{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T10:23:22Z","timestamp":1783592602674,"version":"3.55.0"},"reference-count":62,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2012,10,1]]},"abstract":"<jats:p> To investigate the effect of tumor cell adhesion on microvascular permeability ( P) in intact microvessels, we measured the adhesion rate of human mammary carcinoma MDA-MB-231, the hydraulic conductivity (L<jats:sub>p<\/jats:sub>), the P, and reflection coefficient (\u03c3) to albumin of the microvessels at the initial tumor cell adhesion and after \u223c45 min cell perfusion in the postcapillary venules of rat mesentery in vivo. Rats (Sprague-Dawley, 250\u2013300 g) were anesthetized with pentobarbital sodium given subcutaneously. A midline incision was made in the abdominal wall, and the mesentery was gently taken out and arranged on the surface of a glass coverslip for the measurement. An individual postcapillary venule was perfused with cells at a rate of \u223c1 mm\/s, which is the mean blood flow velocity in this type of microvessels. At the initial tumor cell adhesion, which was defined as one adherent cell in \u223c100- to 145-\u03bcm vessel segment, L<jats:sub>p<\/jats:sub> was 1.5-fold and P was 2.3-fold of their controls, and \u03c3 decreased from 0.92 to 0.64; after \u223c45-min perfusion, the adhesion increased to \u223c5 adherent cells in \u223c100- to 145-\u03bcm vessel segment, while L<jats:sub>p<\/jats:sub> increased to 2.8-fold, P to 5.7-fold of their controls, and \u03c3 decreased from 0.92 to 0.42. Combining these measured data with the predictions from a mathematical model for the interendothelial transport suggests that tumor cell adhesion to the microvessel wall degrades the endothelial surface glycocalyx (ESG) layer. This suggestion was confirmed by immunostaining of heparan sulfate of the ESG on the microvessel wall. Preserving of the ESG by a plasma glycoprotein orosomucoid decreased the P to albumin and reduced the tumor cell adhesion. <\/jats:p>","DOI":"10.1152\/japplphysiol.00479.2012","type":"journal-article","created":{"date-parts":[[2012,8,3]],"date-time":"2012-08-03T04:38:00Z","timestamp":1343968680000},"page":"1141-1153","source":"Crossref","is-referenced-by-count":43,"title":["Adhesion of malignant mammary tumor cells MDA-MB-231 to microvessel wall increases microvascular permeability via degradation of endothelial surface glycocalyx"],"prefix":"10.1152","volume":"113","author":[{"given":"Bin","family":"Cai","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering, The City College of the City University of New York, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, The City College of the City University of New York, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, The City College of the City University of New York, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, The City College of the City University of New York, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bingmei M.","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, The City College of the City University of New York, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1992.sp018934"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.058255"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.bpj.2011.07.036"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1996.271.6.H2520"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.0263b.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvq137"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-010-0118-z"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1995.1146"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/ALN.0b013e3182289988"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1515\/BC.2008.005"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbiomech.2006.01.001"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000085630.24353.3D"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvq115"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvq188"},{"key":"B15","volume-title":"Cardiovascular Physiology. 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