scholarly journals Correction for McMullen et al., “Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor–Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy”

2021 ◽  
Vol 41 (2) ◽  
Author(s):  
Julie R. McMullen ◽  
Tetsuo Shioi ◽  
Li Zhang ◽  
Oleg Tarnavski ◽  
Megan C. Sherwood ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cardiac Hypertrophy ◽  
Insulin Like Growth Factor ◽  
Phosphoinositide 3 Kinase

scholarly journals Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy

2004 ◽  
Vol 24 (14) ◽  
pp. 6231-6240 ◽  
Author(s):  
Julie R. McMullen ◽  
Tetsuo Shioi ◽  
Li Zhang ◽  
Oleg Tarnavski ◽  
Megan C. Sherwood ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transgenic Mice ◽  
Cardiac Hypertrophy ◽  
Physiological Stress ◽  
Pi3k Pathway ◽  
Insulin Like Growth Factor ◽  
Cardiac Phenotype ◽  
Heart Size ◽  
Phosphoinositide 3 Kinase ◽  
Igf1 Receptor

ABSTRACT Ribosomal S6 kinases (S6Ks) have been depicted as critical effectors downstream of growth factor pathways, which play an important role in the regulation of protein synthesis by phosphorylating the ribosomal protein, S6. The goal of this study was to determine whether S6Ks regulate heart size, are critical for the induction of cardiac hypertrophy in response to a pathological or physiological stimulus, and whether S6Ks are critical downstream effectors of the insulin-like growth factor 1 (IGF1)-phosphoinositide 3-kinase (PI3K) pathway. For this purpose, we generated and characterized cardiac-specific S6K1 and S6K2 transgenic mice and subjected S6K1−/−, S6K2−/−, and S6K1−/− S6K2−/− mice to a pathological stress (aortic banding) or a physiological stress (exercise training). To determine the genetic relationship between S6Ks and the IGF1-PI3K pathway, S6K transgenic and knockout mice were crossed with cardiac-specific transgenic mice overexpressing the IGF1 receptor (IGF1R) or PI3K mutants. Here we show that overexpression of S6K1 induced a modest degree of hypertrophy, whereas overexpression of S6K2 resulted in no obvious cardiac phenotype. Unexpectedly, deletion of S6K1 and S6K2 had no impact on the development of pathological, physiological, or IGF1R-PI3K-induced cardiac hypertrophy. These studies suggest that S6Ks alone are not essential for the development of cardiac hypertrophy.

scholarly journals Phosphatidylinositol-3,4,5-Trisphosphate Is Required for Insulin-Like Growth Factor 1-Mediated Survival of 3T3-L1 Preadipocytes**This work was supported by a grant (to A.S.) from the Medical Research Council of Canada.

Endocrinology ◽  
2001 ◽  
Vol 142 (1) ◽  
pp. 205-212 ◽  
Author(s):  
AnneMarie Gagnon ◽  
Patti Dods ◽  
Nicolas Roustan-Delatour ◽  
Ching-Shih Chen ◽  
Alexander Sorisky
Keyword(s):  
Cell Death ◽  
Growth Factor ◽  
Mammalian Target Of Rapamycin ◽  
Inhibitory Effect ◽  
Tunel Staining ◽  
Insulin Like Growth Factor ◽  
Tissue Mass ◽  
Akt Phosphorylation ◽  
Dependent Cell ◽  
Phosphoinositide 3 Kinase

Abstract Adipocyte number, a determinant of adipose tissue mass, reflects the balance between the rates of proliferation/differentiation vs. apoptosis of preadipocytes. The percentage of 3T3-L1 preadipocytes undergoing cell death following serum deprivation was reduced by 10 nm insulin-like growth factor (IGF)-1 (from 50.0 ± 0.7% for control starved cells to 27.5 ± 3.1%). TUNEL staining confirmed the apoptotic nature of the cell death. The protective effect of IGF-1 was blocked by phosphoinositide 3-kinase (PI3K) inhibitors, wortmannin, and LY294002, but was unaffected by rapamycin, PD98059, or SB203580, which inhibit mammalian target of rapamycin (mTOR), ERK kinase (MEK1), and p38 MAPK respectively. Exogenous PI(3,4,5)P3 (10 μm), the principal product of IGF-1-stimulated PI3K in 3T3-L1 preadipocytes, had a modest survival effect on its own, reducing cell death from 47.9± 3.4% to 35.6 ± 3.5%. When added to the combination of IGF-1 and LY294002, PI(3,4,5)P3 reversed most of the inhibitory effect of LY294002 on IGF-1-dependent cell survival, protein kinase B/Akt phosphorylation, and caspase-3 activity. Taken together, these results implicate PI(3,4,5)P3 as a necessary signal for the anti-apoptotic action of IGF-1 on 3T3-L1 preadipocytes.

scholarly journals Insulin-Like Growth Factor I Receptor Signaling Is Required for Exercise-Induced Cardiac Hypertrophy

2008 ◽  
Vol 22 (11) ◽  
pp. 2531-2543 ◽  
Author(s):  
Jaetaek Kim ◽  
Adam R. Wende ◽  
Sandra Sena ◽  
Heather A. Theobald ◽  
Jamie Soto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cardiac Hypertrophy ◽  
Insulin Like Growth Factor ◽  
Receptor Signaling ◽  
Factor I ◽  
Growth Factor I ◽  
Exercise Induced

scholarly journals Transcription Factor GATA4 Is Activated but Not Required for Insulin-like Growth Factor 1 (IGF1)-induced Cardiac Hypertrophy

2012 ◽  
Vol 287 (13) ◽  
pp. 9827-9834 ◽  
Author(s):  
Egbert Bisping ◽  
Sadakatsu Ikeda ◽  
Miriam Sedej ◽  
Paulina Wakula ◽  
Julie R. McMullen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Growth Factor ◽  
Cardiac Hypertrophy ◽  
Insulin Like Growth Factor

Overexpression of Insulin-Like Growth Factor-I in Hearts of Rats with Isoproterenol-Induced Cardiac Hypertrophy

1999 ◽  
Vol 34 (5) ◽  
pp. 635-644 ◽  
Author(s):  
Jun Suzuki ◽  
Isao Ohno ◽  
Jun Nawata ◽  
Shoko Miura ◽  
Jun Ikeda ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cardiac Hypertrophy ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

scholarly journals Insulin and Insulin-like growth factor-1 can activate the phosphoinositide-3-kinase /Akt/FoxO1 pathway in T cells in vitro

2017 ◽  
Vol 9 (1) ◽  
pp. e1356518 ◽  
Author(s):  
Yasaman Mirdamadi ◽  
Ursula Bommhardt ◽  
Alexander Goihl ◽  
Karina Guttek ◽  
Christos C. Zouboulis ◽  
...  
Keyword(s):  
T Cells ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Phosphoinositide 3 Kinase

scholarly journals The Insulin-like Growth Factor 1 Receptor Induces Physiological Heart Growth via the Phosphoinositide 3-Kinase(p110α) Pathway

2003 ◽  
Vol 279 (6) ◽  
pp. 4782-4793 ◽  
Author(s):  
Julie R. McMullen ◽  
Tetsuo Shioi ◽  
Weei-Yuarn Huang ◽  
Li Zhang ◽  
Oleg Tarnavski ◽  
...  
Keyword(s):  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Phosphoinositide 3 Kinase
Sign in / Sign up

Export Citation Format

Share Document