Effects of thyroid hormones on cartilage sulphation in sex-linked dwarf chickens

1989 ◽  
Vol 121 (1) ◽  
pp. 107-111 ◽  
Author(s):  
S. Hoshino ◽  
M. Wakita ◽  
Y. Kobayashi ◽  
T. Kakegawa ◽  
M. Suzuki
Keyword(s):  
Growth Rate ◽  
Growth Factor ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Chick Embryos ◽  
Chicken Serum ◽  
Factor I ◽  
Dwarf Chicken

Abstract. The present investigation was undertaken to see if exogenous thyroid hormone could stimulate cartilage sulphation in vivo and in vitro in sex-linked dwarf chickens. L-thyroxine or L-3,5,3'-triiodothyronine injection for 7 consecutive days stimulated in vivo 35SO2−4 incorporation into trachea cartilages of the dwarf chicken. Both thyroid hormones added to the incubation medium with or without 2.5% dwarf chicken serum also stimulated in vitro 35SO2−4 incorporation into pelvic rudiment from 11-day chick embryos. These data demonstrate that thyroid hormones, like insulin-like growth factor I, might be responsible for the reduced growth rate of dwarf chickens.

scholarly journals Endogenous thyroid hormones modulate pituitary somatotroph differentiation during chicken embryonic development

2004 ◽  
Vol 180 (1) ◽  
pp. 45-53 ◽  
Author(s):  
L Liu ◽  
TE Porter
Keyword(s):  
Thyroid Hormone ◽  
Embryonic Development ◽  
Thyroid Hormones ◽  
Synthesis Inhibitor ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis ◽  
Growth Hormone Cell ◽  
Thyroid Hormone Levels

Growth hormone cell differentiation normally occurs between day 14 and day 16 of chicken embryonic development. We reported previously that corticosterone (CORT) could induce somatotroph differentiation in vitro and in vivo and that thyroid hormones could act in combination with CORT to further augment the abundance of somatotrophs in vitro. The objective of the present study was to test our hypothesis that endogenous thyroid hormones regulate the abundance of somatotrophs during chicken embryonic development. Plasma samples were collected on embryonic day (e) 9-14. We found that plasma CORT and thyroid hormone levels increased progressively in mid-embryogenesis to e 13 or e 14, immediately before normal somatotroph differentiation. Administration of thyroxine (T4) and triiodothyronine (T3) into the albumen of fertile eggs on e 11 increased somatotroph proportions prematurely on e 13 in the developing chick embryos in vivo. Furthermore, administration of methimazole, the thyroid hormone synthesis inhibitor, on e 9 inhibited somatotroph differentiation in vivo, as assessed on e 14; this suppression was completely reversed by T3 replacement on e 11. Since we reported that T3 alone was ineffective in vitro, we interpret these findings to indicate that the effects of treatments in vivo were due to interactions with endogenous glucocorticoids. These results indicate that treatment with exogenous thyroid hormones can modulate somatotroph abundance and that endogenous thyroid hormone synthesis likely contributes to normal somatotroph differentiation.

scholarly journals Selective labelling and inactivation of creatine kinase isoenzymes by the thyroid hormone derivative N-bromoacetyl-3,3′,5-tri-iodo-l-thyronine

1993 ◽  
Vol 291 (2) ◽  
pp. 463-472 ◽  
Author(s):  
M Wyss ◽  
T Wallimann ◽  
J Köhrle
Keyword(s):  
Creatine Kinase ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Rat Heart ◽  
Covalent Modification ◽  
Regulation Of Transcription ◽  
Selective Labelling ◽  
Mitochondrial Fractions

Besides their well-known regulation of transcription by binding to nuclear receptors, thyroid hormones have been suggested to have direct effects on mitochondria. In a previous study, incubation of rat heart mitochondria with 125I-labelled N-bromoacetyl-3,3′,5-tri-iodo-L-thyronine (BrAcT3), a thyroid hormone derivative with an alkylating side chain, resulted in the selective labelling of a protein doublet around M(r) 45,000 on SDS/polyacrylamide gels [Rasmussen, Köhrle, Rokos and Hesch (1989) FEBS Lett. 255, 385-390]. Now, this protein doublet has been identified as mitochondrial creatine kinase (Mi-CK). Immunoblotting experiments with the cytoplasmic and mitochondrial fractions of rat heart, brain and liver, as well as inactivation studies with the purified chicken CK isoenzymes have further demonstrated that all four CK isoenzymes (Mia-, Mib-, M- and B-CK) are indeed selectively labelled by BrAcT3. However, in contrast with their bromoalkyl derivatives, thyroid hormones themselves did not compete for CK labelling, suggesting that not the thyroid hormone moiety but rather the bromoacetyl-driven alkylation of the highly reactive ‘essential’ thiol group of CK accounts for this selective labelling. Therefore the assumption that CK isoenzymes are thyroid-hormone-binding proteins has to be dismissed. Instead, bromoacetyl-based reagents may allow a very specific covalent modification and inactivation of CK isoenzymes in vitro and in vivo.

