{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T04:16:51Z","timestamp":1791001011208,"version":"4.1.0"},"reference-count":25,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2014,4,25]],"date-time":"2014-04-25T00:00:00Z","timestamp":1398384000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biology of the Cell"],"published-print":{"date-parts":[[2014,6]]},"abstract":"<jats:sec><jats:title>Background information<\/jats:title><jats:p>Angiotensin\u2010(1\u20137) [ANG\u2010(1\u20137)] mediates vasodilation, antiproliferation, anti\u2010apoptosis and antifibrosis, therefore, it opposes the effects of angiotensin II (ANG II). However, the detailed signal transduction mechanism following the Mas receptor activated by ANG\u2010(1\u20137) is still poorly understood. Src homology2\u2010containing inositol phosphatase 1 (SHP\u20101), a redoxsensitive protein tyrosine phosphatase, negatively influences downstream signalling molecules, such as mitogen\u2010activated protein kinases (MAPKs), through dephosphorylation, thereby inhibiting proliferative and profibrotic signalling induced by ANG II. Therefore, we hypothesised that SHP\u20101 may mediate the antiproliferative signalling of ANG\u2010(1\u20137) through the regulation of the dynamic balance of MAPKs and SHP\u20101 in isolated cardiac fibroblasts. Primary culture of neonatal Sprague\u2013Dawley rats cardiac fibroblasts was treated separately with different interventions to investigate this issue.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Our data revealed that ANG II increased the phosphorylation of extracellular signal\u2010related kinase (p\u2010ERK1\/2) and the ratio of (p\u2010ERK1\/2)\/(ERK1\/2), but ANG\u2010(1\u20137) decreased them. The effects of ANG\u2010(1\u20137) on the phosphorylation p\u2010ERK1\/2 were blocked by the Mas receptor antagonist A\u2010779. Unlike ANG II, which decreased the activity of SHP\u20101, ANG\u2010(1\u20137) increased its activity. Overexpression of SHP\u20101 attenuated the ANG II\u2010stimulated phosphorylation of c\u2010Src, its downstream molecules ERK1\/2, \u03b1\u2010smooth muscle actin and transforming growth factor\u2010\u03b21 (TGF\u2010\u03b21). These effects were also inhibited by the specific inhibitor of SHP\u20101, sodium stibogluconate. ANG\u2010(1\u20137) had no significant effects on the gene expression of TGF\u2010\u03b21, collagen I or collagen III, but was found to antagonise the stimulatory effects of ANG II on them.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>ANG\u2010(1\u20137), through Mas receptor, activates SHP\u20101 in cardiac fibroblasts, which can negatively modulate ANG II\u2010induced phosphorylation of c\u2010Src and MAPKs, and inhibits profibrotic factors TGF\u2010\u03b21 and collagen production. ANG\u2010(1\u20137) can thereby serve as a protective role by counteracting the effects of ANG II.<\/jats:p><\/jats:sec>","DOI":"10.1111\/boc.201400015","type":"journal-article","created":{"date-parts":[[2014,3,18]],"date-time":"2014-03-18T18:21:05Z","timestamp":1395166865000},"page":"182-192","source":"Crossref","is-referenced-by-count":29,"title":["Angiotensin\u2010(1\u20137) attenuates angiotensin II\u2010induced signalling associated with activation of a tyrosine phosphatase in Sprague\u2013Dawley rats cardiac fibroblasts"],"prefix":"10.1111","volume":"106","author":[{"given":"Xiaoling","family":"Tao","sequence":"first","affiliation":[{"name":"Department of Cardiology The Second Affiliated Hospital of Chongqing Medical University, The Chongqing Cardiac Arrhythmias Service Center  Chongqing 400010 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinqi","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Cardiology The Second Affiliated Hospital of Chongqing Medical University, The Chongqing Cardiac Arrhythmias Service Center  Chongqing 400010 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guoying","family":"Kao","sequence":"additional","affiliation":[{"name":"Department of Cardiology The Second Affiliated Hospital of Chongqing Medical University, The Chongqing Cardiac Arrhythmias Service Center  Chongqing 400010 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoge","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Cardiology The Second Affiliated Hospital of Chongqing Medical University, The Chongqing Cardiac Arrhythmias Service Center  Chongqing 400010 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Cardiology The Second Affiliated Hospital of Chongqing Medical University, The Chongqing Cardiac Arrhythmias Service Center  Chongqing 400010 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuehui","family":"Yin","sequence":"additional","affiliation":[{"name":"Department of Cardiology The Second Affiliated Hospital of Chongqing Medical University, The Chongqing Cardiac Arrhythmias Service Center  Chongqing 400010 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernhard","family":"Zrenner","sequence":"additional","affiliation":[{"name":"Medizinische Klinik I Krankenhaus Landshut\/Achdorf  Landshut 84036 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