptosis process. Here, we review our evidence linking ER stress, β-cell apoptosis and iPLA(2)β. Continued studies in this area will increase our understanding of the contribution of iPLA(2)β to the evolution of diabetes mellitus and will further our knowledge of factors that influence β-cell health in diabetes mellitus and identify potential targets for future therapeutic interventions to prevent β-cell death.

Duke Scholars

Published In

Diabetes Obes Metab

DOI

EISSN

1463-1326

Publication Date

October 2010

Volume

12 Suppl 2

Issue

0 2

Start / End Page

93 / 98

Location

England

Related Subject Headings

  • Stress, Physiological
  • Mitochondria
  • Insulin-Secreting Cells
  • Humans
  • Group VI Phospholipases A2
  • Endoplasmic Reticulum
  • Endocrinology & Metabolism
  • Diabetes Mellitus, Type 2
  • Ceramides
  • Calcium
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Lei, X., Zhang, S., Emani, B., Barbour, S. E., & Ramanadham, S. (2010). A link between endoplasmic reticulum stress-induced β-cell apoptosis and the group VIA Ca2+-independent phospholipase A2 (iPLA2β). Diabetes Obes Metab, 12 Suppl 2(0 2), 93–98. https://doi.org/10.1111/j.1463-1326.2010.01270.x
Lei, X., S. Zhang, B. Emani, S. E. Barbour, and S. Ramanadham. “A link between endoplasmic reticulum stress-induced β-cell apoptosis and the group VIA Ca2+-independent phospholipase A2 (iPLA2β).Diabetes Obes Metab 12 Suppl 2, no. 0 2 (October 2010): 93–98. https://doi.org/10.1111/j.1463-1326.2010.01270.x.
Lei X, Zhang S, Emani B, Barbour SE, Ramanadham S. A link between endoplasmic reticulum stress-induced β-cell apoptosis and the group VIA Ca2+-independent phospholipase A2 (iPLA2β). Diabetes Obes Metab. 2010 Oct;12 Suppl 2(0 2):93–8.
Lei, X., et al. “A link between endoplasmic reticulum stress-induced β-cell apoptosis and the group VIA Ca2+-independent phospholipase A2 (iPLA2β).Diabetes Obes Metab, vol. 12 Suppl 2, no. 0 2, Oct. 2010, pp. 93–98. Pubmed, doi:10.1111/j.1463-1326.2010.01270.x.
Lei X, Zhang S, Emani B, Barbour SE, Ramanadham S. A link between endoplasmic reticulum stress-induced β-cell apoptosis and the group VIA Ca2+-independent phospholipase A2 (iPLA2β). Diabetes Obes Metab. 2010 Oct;12 Suppl 2(0 2):93–98.
Journal cover image

Published In

Diabetes Obes Metab

DOI

EISSN

1463-1326

Publication Date

October 2010

Volume

12 Suppl 2

Issue

0 2

Start / End Page

93 / 98

Location

England

Related Subject Headings

  • Stress, Physiological
  • Mitochondria
  • Insulin-Secreting Cells
  • Humans
  • Group VI Phospholipases A2
  • Endoplasmic Reticulum
  • Endocrinology & Metabolism
  • Diabetes Mellitus, Type 2
  • Ceramides
  • Calcium