Thyrotropin‐releasing hormone in rat heart: effect of swelling, angiotensin II and renin gene

Bačová, Zuzana; Baqi, L; Beňačka, O.; Payer, Juraj; Križanová, Oľga; Zeman, Michal; Smreková, Lucia; Zórad, Štefan; Štrbák, Vladimír

doi:10.1111/j.1748-1716.2006.01545.x

Cited by 12 publications

(12 citation statements)

References 19 publications

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“…In 1992, a cardiac TRH system was reported, and, since then, many authors have studied the role of local TRH in cardiac physiology (1,9,26). An increase in TRH expression in the ventricle of infarcted rats after an 8-wk injury has been reported, suggesting the participation of the tripeptide in the cardiac damage (11).…”

Section: Discussionmentioning

confidence: 99%

Thyrotropin-releasing hormone overexpression induces structural changes of the left ventricle in the normal rat heart

Schuman

Diaz

Landa³

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Schuman ML, Peres Diaz LS, Landa MS, Toblli JE, Cao G, Alvarez AL, Finkielman S, Pirola CJ, García SI. Thyrotropin-releasing hormone overexpression induces structural changes of the left ventricle in the normal rat heart. Am J Physiol Heart Circ Physiol 307: H1667-H1674, 2014. First published October 3, 2014; doi:10.1152/ajpheart.00494.2014.-Thyrotropin-releasing hormone (TRH) hyperactivity has been observed in the left ventricle of spontaneously hypertensive rats. Its long-term inhibition suppresses the development of hypertrophy, specifically preventing fibrosis. The presence of diverse systemic abnormalities in spontaneously hypertensive rat hearts has raised the question of whether specific TRH overexpression might be capable of inducing structural changes in favor of the hypertrophic phenotype in normal rat hearts. We produced TRH overexpression in normal rats by injecting into their left ventricular wall a plasmid driving expression of the preproTRH gene (PCMV-TRH). TRH content and expression of preproTRH, collagen type III, brain natriuretic peptide, ␤-myosin heavy chain, Bax-toBcl-2 ratio, and caspase-3 were measured. The overexpression maneuver was a success, as we found a significant increase in both tripeptide and preproTRH mRNA levels in the PCMV-TRH group compared with the control group. Immunohistochemical staining against TRH showed markedly positive brown signals only in the PCMV-TRH group. TRH overexpression induced a significant increase in fibrosis, evident in the increase of collagen type III expression accompanied by a significant increase in extracellular matrix expansion. We found a significant increase in brain natriuretic peptide and ␤-myosin heavy chain expression (recognized markers of hypertrophy). Moreover, TRH overexpression induced a slight but significant increase in myocyte diameter, indicating the onset of cell hypertrophy. We confirmed the data "in vitro" using primary cardiac cell cultures (fibroblasts and myocytes). In conclusion, these results show that a specific TRH increase in the left ventricle induced structural changes in the normal heart, thus making the cardiac TRH system a promising therapeutic target.heart; rat; thyrotropin-releasing hormone; fibrosis THYROTROPIN-RELEASING HORMONE (TRH), a small neuropeptide (p-Glu-His-Pro-NH 2 ) initially identified in the hypothalamus, is amply distributed in the central nervous system (17) and in other extra neural tissues (4). TRH also acts on the cardiovascular system of rodents, increasing blood pressure, heart rate, and contractility after its intracerebroventricular or intravenous administration (15). The hypertensive effect of TRH seems to be independent from the TRH-thyroid stimulating hormone (TSH)-triiodothyronine (T 3 ) system. In fact, in almost all of our protocols, we measured thyroid hormones [T 3 and thyroxine (T 4 )] and TSH, confirming these results (6). Indeed, other laboratories have demonstrated the existence of different pools of TRH neurons around the central nervous system, indicating that there are many T...

