In:
Journal of Cellular Physiology, Wiley, Vol. 206, No. 2 ( 2006-02), p. 309-321
Abstract:
3,5,3′‐triiodothyronine (T 3 ) is essential for the growth and the regulation of metabolic functions, moreover, the growth‐stimulatory effect of T 3 has largely been demonstrated and the pathways via which T 3 promotes cell growth have been recently investigated. Type 1 diabetes (T1D) is due to the destruction of β‐cells, which occurs even through apoptosis. Aim of our study was to analyze whether T 3 could have an antiapoptotic effect on cultured β‐cells undergoing apoptosis. We have demonstrated that T 3 promotes cell proliferation in islet β‐cell lines (rRINm5F and hCM) provoking an increment in cell number (up to 55%: rRINm5F and 45%: hCM), cell viability, and BrdU incorporation, and regulating the cell cycle‐related molecules (cyc A, D1, E, and p27 kip1 ). T 3 inhibited the apoptotic process induced by streptozocin, S‐Nitroso‐N‐Acetylpenicylamine (SNAP), and H 2 O 2 via regulation of the pro‐ and anti‐apoptotic factors Bcl‐2, Bcl‐X L , Bad, Bax, and Caspase 3. The T 3 protective effect was PI‐3 K‐, but not MAPK‐ or PKA‐mediated, involving pAkt Thr308 . Thus, T 3 could be considered a survival factor protecting islet β‐cells from apoptosis. J. Cell. Physiol. 206: 309–321, 2006. © 2005 Wiley‐Liss, Inc.
Type of Medium:
Online Resource
ISSN:
0021-9541
,
1097-4652
Language:
English
Publisher:
Wiley
Publication Date:
2006
detail.hit.zdb_id:
1478143-8
SSG:
12
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