{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T16:51:41Z","timestamp":1792083101186,"version":"4.4.0"},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[1999,7]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014We have previously demonstrated that elevating intraluminal pressure from 90 to 140 mm Hg in isolated mesenteric arteries increases the expression of proto-oncogenes. These proto-oncogenes encode nuclear transcription factors that regulate the expression of target genes during various stages of the cell cycle. Thus, pressure-induced proto-oncogene expression may represent a mechanism by which pressure can induce growth and\/or proliferation of vascular smooth muscle. The purpose of this study was to determine the intracellular signals that contribute to the pressure-induced increase in c-\n            <jats:italic>fos<\/jats:italic>\n            expression. Small mesenteric arteries were isolated from male Wistar rats and transferred to a dual-vessel chamber. The arteries were cannulated and slowly equilibrated to initial conditions (90 mm Hg, 37\u00b0C) while being continuously superfused with a HEPES-bicarbonate\u2013buffered Krebs\u2019 solution. After the equilibration period, the intraluminal pressure in 1 artery was increased to 140 mm Hg for 1 hour. In experiments designed to determine the intracellular signals involved in the pressure-induced increase in c-\n            <jats:italic>fos<\/jats:italic>\n            expression, specific inhibitors were introduced to the superfusate reservoir of both arteries before the pressure increase. The arteries were then fixed in phosphate-buffered formalin and embedded in paraffin blocks. Sections of paraffin-embedded arteries were fixed on slides, and the expression of c-\n            <jats:italic>fos<\/jats:italic>\n            was determined by in situ hybridization with the use of\n            <jats:sup>35<\/jats:sup>\n            S-labeled riboprobes. The pressure-induced expression of c-\n            <jats:italic>fos<\/jats:italic>\n            was not inhibited by nitrendipine (10 \u03bcmol\/L), a calcium-free Krebs\u2019 solution containing EGTA (1 to 2 mmol\/L), calphostin C (0.1 \u03bcmol\/L), or cytochalasin D (0.4 \u03bcmol\/L) but was inhibited by genistein (30 \u03bcmol\/L). The results suggest that activation of a tyrosine kinase is required for pressure-induced c-\n            <jats:italic>fos<\/jats:italic>\n            expression, but the signaling pathway does not require extracellular calcium entry, intact actin filaments, or protein kinase C. As we have shown previously, the expression of c\n            <jats:italic>-fos<\/jats:italic>\n            correlated with wall stress.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.34.1.132","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"132-137","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":12,"title":["Genistein Inhibits Pressure-Induced Expression of c-\n            <i>fos<\/i>\n            in Isolated Mesenteric Arteries"],"prefix":"10.1161","volume":"34","author":[{"given":"Victor A.","family":"Miriel","sequence":"first","affiliation":[{"name":"From the Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Va."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven P.","family":"Allen","sequence":"additional","affiliation":[{"name":"From the Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Va."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suzanne D.","family":"Schriver","sequence":"additional","affiliation":[{"name":"From the Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Va."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Russell L.","family":"Prewitt","sequence":"additional","affiliation":[{"name":"From the Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Va."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1159\/000159102"},{"key":"e_1_3_2_2_2","first-page":"H933","volume":"253","year":"1987","unstructured":"Hashimoto H, Prewitt RL, Efaw CW. 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