Influence of vasoactive intestinal peptide (VIP), atrial natriuretic peptide (ANP) and insulin-like growth factor-I (IGF-I) on in vitro maturation of prepubertal and adult sheep oocytes

Zygote ◽  
1996 ◽  
Vol 4 (04) ◽  
pp. 343-348 ◽  
Author(s):  
S. Ledda ◽  
L. Bogliolo ◽  
G. Leoni ◽  
P. Calvia ◽  
S. Naitana
Keyword(s):  
Growth Factor ◽  
Atrial Natriuretic Peptide ◽  
Oocyte Maturation ◽  
In Vitro Maturation ◽  
Optimal Conditions ◽  
Factor I ◽  
Igf I

Much effort has been focused on establishing optimal conditions for obtainingin vitromaturation of oocytes from different species with results comparable to those achieved afterin vivodevelopment (reviewed by Brackett, 1992). However, even though extraordinary progress has been made, thein vitrotechnology for oocyte maturation lags far behind thatin vivoand improvements are needed to increase the quantity and quality of the embryos produced from these matured oocytes.

Parathyroid hormone potentiates the effect of insulin-like growth factor-I on bone formation

1989 ◽  
Vol 121 (3) ◽  
pp. 435-442 ◽  
Author(s):  
E. Martin Spencer ◽  
Erwin C. C. Si ◽  
Chung C. Liu ◽  
Guy A. Howard
Keyword(s):  
Parathyroid Hormone ◽  
Growth Factor ◽  
Bone Formation ◽  
Trabecular Bone ◽  
Thymidine Incorporation ◽  
Bone Apposition ◽  
Factor I ◽  
Igf I

Abstract. Insulin-like growth factor-I and parathyroid hormone are both known regulators of bone formation. In this study, human recombinant IGF-I and bovine PTH (1–34) and their combination were studied for their effects in vitro on the proliferation of embryonic chick osteoblast-like cells (osteoblasts) and in vivo on bone formation in normal rats. Osteoblasts from 17-day-old chick embryos were cultured in serum-free BGJb medium containing 0.1% bovine albumin. After 2 days, IGF-I and/or PTH were added. Twenty-four hours later [3H]thymidine incorporation into trichloroacetic acid precipitable material was quantified as an index of cell proliferation. This has previously been shown to reflect actual cell division. IGF-I at doses ranging from 0.85 to 13.6 nmol/l caused a dose-dependent increase in [3H]thymidine incorporation into osteoblasts. PTH alone (10 to 1000 pmol/l) had no significant effect. However, when combined with IGF-I, PTH potentiated the mitogenic effect of IGF-I and achieved statistical significance at 30 and 100 pmol/l (p <0.05). This potentiation was also studied in vivo. The right hindlimbs of rats weighing 150 g were infused intra-arterially by an osmotic minipump with graded doses of IGF-I (0.1 to 0.4 nmol/day) and/or PTH (0.27 nmol/day) for 7 days. The rate of trabecular bone apposition (formation) was measured by double tetracycline labelling and compared with the contralateral uninfused limb which acted as the control. Histomorphometric data revaled that neither IGF-I nor PTH alone had a significant effect on trabecular bone apposition rate compared with control limbs. The co-infusion of IGF-I (0.4 nmol/day) and PTH (0.27 nmol/day) resulted in a marked increase in trabecular bone apposition rate. The results of 2 studies were significant at p < 0.01. These data suggest that PTH potentiates the effect of IGF-I on bone formation both in vivo and in vitro.

scholarly journals Viral expression of insulin-like growth factor I E-peptides increases skeletal muscle mass but at the expense of strength

2014 ◽  
Vol 306 (8) ◽  
pp. E965-E974 ◽  
Author(s):  
Becky K. Brisson ◽  
Janelle Spinazzola ◽  
SooHyun Park ◽  
Elisabeth R. Barton
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Muscle Mass ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Insulin-like growth factor I (IGF-I) is a protein that regulates and promotes growth in skeletal muscle. The IGF-I precursor polypeptide contains a COOH-terminal extension called the E-peptide. Alternative splicing in the rodent produces two isoforms, IA and IB, where the mature IGF-I in both isoforms is identical yet the E-peptides, EA and EB, share less than 50% homology. Recent in vitro studies show that the E-peptides can enhance IGF-I signaling, leading to increased myoblast cell proliferation and migration. To determine the significance of these actions in vivo and to evaluate if they are physiologically beneficial, EA and EB were expressed in murine skeletal muscle via viral vectors. The viral constructs ensured production of E-peptides without the influence of additional IGF-I through an inactivating mutation in mature IGF-I. E-peptide expression altered ERK1/2 and Akt phosphorylation and increased satellite cell proliferation. EB expression resulted in significant muscle hypertrophy that was IGF-I receptor dependent. However, the increased mass was associated with a loss of muscle strength. EA and EB have similar effects in skeletal muscle signaling and on satellite cells, but EB is more potent at increasing muscle mass. Although sustained EB expression may drive hypertrophy, there are significant physiological consequences for muscle.

