scholarly journals Improved mitochondrial stress response in long‐lived Snell dwarf mice

Aging Cell ◽  
2019 ◽  
Vol 18 (6) ◽  
Author(s):  
Ulas Ozkurede ◽  
Richard A. Miller
Keyword(s):  
Stress Response ◽  
Mitochondrial Stress ◽  
Snell Dwarf ◽  
Dwarf Mice

scholarly journals FAST Is a Survival Protein That Senses Mitochondrial Stress and Modulates TIA-1-Regulated Changes in Protein Expression

2004 ◽  
Vol 24 (24) ◽  
pp. 10718-10732 ◽  
Author(s):  
Wei Li ◽  
Maria Simarro ◽  
Nancy Kedersha ◽  
Paul Anderson
Keyword(s):  
Protein Synthesis ◽  
Rna Interference ◽  
Stress Response ◽  
Mitochondrial Membrane ◽  
Binding Domain ◽  
Outer Mitochondrial Membrane ◽  
Mitochondrial Stress ◽  
Inhibitors Of Apoptosis ◽  
Reporter Proteins ◽  
Induced Apoptosis

ABSTRACT The Fas-activated serine/threonine phosphoprotein (FAST) is tethered to the outer mitochondrial membrane, where it interacts with BCL-XL (17). Here we show that RNA interference-mediated knockdown of endogenous FAST results in apoptosis, whereas overexpressed recombinant FAST inhibits Fas- and UV-induced apoptosis, indicating that FAST is a survival protein. The antiapoptotic effects of FAST are regulated by interactions with the translational silencer TIA-1: a FAST mutant lacking its TIA-1-binding domain does not inhibit apoptosis, and overexpressed recombinant TIA-1 inhibits the antiapoptotic effects of FAST. Because the antiapoptotic effects of FAST require ongoing protein synthesis, we hypothesized that FAST might function by preventing TIA-1-mediated silencing of mRNAs encoding inhibitors of apoptosis. Consistent with this hypothesis, FAST promotes the expression of cotransfected reporter proteins, a process that requires its TIA-1-binding domain and is inhibited by overexpressed recombinant TIA-1. More compellingly, recombinant FAST increases the expression of endogenous cIAP-1 and XIAP, but not GAPDH, in transfected HeLa cells. Because FAST is released from mitochondria in cells undergoing Fas- or UV-induced apoptosis, we propose that FAST serves as a sensor of mitochondrial stress that modulates a TIA-1-regulated posttranscriptional stress response program.

scholarly journals Mitochondrial Stress Response and Cancer

2020 ◽  
Vol 6 (8) ◽  
pp. 688-701 ◽  
Author(s):  
Jordan O’Malley ◽  
Rahul Kumar ◽  
Joseph Inigo ◽  
Nagendra Yadava ◽  
Dhyan Chandra
Keyword(s):  
Stress Response ◽  
Mitochondrial Stress

scholarly journals Dexamethasone Differentially Inhibits Thyroxine- or Growth Hormone-Induced Body and Organ Growth of Snell Dwarf Mice

Endocrinology ◽  
2003 ◽  
Vol 144 (6) ◽  
pp. 2553-2558 ◽  
Author(s):  
Raoul P. A. Rooman ◽  
Gilliam Kuijpers ◽  
Ria Gresnigt ◽  
Ruud Bloemen ◽  
Johanna G. Koster ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Organ Growth ◽  
Snell Dwarf ◽  
Dwarf Mice

Meiotic nondisjunction in male Snell dwarf mice

1982 ◽  
Vol 73 (5) ◽  
pp. 365-369 ◽  
Author(s):  
Paulette J. J. Wauben-Penris ◽  
Sylvia C. van Buul-Offers
Keyword(s):  
Snell Dwarf ◽  
Meiotic Nondisjunction ◽  
Dwarf Mice

scholarly journals Impaired mitochondrial stress response in cumulus cells is associated with increased apoptosis and accelerated follicular depletion

