Abstract
Fas is an apoptosis-inducing surface receptor involved in controlling tissue homeostasis and function at multiple sites. Here we show that β cells from the pancreata of newly diagnosed insulin-dependent diabetes mellitus (IDDM) patients express Fas and show extensive apoptosis among those cells located in proximity to Fas ligand-expressing T lymphocytes infiltrating the IDDM islets. Normal human pancreatic β cells that do not constitutively express Fas, become strongly Fas positive after interleuken (IL)-β exposure, and are then susceptible to Fas-mediated apoptosis. N(G)-monomethyl-L- arginine, an inhibitor of nitric oxide (NO) synthase, prevents IL-β-induced Fas expression, whereas the NO donors sodium nitroprusside and nitric oxide releasing compound (NOC)-18, induce functional Fas expression in normal pancreatic β cells. These findings suggest that NO-mediated upregulation of Fas contributes to pancreatic β cell damage in IDDM.
| Original language | English |
|---|---|
| Pages (from-to) | 1193-1200 |
| Number of pages | 8 |
| Journal | Journal of Experimental Medicine |
| Volume | 186 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - Oct 20 1997 |
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ASJC Scopus subject areas
- Immunology
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Nitric oxide primes pancreatic β cells for Fas-mediated destruction in insulin-dependent diabetes mellitus. / Stassi, Giorgio; De Maria, Ruggero; Trucco, Giuliana; Rudert, William; Testi, Roberto; Galluzzo, Aldo; Giordano, Carla; Trucco, Massimo.
In: Journal of Experimental Medicine, Vol. 186, No. 8, 20.10.1997, p. 1193-1200.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Nitric oxide primes pancreatic β cells for Fas-mediated destruction in insulin-dependent diabetes mellitus
AU - Stassi, Giorgio
AU - De Maria, Ruggero
AU - Trucco, Giuliana
AU - Rudert, William
AU - Testi, Roberto
AU - Galluzzo, Aldo
AU - Giordano, Carla
AU - Trucco, Massimo
PY - 1997/10/20
Y1 - 1997/10/20
N2 - Fas is an apoptosis-inducing surface receptor involved in controlling tissue homeostasis and function at multiple sites. Here we show that β cells from the pancreata of newly diagnosed insulin-dependent diabetes mellitus (IDDM) patients express Fas and show extensive apoptosis among those cells located in proximity to Fas ligand-expressing T lymphocytes infiltrating the IDDM islets. Normal human pancreatic β cells that do not constitutively express Fas, become strongly Fas positive after interleuken (IL)-β exposure, and are then susceptible to Fas-mediated apoptosis. N(G)-monomethyl-L- arginine, an inhibitor of nitric oxide (NO) synthase, prevents IL-β-induced Fas expression, whereas the NO donors sodium nitroprusside and nitric oxide releasing compound (NOC)-18, induce functional Fas expression in normal pancreatic β cells. These findings suggest that NO-mediated upregulation of Fas contributes to pancreatic β cell damage in IDDM.
AB - Fas is an apoptosis-inducing surface receptor involved in controlling tissue homeostasis and function at multiple sites. Here we show that β cells from the pancreata of newly diagnosed insulin-dependent diabetes mellitus (IDDM) patients express Fas and show extensive apoptosis among those cells located in proximity to Fas ligand-expressing T lymphocytes infiltrating the IDDM islets. Normal human pancreatic β cells that do not constitutively express Fas, become strongly Fas positive after interleuken (IL)-β exposure, and are then susceptible to Fas-mediated apoptosis. N(G)-monomethyl-L- arginine, an inhibitor of nitric oxide (NO) synthase, prevents IL-β-induced Fas expression, whereas the NO donors sodium nitroprusside and nitric oxide releasing compound (NOC)-18, induce functional Fas expression in normal pancreatic β cells. These findings suggest that NO-mediated upregulation of Fas contributes to pancreatic β cell damage in IDDM.
UR - http://www.scopus.com/inward/record.url?scp=0030731917&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030731917&partnerID=8YFLogxK
U2 - 10.1084/jem.186.8.1193
DO - 10.1084/jem.186.8.1193
M3 - Article
C2 - 9334358
AN - SCOPUS:0030731917
VL - 186
SP - 1193
EP - 1200
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
SN - 0022-1007
IS - 8
ER -