Faculty Opinions recommendation of Proangiogenesis action of the thyroid hormone analog 3,5-diiodothyropropionic acid (DITPA) is initiated at the cell surface and is integrin mediated.

2006 ◽  
Author(s):  
Juan Bernal
Keyword(s):  
Thyroid Hormone ◽  
Cell Surface ◽  
Hormone Analog

scholarly journals Proangiogenesis Action of the Thyroid Hormone Analog 3,5-Diiodothyropropionic Acid (DITPA) Is Initiated at the Cell Surface and Is Integrin Mediated

Endocrinology ◽  
2006 ◽  
Vol 147 (4) ◽  
pp. 1602-1607 ◽  
Author(s):  
Shaker A. Mousa ◽  
Laura O’Connor ◽  
Faith B. Davis ◽  
Paul J. Davis
Keyword(s):  
Growth Factor ◽  
Thyroid Hormone ◽  
Cell Surface ◽  
Vascular Endothelial Cell ◽  
Three Dimensional ◽  
Integrin Αvβ3 ◽  
Hormone Analog ◽  
Microvascular Endothelial ◽  
Cam Model

We have recently described the proangiogenesis effects of thyroid hormone in the chick chorioallantoic membrane (CAM) model. Generation of new blood vessels from existing vessels was promoted 2- to 3-fold by either T4 or T3 at 10−8–10−7m total hormone concentrations. In the present studies, nanomolar concentrations of 3,5-diiodothyropropionic acid (DITPA), a thyroid hormone analog with inotropic but not chronotropic properties, exhibited potent proangiogenic activity that was comparable to that obtained with T3 and T4 in both the CAM model and in an in vitro three-dimensional human microvascular endothelial sprouting assay. The proangiogenesis effect of DITPA was inhibited by tetraiodothyroacetic acid, a thyroid hormone analog that competes with T4 and T3 for a novel cell surface hormone receptor site on integrin αvβ3. The thyroid hormone analogs DITPA, T4, and T4-agarose, as well as basic fibroblast growth factor (b-FGF) and vascular endothelial cell growth factor, demonstrated comparable proangiogenic effects in the CAM model and in the three-dimensional human microvascular endothelial sprouting model. The proangiogenesis effect of either DITPA or b-FGF was blocked by PD 98059, an inhibitor of the ERK1/2 signal transduction cascade. Additionally, a specific integrin αvβ3 small molecule antagonist, XT199, effectively inhibited the proangiogenesis effect of DITPA and b-FGF. Thus, the proangiogenesis actions of thyroid hormone and its analog DITPA are initiated at the plasma membrane, apparently at integrin αvβ3, and are MAPK dependent.

Pilot Studies on the Use of 3,5-Diiodothyropropionic Acid, a Thyroid Hormone Analog, in the Treatment of Congestive Heart Failure

Cardiology ◽  
2002 ◽  
Vol 97 (4) ◽  
pp. 218-225 ◽  
Author(s):  
Eugene Morkin ◽  
Gregory Pennock ◽  
Peter H. Spooner ◽  
Joseph J. Bahl ◽  
Katherine Underhill Fox ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Thyroid Hormone ◽  
Pilot Studies ◽  
Hormone Analog

DITPA, A Thyroid Hormone Analog, Reduces Infarct Size and Attenuates the Inflammatory Response Following Myocardial Ischemia

2011 ◽  
Vol 171 (2) ◽  
pp. 379-385 ◽  
Author(s):  
Abdelrahman A. Abohashem-Aly ◽  
Xianzhong Meng ◽  
Jilin Li ◽  
Miral R. Sadaria ◽  
Lihua Ao ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Myocardial Ischemia ◽  
Inflammatory Response ◽  
Infarct Size ◽  
Hormone Analog

The thyroid hormone analog DITPA restoresI to in rats after myocardial infarction

2000 ◽  
Vol 278 (4) ◽  
pp. H1105-H1116 ◽  
Author(s):  
Alan D. Wickenden ◽  
Roger Kaprielian ◽  
Xiao-Mang You ◽  
Peter H. Backx
Keyword(s):  
Myocardial Infarction ◽  
Thyroid Hormone ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Monophasic Action Potential ◽  
Mrna Levels ◽  
Hormone Analog ◽  
Life Threatening ◽  
The Right