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Section: Discussionmentioning

confidence: 99%

Thyrotropin-releasing hormone overexpression induces structural changes of the left ventricle in the normal rat heart

Schuman

Diaz

Landa³

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…Secretion of essentially all so-packaged hormones, including pituitary luteinizing hormone, follicle-stimulating hormone, adrenocorticotropic hormone, melanocyte-stimulating hormone, thyroid-stimulating hormone, prolactin (Greer et al 1983(Greer et al , 1985(Greer et al , 1990Wang et al 1989;Sato et al 1990aSato et al , 1991, β-endorphin (Back et al 2000), hypothalamic gonadotropin-releasing hormone (Inukai et al 1992), pancreatic insulin (Blackard et al 1975), and glucagon (Blackard et al 1975), is stimulated by cell swelling. Swelling-induced thyrotropin-releasing hormone (TRH) secretion from pancreatic islets (Benicky et al 1997(Benicky et al , 2000, hypothalamic structures (Kucerova & Strbak 2001;Najvirtova et al, 2003;Bacova et al 2006b) and heart (Bacova et al 2006a) was demonstrated. Nevertheless, cell swelling-induced exocytosis possesses lim-1040 R. Hafko et al ited selectivity; cells specifically engaged in water and salt regulation retain their specific response to osmotic stimuli (Najvirtova et al 2003;Bacova et al 2006a,b).…”

Section: Introductionmentioning

confidence: 99%

“…Swelling evokes an immediate secretory burst of hormones stored in secretory vesicles with dynamics, which is indistinguishable from that induced by natural secretagogue (Bacova et al, 2006a). Secretion of essentially all so-packaged hormones, including pituitary luteinizing hormone, follicle-stimulating hormone, adrenocorticotropic hormone, melanocyte-stimulating hormone, thyroid-stimulating hormone, prolactin (Greer et al 1983(Greer et al , 1985(Greer et al , 1990Wang et al 1989;Sato et al 1990aSato et al , 1991, β-endorphin (Back et al 2000), hypothalamic gonadotropin-releasing hormone (Inukai et al 1992), pancreatic insulin (Blackard et al 1975), and glucagon (Blackard et al 1975), is stimulated by cell swelling.…”

Section: Introductionmentioning

confidence: 99%

Ethanol and urea affect insulin secretion from islets and insulinoma cells by different mechanisms

et al. 2009

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Secretion of insulin could be stimulated by several ways. Comparison of glucose-and swelling-induced mechanisms in pancreatic islets revealed the involvement of a novel signal transduction pathway with specific features of osmotically stimulated peptide hormone release including Ca 2+ independence and resistance to noradrenalin (NA) inhibition. Cell swelling can be induced by hypotonicity or small permeant molecules (e.g. ethanol, urea). Our experiments were aimed to compare the effect of these permeants on insulin secretion from natural system -freshly isolated pancreatic islets and rat insulinoma cell lines INS-1 and INS-1E. As expected glucose and both permeants (80 mM ethanol and urea in isosmotic medium) induced insulin release from islets and NA did not inhibit permeant-induced secretion. Although ethanol and urea induced similar swelling of tumor cells, they produced opposite effect on insulin secretion; while exposure to ethanol led to stimulation of insulin secretion, exposure to urea led to suppression in both types of neoplastic cells. Surprisingly, stimulating effect of ethanol was completely suppressed by NA in both tumor cell lines. Ethanol in hyperosmotic medium failed to stimulate and even inhibited insulin release from both tumor cell lines in present study indicating thus involvement of an osmotic component. In conclusion, the opposite effect of ethanol and urea on insulin secretion from insulinoma cells and sensitivity of ethanol stimulation to NA indicate utilization of different cellular signaling pathways in tumor cells as compared to natural β-cells. Participation of permeant effect in the mechanism of ethanol stimulation remains to be clarified.

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“…Furthermore, as suggested by the wide tissue-distribution of TRH and TRH receptors, TRH is implicated in many physiological and pathological processes of prostate, pancreas, testis, adrenal gland, heart, skin and thyroid tissues [112][113][114][115][116][117][118][119].…”

Section: Trhmentioning

confidence: 99%

Paracrine Regulation of Thyroid-Hormone Synthesis by C Cells

Fernández-Santos¹,

García-Marín²,

Utrilla³

et al. 2012

Thyroid Hormone

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Thyrotropin‐releasing hormone in rat heart: effect of swelling, angiotensin II and renin gene

Cited by 12 publications

References 19 publications

Thyrotropin-releasing hormone overexpression induces structural changes of the left ventricle in the normal rat heart

Thyrotropin-releasing hormone overexpression induces structural changes of the left ventricle in the normal rat heart

Ethanol and urea affect insulin secretion from islets and insulinoma cells by different mechanisms

Paracrine Regulation of Thyroid-Hormone Synthesis by C Cells

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