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The counterregulating role of ACE2 and ACE2-mediated angiotensin 1-7 signaling against angiotensin II stimulation in vascular cells.
Hypertens Res. 2010 Nov; 33(11):1182-5.HR

Abstract

To clarify the role of endogenous angiotensin (Ang)-converting enzyme 2 (ACE2) and its cleavage product, Ang 1-7, in the atherogenic stimulation of vascular cells, we investigated the effect of pharmacological inhibition of ACE2 and Mas, an Ang 1-7 receptor, on cellular responses against Ang II stimulation. We measured extracellular signal-regulated kinase (ERK) 1/2 phosphorylation by western blot, smooth muscle cell (SMC) proliferation by WST assay and the adhesion of monocytes labeled with PKH67 to endothelial cells (ECs) by fluorescence microplate reader. Cells were pretreated with Ang 1-7, olmesartan (Ang II type 1 receptor (AT1) blocker), DX600 (ACE2 inhibitor), -Ala7-Ang1-7 (D-Ala; Mas antagonist), or combinations of treatments before the application of Ang II. Treatment with Ang II increased phosphorylated ERK 1/2 of SMC and EC, proliferation of SMC and adhesion of monocyte to EC, which were blocked by olmesartan. Pretreatment with DX600 either did not accelerate or only slightly accelerated these cellular responses. However, when Ang II signaling through AT1 was reduced by olmesartan, the additional treatment with DX600 significantly blunted some of the effect of olmesartan. Similarly, pretreatment with D-Ala reduced the inhibitory effect of olmesartan in response to Ang II stimulation. Endogenous ACE2 in vascular cells may contribute to counteracting the Ang II-mediated cellular response partly by upregulating the Ang 1-7 signaling through Mas.

Authors+Show Affiliations

Department of Geriatric Medicine, Osaka University Graduate School of Medicine, Suita, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20703229

Citation

Hayashi, Norihiro, et al. "The Counterregulating Role of ACE2 and ACE2-mediated Angiotensin 1-7 Signaling Against Angiotensin II Stimulation in Vascular Cells." Hypertension Research : Official Journal of the Japanese Society of Hypertension, vol. 33, no. 11, 2010, pp. 1182-5.
Hayashi N, Yamamoto K, Ohishi M, et al. The counterregulating role of ACE2 and ACE2-mediated angiotensin 1-7 signaling against angiotensin II stimulation in vascular cells. Hypertens Res. 2010;33(11):1182-5.
Hayashi, N., Yamamoto, K., Ohishi, M., Tatara, Y., Takeya, Y., Shiota, A., Oguro, R., Iwamoto, Y., Takeda, M., & Rakugi, H. (2010). The counterregulating role of ACE2 and ACE2-mediated angiotensin 1-7 signaling against angiotensin II stimulation in vascular cells. Hypertension Research : Official Journal of the Japanese Society of Hypertension, 33(11), 1182-5. https://doi.org/10.1038/hr.2010.147
Hayashi N, et al. The Counterregulating Role of ACE2 and ACE2-mediated Angiotensin 1-7 Signaling Against Angiotensin II Stimulation in Vascular Cells. Hypertens Res. 2010;33(11):1182-5. PubMed PMID: 20703229.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The counterregulating role of ACE2 and ACE2-mediated angiotensin 1-7 signaling against angiotensin II stimulation in vascular cells. AU - Hayashi,Norihiro, AU - Yamamoto,Koichi, AU - Ohishi,Mitsuru, AU - Tatara,Yuji, AU - Takeya,Yasushi, AU - Shiota,Atsushi, AU - Oguro,Ryosuke, AU - Iwamoto,Yoshihiro, AU - Takeda,Masao, AU - Rakugi,Hiromi, Y1 - 2010/08/12/ PY - 2010/8/13/entrez PY - 2010/8/13/pubmed PY - 2011/3/1/medline SP - 1182 EP - 5 JF - Hypertension research : official journal of the Japanese Society of Hypertension JO - Hypertens Res VL - 33 IS - 11 N2 - To clarify the role of endogenous angiotensin (Ang)-converting enzyme 2 (ACE2) and its cleavage product, Ang 1-7, in the atherogenic stimulation of vascular cells, we investigated the effect of pharmacological inhibition of ACE2 and Mas, an Ang 1-7 receptor, on cellular responses against Ang II stimulation. We measured extracellular signal-regulated kinase (ERK) 1/2 phosphorylation by western blot, smooth muscle cell (SMC) proliferation by WST assay and the adhesion of monocytes labeled with PKH67 to endothelial cells (ECs) by fluorescence microplate reader. Cells were pretreated with Ang 1-7, olmesartan (Ang II type 1 receptor (AT1) blocker), DX600 (ACE2 inhibitor), -Ala7-Ang1-7 (D-Ala; Mas antagonist), or combinations of treatments before the application of Ang II. Treatment with Ang II increased phosphorylated ERK 1/2 of SMC and EC, proliferation of SMC and adhesion of monocyte to EC, which were blocked by olmesartan. Pretreatment with DX600 either did not accelerate or only slightly accelerated these cellular responses. However, when Ang II signaling through AT1 was reduced by olmesartan, the additional treatment with DX600 significantly blunted some of the effect of olmesartan. Similarly, pretreatment with D-Ala reduced the inhibitory effect of olmesartan in response to Ang II stimulation. Endogenous ACE2 in vascular cells may contribute to counteracting the Ang II-mediated cellular response partly by upregulating the Ang 1-7 signaling through Mas. SN - 1348-4214 UR - https://www.unboundmedicine.com/medline/citation/20703229/The_counterregulating_role_of_ACE2_and_ACE2_mediated_angiotensin_1_7_signaling_against_angiotensin_II_stimulation_in_vascular_cells_ L2 - http://amigo.geneontology.org/amigo/reference/PMID:20703229 DB - PRIME DP - Unbound Medicine ER -