Previous studies have established that reductions in repolarizing currents occur in heart disease and can contribute to life-threatening arrhythmias in myocardium. In this study, we investigated whether the thyroid hormone analog 3,5-diiodothyropropionic acid (DITPA) could restore repolarizing transient outward K+ current ( I to) density and gene expression in rat myocardium after myocardial infarction (MI). Our findings show that I to density was reduced after MI (14.0 ± 1.0 vs. 10.2 ± 0.9 pA/pF, sham vs. post-MI at +40 mV). mRNA levels of Kv4.2 and Kv4.3genes were decreased but Kv1.4 mRNA levels were increased post-MI. Corresponding changes in Kv4.2 and Kv1.4 protein were also observed. Chronic treatment of post-MI rats with 10 mg/kg DITPA restored I to density (to 15.2 ± 1.1 pA/pF at +40 mV) as well as Kv4.2 and Kv1.4 expression to levels observed in sham-operated controls. Other membrane currents (Na+, L-type Ca2+, sustained, and inward rectifier K+ currents) were unaffected by DITPA treatment. Associated with the changes in I toexpression, action potential durations (current-clamp recordings in isolated single right ventricular myocytes and monophasic action potential recordings from the right free wall in situ) were prolonged after MI and restored with DITPA treatment. Our results demonstrate that DITPA restores I to density in the setting of MI, which may be useful in preventing complications associated with I to downregulation.

Thyroid hormone analog inhibition of hepatic 5′-iodothyrohine deiodinase activity

1988 ◽  
Vol 11 (9) ◽  
pp. 657-661 ◽  
Author(s):  
B. L. Shulkin ◽  
M. B. Bolger ◽  
R. D. Utiger
Keyword(s):  
Thyroid Hormone ◽  
Deiodinase Activity ◽  
Hormone Analog

scholarly journals Acting via a Cell Surface Receptor, Thyroid Hormone Is a Growth Factor for Glioma Cells

2006 ◽  
Vol 66 (14) ◽  
pp. 7270-7275 ◽  
Author(s):  
Faith B. Davis ◽  
Heng-Yuan Tang ◽  
Ai Shih ◽  
Travis Keating ◽  
Lawrence Lansing ◽  
...  
Keyword(s):  
Growth Factor ◽  
Thyroid Hormone ◽  
Cell Surface ◽  
Glioma Cells ◽  
Cell Surface Receptor ◽  
Surface Receptor ◽  
A Cell

Thyroid Hormone Excess Increases Basal and Insulin-stimulated Recruitment of GLUT3 Glucose Transporters on Cell Surface

2005 ◽  
Vol 37 (1) ◽  
pp. 15-20 ◽  
Author(s):  
G. Dimitriadis ◽  
E. Maratou ◽  
M. Alevizaki ◽  
E. Boutati ◽  
K. Psara ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Cell Surface ◽  
Glucose Transporters

Translational implications of nongenomic actions of thyroid hormone initiated at its integrin receptor

2009 ◽  
Vol 297 (6) ◽  
pp. E1238-E1246 ◽  
Author(s):  
Paul J. Davis ◽  
Faith B. Davis ◽  
Hung-Yun Lin ◽  
Shaker A. Mousa ◽  
Min Zhou ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Cell Surface ◽  
Tumor Cell ◽  
Cell Biology ◽  
Thyroid Hormone Receptor ◽  
Integrin Αvβ3 ◽  
Integrin Receptor ◽  
Cell Functions ◽  
Mediated Effects ◽  
Hormone Analogs

A thyroid hormone receptor on integrin αvβ3 that mediates cell surface-initiated nongenomic actions of thyroid hormone on tumor cell proliferation and on angiogenesis has been described. Transduction of the hormone signal into these recently recognized proliferative effects is by extracellular-regulated kinases 1/2 (ERK1/2). Other nongenomic actions of the hormone may be transduced by phosphatidylinositol 3-kinase (PI3K) and are initiated in cytoplasm or at the cell surface. PI3K-mediated effects are important to angiogenesis or other recently appreciated cell functions but apparently not to tumor cell division. For those actions of thyroid hormone [l-thyroxine (T4) and 3,3′-5-triiodo-l-thyronine (T3)] that begin at the integrin receptor, tetraiodothyroacetic acid (tetrac) is an inhibitor of and probe for the participation of the receptor in downstream intracellular events. In addition, tetrac has actions initiated at the integrin receptor that are unrelated to inhibition of the effects of T4 and T3 but do involve gene transcription in tumor cells. Discussed here are the implications of translating these nongenomic mechanisms of thyroid hormone analogs into clinical cancer cell biology, tumor-related angiogenesis, and modulation of angiogenesis that is not related to cancer.

scholarly journals DITPA (3,5-Diiodothyropropionic Acid), a Thyroid Hormone Analog to Treat Heart Failure

Circulation ◽  
2009 ◽  
Vol 119 (24) ◽  
pp. 3093-3100 ◽  
Author(s):  
Steven Goldman ◽  
Madeline McCarren ◽  
Eugene Morkin ◽  
Paul W. Ladenson ◽  
Robert Edson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Thyroid Hormone ◽  
Treat Heart Failure ◽  
Hormone Analog
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