Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/76705
Title: Regulation of expression of Suppressors of Cytokine Signalling (SOCS) genes in hypothyroid male rats by Growth hormone, Thyroid Hormones and Estradiol
Authors: Santana-Farre, Ruyman
Flores Morales, Amilcar 
Alvarez Valtuena, Natalia
Cabrera-Galvan, Juan J. 
Novoa Mogollón, Francisco 
Norstedt, Gunnar
Fernandez-Perez, Leandro 
UNESCO Clasification: 32 Ciencias médicas
3209 Farmacología
Keywords: Cytokine signalling (SOCS)
Thyroid hormone
Estradiol
Issue Date: 2008
Journal: FASEB Journal 
Abstract: SOCS proteins act as negative regulators of GH signalling. Recently, E2 was demonstrated to induce SOCS‐2 synthesis and inhibit GH signalling in liver and kidney cells. To evaluate the role of E2 on GH‐regulated SOCS in vivo, this work used orchidectomized‐hypothyroid (TX‐OX) male rats to minimize the influence of internal hormones on treatment. OX‐TX rats were treated 3 weeks with vehicle or E2 before hormonal replacement with GH, T3, or T3 plus GH during 7 days. We analyzed body growth, serum lipids and steady‐state levels of SOCS‐2, ‐3, and CIS mRNA expression in liver in relation to cited hormones. Hypothyroidism resulted in an over 2‐fold increase in serum cholesterol (Cho) levels and 2‐fold reduction in serum triglyceride (Tg) levels. T3 treatment decreased Cho and GH treatment resulted in 3‐4‐fold reduction in serum FFAs levels. Hypothyroidism reduced the levels of SOCS‐2 and CIS mRNA and induced SOCS‐3. E2 reversed the effects of hypothyroidism on SOCS2 and CIS but not on SOCS3 mRNA levels. Unlike T3, the effects of hypothyroidism on SOCS2 and CIS mRNA levels were reversed by GH. T3 reversed the effects of hypothyroidism on SOCS3. Whereas E2 enhanced the effect of T3 on SOCS2 and CIS, T3 effect on SOCS3 was antagonized. These results indicate that SOCS are differently regulated in vivo and an important physiological role for E2, GH and T3 in maintaining levels of SOCS in male liver.
URI: http://hdl.handle.net/10553/76705
ISSN: 0892-6638
DOI: 10.1096/fasebj.22.1_supplement.1133.9
Source: Faseb Journal [ISSN 0892-6638], v. 22, (Abril 2008)
Appears in Collections:Actas de congresos
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