Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons.

Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons. Research Abstract Details 

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Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons. Abstract Text:

Chengwen Sun,Hongwei Li,Yongxin Gao,Tomokazu Matsuura,Patrick A Upchurch,Mohan K Raizada,Colin Sumners,

Macrophage migration inhibitory factor acts via its intrinsic thiol-protein oxidoreductase activity to negatively regulate the neuronal chronotropic actions of angiotensin II in normotensive rat neurons. Because the chronotropic action of angiotensin II is potentiated in spontaneously hypertensive rat neurons, we investigated whether this negative regulatory mechanism is absent in these rats. Angiotensin II (100 nM) elicited an approximately 89% increase in neuronal firing in Wistar-Kyoto rat hypothalamus and brain stem cultured neurons and an increase in intracellular macrophage migration inhibitory factor levels in the same cells. The chronotropic action of angiotensin II was significantly greater (approximately 212% increase) in spontaneously hypertensive rat neurons, but angiotensin II failed to alter macrophage migration inhibitory factor expression in these cells. Intracellular application of recombinant macrophage migration inhibitory factor (0.8 nM) or its specific neuronal overexpression via Ad5-SYN-MIF (1x10(7) infectious units) significantly attenuated the chronotropic action of angiotensin II in spontaneously hypertensive rat neurons, similar to results from Wistar-Kyoto rat neurons. In contrast, C60S-macrophage migration inhibitory factor (0.8 nM), which lacks thiol-protein oxidoreductase activity, failed to alter the chronotropic action of angiotensin II in neurons from either rat strain. Thus, whereas macrophage migration inhibitory factor has the potential to depress the chronotropic action of angiotensin II in spontaneously hypertensive rat neurons, it is unlikely that this regulatory mechanism occurs, because angiotensin II does not increase the expression of this protein. The lack of this regulatory mechanism may contribute to the increased chronotropic action of angiotensin II in spontaneously hypertensive rat neurons.

Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons. Publishing Authors By Initials

C Sun,H Li,Y Gao,T Matsuura,PA Upchurch,MK Raizada,C Sumners,

For similar proteins: membrane proteins: receptors, cell surface: receptors, immunologic: receptors, cytokine: receptors, thrombopoietin research abstracts see: proteins: membrane proteins: receptors, cell surface: receptors, immunologic: receptors, cytokine: receptors, thrombopoietin research

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Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Hypertension

VOLUME: 49

Page Numbers: 528-34

Journal Abbreviation: Hypertension

ISSN: 1524-4563

DAY: 29

MONTH: 01

YEAR: 2007

Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7906255

Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons. Keywords Mesh Terms:

KEYWORDS: Receptors, Thrombopoietin

MESH TERMS: physiology

Chemical & Substance for Abstract: Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons. Information

Substance Name: Angiotensin II

Registry Number: 11128-99-7

Grant and Affiliation Information for Lack of macrophage migration inhibitory factor regulation is linked to the increased chronotropic action of angiotensin II in SHR neurons.

AFFILIATION: Department of Physiology and Functional Genomics and McKnight Brain Institute, University of Florida, Gainesville, FL 32610-0274, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: 1R01HL-076803

ACRONYM: HL

MEDLINETA: Hypertension

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