Suppressor of Cytokine Signaling 3 Is Induced by Angiotensin II in Heart and Isolated Cardiomyocytes, and Participates in Desensitization

Calegari, Vivian C.; Bezerra, Rosângela Maria Neves; Torsoni, Márcio Alberto; Torsoni, Adriana Souza; Franchini, Kleber G.; Saad, Mário José Abdalla; Velloso, Lı́cio A.

doi:10.1210/en.2003-0046

Cited by 36 publications

(45 citation statements)

References 48 publications

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“…Aliquots of the resulting supernatants containing 5.0 mg of total protein were used for immunoprecipitation with antibodies against IR at 4°C overnight followed by SDS-PAGE, transfer to nitrocellulose membranes, and blotting with antiphosphotyrosine or anti-IR antibodies. In direct immunoblot experiments, 0.2 mg of protein extracts from each tissue was separated by SDS-PAGE, transferred to nitrocellulose membranes, and blotted with anti-IR, antiphospho-Akt, antiphospho-ERK, anti-GLUT4, anti-GLUT-1, anti-PGC-1␣, anti-UCP-3, antiphospho-AMPK, and antiphosphoacetyl-CoA carboxylase antibodies, as described previously (3).…”

Section: Methodsmentioning

confidence: 99%

Cold-induced PGC-1α expression modulates muscle glucose uptake through an insulin receptor/Akt-independent, AMPK-dependent pathway

Oliveira¹,

Ueno²,

Souza³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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Section: Methodsmentioning

confidence: 99%

Cold-induced PGC-1α expression modulates muscle glucose uptake through an insulin receptor/Akt-independent, AMPK-dependent pathway

Oliveira¹,

Ueno²,

Souza³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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“…Both insulin and Ang II are individually able to induce the expression of SOCS proteins in tissues of living animals and in cultivated cell-lines [68][69][70][71][72]. Depending on the tissue or cell line studied, insulin is able to induce the expression of SOCS-2 [69] and/or SOCS-3 [68,73] through the activation of STAT-5b.…”

Section: The Late Events Affected By the Insulin-ang II Cross-talkmentioning

confidence: 99%

“…Moreover, SOCS-3 is also able to bind directly to IRS proteins and drive them to proteosomic degradation through an ubiquitin-dependent mechanism [67]. In turn, Ang II, acting in the heart, in isolated cardiomyocytes and in the hypothalamus, induces the tyrosine phosphorylation of JAK-2 and the recruitment and activation of STAT-5b, which mediates Ang II-induced expression of SOCS-3 [71,72]. In all these experimental systems, the steady-state expression of SOCS-3 is very low.…”

Section: The Late Events Affected By the Insulin-ang II Cross-talkmentioning

confidence: 99%

“…In all these experimental systems, the steady-state expression of SOCS-3 is very low. However, 10 min after Ang II stimulation, both mRNA and protein levels of SOCS-3 start to increase, reaching a peak at 120 min and returning to pre-stimulus levels after 360 min [71,72]. During this time frame, SOCS-3 associates with JAK-2 and STAT-5b and inhibits further stimulation of the pathway.…”

Section: The Late Events Affected By the Insulin-ang II Cross-talkmentioning

confidence: 99%

“…During this time frame, SOCS-3 associates with JAK-2 and STAT-5b and inhibits further stimulation of the pathway. As a consequence of this inhibition, Ang II-dependent c-fos expression in the heart and cardiomyocytes is blunted [71] and hypothalamic Ang II-induced water intake is suppressed [72].…”

Section: The Late Events Affected By the Insulin-ang II Cross-talkmentioning

confidence: 99%

See 2 more Smart Citations

The multi‐faceted cross‐talk between the insulin and angiotensin II signaling systems

Velloso

Folli

Perego

et al. 2006

Diabetes Metabolism Res

103

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SummaryInsulin and angiotensin II are hormones that play pivotal roles in the control of two vital and closely related systems, the metabolic and the circulatory systems, respectively. A failure in the proper action of each of these hormones results, to a variable degree, in the development of two highly prevalent and commonly overlapping diseases -diabetes mellitus and hypertension. In recent years, a series of studies has revealed a tight connection between the signal transduction pathways that mediate insulin and angiotensin II actions in target tissues. This molecular cross-talk occurs at multiple levels and plays an important role in phenomena that range from the action of anti-hypertensive drugs to cardiac hypertrophy and energy acquisition by the heart. At the extracellular level, the angiotensin-converting enzyme controls angiotensin II synthesis but also interferes with insulin signaling through the proper regulation of angiotensin II and through the accumulation of bradykinin. At an early intracellular level, angiotensin II, acting through JAK-2/IRS-1/PI3-kinase, JNK and ERK, may induce the serine phosphorylation and inhibition of key elements of the insulin-signaling pathway. Finally, by inducing the expression of the regulatory protein SOCS-3, angiotensin II may impose a late control on the insulin signal. This review will focus on the main advances obtained in this field and will discuss the implications of this molecular cross-talk in the common clinical association between diabetes mellitus and hypertension.

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Suppressors of cytokine signaling in health and disease

Tan

Rabkin

2005

Pediatr Nephrol

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Cytokines consist of a large family of secreted proteins, including pro-inflammatory agents, growth hormone and erythropoietin, that utilize the Janus kinase (JAK) signal transducer and activator of transcription (STAT) signal transduction pathway to mediate many of their key physiologic and pathologic actions. These actions include cytokine-mediated inflammation, immunoregulation, hematopoiesis and growth. The JAK-STAT pathway is regulated by several processes, among which negative feedback regulation by the suppressors of cytokine signaling (SOCS), members of a family of eight proteins, is particularly important. Each cytokine induces one or more specific SOCS proteins that in turn down-regulate the signal initiated by the cytokine. Through their impact on the cytokine-activated JAK-STAT pathway, the SOCS proteins are involved in many diseases that come to the attention of the pediatric nephrologist. For example, an increase in the expression of SOCS-2 and -3 may be a cause of growth hormone resistance and thus may contribute to the growth retardation that affects children with chronic renal failure. Because of their obvious biologic importance, the SOCS proteins have been the subject of intense research that includes the development of strategies to utilize these proteins to control cytokine-induced JAK/STAT signal transduction for therapeutic purposes.

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Suppressor of Cytokine Signaling 3 Is Induced by Angiotensin II in Heart and Isolated Cardiomyocytes, and Participates in Desensitization

Cited by 36 publications

References 48 publications

Cold-induced PGC-1α expression modulates muscle glucose uptake through an insulin receptor/Akt-independent, AMPK-dependent pathway

Cold-induced PGC-1α expression modulates muscle glucose uptake through an insulin receptor/Akt-independent, AMPK-dependent pathway

The multi‐faceted cross‐talk between the insulin and angiotensin II signaling systems

Suppressors of cytokine signaling in health and disease

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