| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
in INS-1 insulinoma cells
1 Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029; and 2 Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Accumulating evidence
suggests that the cytosolic calcium-independent phospholipase
A2 (iPLA2
) manifests a signaling role in
insulin-secreting (INS-1) -cells. Earlier, we reported that insulin-secretory responses to cAMP-elevating agents are amplified in
iPLA2-overexpressing INS-1 cells (Ma Z, Ramanadham S,
Bohrer A, Wohltmann M, Zhang S, and Turk J. J Biol Chem
276: 13198-13208, 2001). Here, immunofluorescence, immunoaffinity,
and enzymatic activity analyses are used to examine distribution of
iPLA2 in stimulated INS-1 cells in greater detail.
Overexpression of iPLA2 in INS-1 cells leads to
increased accumulation of iPLA2 in the nuclear fraction.
Increasing glucose concentrations alone results in modest increases in
insulin secretion, relative to parental cells, and in nuclear
accumulation of the iPLA2 protein. In contrast, cAMP-elevating agents induce robust increases in insulin secretion and
in time-dependent nuclear accumulation of iPLA2
fluorescence, which is reflected by increases in nuclear
iPLA2 protein content and specific enzymatic activity.
The stimulated effects are significantly attenuated in the presence of
cell-permeable inhibitors of protein phosphorylation and glycosylation.
These findings suggest that conditions that amplify insulin secretion
promote translocation of -cell iPLA2 to the nuclei,
where it may serve a crucial signaling role.
immunofluorescence; immunoaffinity; enzymatic activity; insulin secretion; nuclear localization
This article has been cited by other articles:
|
|
 |
|
  E. K. Hoffmann, I. H. Lambert, and S. F. Pedersen Physiology of Cell Volume Regulation in Vertebrates Physiol Rev, January 1, 2009; 89(1): 193 - 277. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Bao, D. A. Jacobson, M. Wohltmann, A. Bohrer, W. Jin, L. H. Philipson, and J. Turk Glucose homeostasis, insulin secretion, and islet phospholipids in mice that overexpress iPLA2{beta} in pancreatic {beta}-cells and in iPLA2{beta}-null mice Am J Physiol Endocrinol Metab, February 1, 2008; 294(2): E217 - E229. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. H. Zhang, C. Zhao, and Z. A. Ma The increase of cell-membranous phosphatidylcholines containing polyunsaturated fatty acid residues induces phosphorylation of p53 through activation of ATR J. Cell Sci., December 1, 2007; 120(23): 4134 - 4143. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Bao, C. Jin, S. Zhang, J. Turk, Z. Ma, and S. Ramanadham {beta}-Cell Calcium-Independent Group VIA Phospholipase A2 (iPLA2{beta}): Tracking iPLA2{beta} Movements in Response to Stimulation With Insulin Secretagogues in INS-1 Cells Diabetes, February 1, 2004; 53(90001): S186 - 189. [Abstract] [Full Text]
|
|
|
|
 |
|
 M. A. Balboa and J. Balsinde Involvement of Calcium-independent Phospholipase A2 in Hydrogen Peroxide-induced Accumulation of Free Fatty Acids in Human U937 Cells J. Biol. Chem., October 18, 2002; 277(43): 40384 - 40389. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