2018 ◽  
Vol 110 (4) ◽  
pp. e99-e100
Author(s):  
E. Esencan ◽  
Z. Jiang ◽  
T. Wang ◽  
M. Zhang ◽  
M.B. Bener ◽  
...  
Keyword(s):  
Stress Response ◽  
Cumulus Cells ◽  
Mitochondrial Stress

Cellular growth in organs of dwarf mice during treatment with growth hormone, thyroxine and plasma fractions containing somatomedin activity

1982 ◽  
Vol 99 (1) ◽  
pp. 150-160 ◽  
Author(s):  
Sylvia van Buul-Offers ◽  
Jan Leo Van den Brande ◽  
L. Dumoleijn ◽  
M. Feijlbrief ◽  
C. M. Hoogerbrugge ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Human Growth ◽  
Cell Number ◽  
Small Degree ◽  
Cellular Growth ◽  
Nucleic Acid Metabolism ◽  
Plasma Fractions ◽  
Snell Dwarf ◽  
Division Cell ◽  
Dwarf Mice

Abstract. DNA, RNA and protein content of the liver, kidneys and spleen were studied in dwarf mice during treatment with human growth hormone (hGH), thyroxine and plasma fractions containing somatomedin activity (SM-P1 and SM-P4). This investigation has revealed that part of the growth of the liver and all growth of the spleen obtained with the administered preparations, are a consequence of nuclear division. Cell enlargement is not induced in the spleen by either of the preparations used. In the liver a small degree of hypertrophy is obtained with SM-P1. In the kidney both cell number and cell size are stimulated by thyroxine and to a lesser extent by hGH and SM-P1. With regards to the RNA content per cell an increase is obtained with hGH and thyroxine in the liver and in the kidneys also with SM-P1, but not in the spleen. These data demonstrate that semi-purified SM-preparations, like hGH and thyroxine, might be potent stimuli for the restoration of the impaired nucleic acid metabolism in these organs of the Snell dwarf mouse.

Testicular growth and hormonal parameters in the male Snell dwarf mouse

1987 ◽  
Vol 115 (3) ◽  
pp. 399-405 ◽  
Author(s):  
M. T. Hochereau-de Reviers ◽  
M. M. de Reviers ◽  
C. Monet-Kuntz ◽  
C. Perreau ◽  
I. Fontaine ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Normal Values ◽  
Accessory Gland ◽  
Plasma Testosterone ◽  
Cell Multiplication ◽  
Daily Production ◽  
Testicular Growth ◽  
Adult Mice ◽  
Snell Dwarf ◽  
Dwarf Mice

Abstract. Dwarf mice show delayed testicular growth and their adult testis weights are half the normal value. The aims of the present work were firstly, to compare the developmental profiles of plasma gonadotropins and of testicular cell multiplication and differentiation in dwarf vs normal mice and secondly, to determine the effect of hMG supplementation on dwarf mice. In the dwarf mice no pubertal rise in plasma FSH was observed, and the adult values remained very low when compared with those of normal mice; plasma LH decreased after 40 days of age and remained equal to half the normal values. In adults, testicular testosterone content was greatly increased in dwarf mice compared with normal mice, whereas plasma testosterone and accessory gland weights were reduced. At 24 days of age, the total numbers per testis of Leydig and Sertoli cells were reduced in dwarf vs normal mice, whereas in adult mice their differentiation, but not their total numbers, was reduced. This resulted in lower daily production of leptotene primary spermatocytes and of round spermatids in dwarf than in normal mice. hMG supplementation promoted Leydig and Sertoli cell multiplication, but did not produce full differentiation, resulting in increased daily production of round spermatids. In conclusion, in adult dwarf mice a deficiency in plasma gonadotropins prevents full differentiation of Leydig and Sertoli cells without affecting the number of these cells.

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