Growth and serum thyroid hormone and insulin-like growth factor I (IGF-I) responses to natural passive immunization against somatostatin in the lamb

1993 ◽  
Vol 73 (3) ◽  
pp. 509-516 ◽  
Author(s):  
A. G. Van Kessel ◽  
R. S. Korchinski ◽  
B. Laarveld
Keyword(s):  
Growth Rate ◽  
Growth Factor ◽  
Thyroid Hormone ◽  
Serum Insulin ◽  
Passive Immunization ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Ad Libitum ◽  
Growth Factor I

The colostral transfer of maternal humoral immunity against somatostatin (SRIF) was examined as a mechanism of improving growth performance of the lamb. Lambs were the offspring of 15 ewes actively immunized against an SRIF-ovalbumin conjugate (SI; 14 male, 7 female) and of 13 ewes actively immunized against ovalbumin (C; 10 male, 5 female). At 5 d of age, lambs were removed from the ewes and received a 50:50 mixture of whole cow's milk and milk replacer ad libitum. At 46 d of age lambs were weaned and provided with an 18% crude protein pelleted grower ration ad libitum. Lamb weight was recorded and blood samples were obtained at regular intervals from 5 to 46 d of age and at 102 d of age. From 5 to 46 d of age, immunization increased growth rate of male (P < 0.001) but not female lambs. Serum thyroxine (T4) was lower (P < 0.001) in male than in female lambs. Serum triiodothyronine (T3) was higher (P < 0.05) in SI male than in C male lambs. SI female lambs initially demonstrated higher serum T3 levels than C female lambs, but this effect reversed after 19 d of age. Serum insulin-like growth factor I (IGF-I) levels were higher (P = 0.08) in SI than in C lambs without significant influence of sex. From 46 to 102 d of age, somatostatin immunization increased growth rate of male (P = 0.08) but not female lambs. Serum levels of T4, T3 and IGF-I at 102 d of age were not affected by immunization. Passive immunization against SRIF through colostral transfer of immunity may improve growth rate of the lamb via an influence on thyroid hormone metabolism. Key words: Sheep, somatostatin, immunoneutralization. growth, thyroid, IGF-I

scholarly journals Growth factor gene activation and clonal heterogeneity in an autostimulatory myeloid leukemia.

1989 ◽  
Vol 9 (6) ◽  
pp. 2414-2423 ◽  
Author(s):  
K B Leslie ◽  
J W Schrader
Keyword(s):  
Growth Rate ◽  
Growth Factor ◽  
Leukemia Virus ◽  
Class I ◽  
Class Iii ◽  
Gm Csf ◽  
Rna Transcripts ◽  
Cell Densities

Cell lines were isolated from an in vivo-passaged myelomonocytic leukemia, WEHI-274, that arose in a mouse infected with the Abelson leukemia virus-Moloney leukemia virus complex. Clones were isolated in vitro in the presence or absence of a source of a hemopoietic growth factor, interleukin-3 (IL-3), and were divisible into three distinct classes. All three classes were leukemogenic in vivo. In vitro, the class I clone grew slowly at low cell density but responded with an increased growth rate to IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), and autoconditioned medium. Supernatants of these cultures contained a factor with the biological, biochemical, and antigenic properties of IL-3. Class II clones grew better in vitro at low cell densities than did the class I clone and also responded with an increased growth rate to IL-3, GM-CSF, and autoconditional medium but produced GM-CSF rather than IL-3. In contrast, class III clones died in vitro at all cell densities unless exogenous IL-3 or GM-CSF was added. Moreover, they produced no autostimulatory factors. In the class I and class II clones, one allele of the respective IL-3 or GM-CSF gene is rearranged, and in each case, grossly abnormal RNA transcripts of the rearranged gene are present. Neither rearrangements nor abnormal RNA transcripts of the IL-3 or GM-CSF gene were detected in the class III clones. All three classes exhibited a common rearrangement of the c-myb gene, which suggested that all were derived from the one ancestral cell. These experiments demonstrate that two distinct and independent autostimulatory events were involved in the progression of a single disease.

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