Activation of ERK, JNK, Akt, and G‐protein coupled signaling by hybrid angiotensin II AT1/bradykinin B2 receptors expressed in HEK‐293 cells

Yu, Jun; Lubinsky, David; Tsomaia, Natia; Huang, Zhenhua; Taylor, Linda; Mierke, Dale F.; Navarro, Javier; Miraz, Osman; Polgár, Péter

doi:10.1002/jcb.21161

Cited by 13 publications

(17 citation statements)

References 31 publications

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“…Mice with a null mutation of the B 2 BK receptor also have reduced secondary mechanical allodynia in the capsaicin model (Wang et al, 2005). Interestingly, bradykinin via B 2 activates ERK in several other cells Hsieh et al, 2007;Yu et al, 2007). PKC activates Raf and PKA Rap1, and thereby B-Raf (Gutkind, 2000).…”

Section: Discussionmentioning

confidence: 99%

Bradykinin Enhances AMPA and NMDA Receptor Activity in Spinal Cord Dorsal Horn Neurons by Activating Multiple Kinases to Produce Pain Hypersensitivity

Kohno¹,

Wang²,

Amaya³

et al. 2008

J. Neurosci.

101

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-1). Extracellular signal-regulated kinase (ERK) activation is involved after the PKC and PKA coactivation, and intrathecal administration of bradykinin induces a thermal hyperalgesia in vivo, which is reduced by inhibition of ERK, PKA, and PKC. We conclude that bradykinin, by activating multiple kinases in dorsal horn neurons, potentiates glutamatergic synaptic transmission to produce pain hypersensitivity.

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Section: Discussionmentioning

confidence: 99%

Bradykinin Enhances AMPA and NMDA Receptor Activity in Spinal Cord Dorsal Horn Neurons by Activating Multiple Kinases to Produce Pain Hypersensitivity

Kohno¹,

Wang²,

Amaya³

et al. 2008

J. Neurosci.

101

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“…In the process we successfully replaced major portions of the signaling segments within the intracellular face of the AT1 receptor 6. In the communication we showed that the hybrids possess a number of signaling characteristics of the BKB2 receptor.…”

Section: Introductionmentioning

confidence: 99%

Attenuation of Angiotensin II-Induced Hypertension and Cardiac Hypertrophy in Transgenic Mice Overexpressing a Type 1 Receptor Mutant

Ahmad

Cesana

Lamperti

et al. 2009

American Journal of Hypertension

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Background The angiotensin II (AngII) type 1 receptor (AT1) regulates cardiovascular function by activating various signal pathways. The purpose of this study was to evaluate the effects of a mutant AT1 receptor on AngII responding blood pressure and cardiac hypertrophy in conjunction with altered AngII activation of RhoA and Akt. Methods A mutant AT1 receptor was constructed and overexpressed in FVB mice using a ubiquitous-expression vector pCAGGS. The phenotype and signal transduction of the transgenic mice were compared with the wild type (WT) mice. Results The transgenic mice showed a similar baseline phenotype as WT mice, but their blood pressure in response to continuous AngII infusion was significantly lower, as measured on day 3, 4, 7 and 14, with a difference of 20 mmHg by day 14. There was also a significantly larger heart to total body weight ratio in the WT mice, whose heart weight was 0.441 ± 0.008 % of total body weight compared to the transgenic mice at 0.416 ± 0.008 %. Aortic endothelial cells isolated from these transgenic mice displayed an altered signaling profile, such as diminished activation of Akt and RhoA in response to AngII. In contrast, Gαq coupling and ERK/JNK activation did not change. Conclusion The expression of an AT1 mutant receptor in the presence of WT receptor can effectively modulate AngII effected signaling. Furthermore, the elimination of Akt and RhoA activation by AngII significantly reduces but does not eliminate its hypertensive effect.

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“…It involves the PLC-PKC [4,5], Ras-Raf-MEK-ERK [6,7], and PI3K-Akt [8,9] signaling pathways. We focused on what signaling pathway will be involved in up-expression of B2 receptor mediated by BK.…”

Section: Discussionmentioning

confidence: 99%

Effect of bradykinin on bradykinin-B2 receptor in rat aortic vascular smooth muscle cells and the involved signal transduction pathways

et al. 2010

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The aim of this paper is to study the effect of bradykinin (BK) on bradykinin-B2 receptor as well as the possible involved signal transduction pathways in cultured rat aortic vascular smooth muscle cells (VSMCs). Rat aortic VSMCs were cultured. Cells after 4-6 passages were used in the experiment. VSMCs were incubated with BK, BK + B2 receptor inhibitor (HOE-140), BK + MEK inhibitor (PD98059), BK + mitogen-activated protein kinase (MAPK) inhibitor (apigenin), BK + phosphoinositide 3-kinase (PI3K) inhibitor (LY294002), and BK + Akt inhibitor to evaluate the expression of B2 receptor and phosphorylation of signaling molecules MAPK, Akt, and PI3K by Western blot. (1) BK markedly up-regulated the expression of B2 receptor in VSMC. (2) Apigenin, PD98059, Akt inhibitor, and LY294002 inhibited upregulation of B2 receptor induced by BK. (3) Signal transduction pathways of MAPK and PI3K were involved in the up-regulation of B2 receptor by BK mediation. Results suggest that bradykinin can up-regulate the expression of B2 receptor in VSMCs.

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Activation of ERK, JNK, Akt, and G‐protein coupled signaling by hybrid angiotensin II AT1/bradykinin B2 receptors expressed in HEK‐293 cells

Cited by 13 publications

References 31 publications

Bradykinin Enhances AMPA and NMDA Receptor Activity in Spinal Cord Dorsal Horn Neurons by Activating Multiple Kinases to Produce Pain Hypersensitivity

Bradykinin Enhances AMPA and NMDA Receptor Activity in Spinal Cord Dorsal Horn Neurons by Activating Multiple Kinases to Produce Pain Hypersensitivity

Attenuation of Angiotensin II-Induced Hypertension and Cardiac Hypertrophy in Transgenic Mice Overexpressing a Type 1 Receptor Mutant

Effect of bradykinin on bradykinin-B2 receptor in rat aortic vascular smooth muscle cells and the involved signal transduction pathways

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