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Cellular targets of propranolol in i...

Lee, Daniel K.

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Cellular targets of propranolol in infantile hemangioma.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Cellular targets of propranolol in infantile hemangioma./
作者:	Lee, Daniel K.
面頁冊數:	133 p.
附註:	Source: Dissertation Abstracts International, Volume: 75-06(E), Section: B.
Contained By:	Dissertation Abstracts International75-06B(E).
標題:	Biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3611549
ISBN:	9781303724336

Cellular targets of propranolol in infantile hemangioma.
Lee, Daniel K.

Cellular targets of propranolol in infantile hemangioma. - 133 p.

Source: Dissertation Abstracts International, Volume: 75-06(E), Section: B.

Thesis (Ph.D.)--Harvard University, 2014.

This item is not available from ProQuest Dissertations & Theses.

Infantile hemangioma (IH) is a vascular neoplasm that affects 4-10 percent of infants. Propranolol, a non-selective beta-adrenergic receptor (AR) antagonist, was serendipitously discovered to accelerate regression of IH in 2008; however, its mechanism in IH is unclear. A number of approaches were used to investigate the mechanism(s) by which propranolol accelerates the involution of IH. Two of the likely targets of propranolol, beta1- and beta2-ARs, were found expressed in IH tissues by quantitative real time polymerase chain reaction (qRT-PCR). In vitro contractility assays were developed to examine effects of propranolol on cellular activities, and they showed that wrinkles formed by hemangioma-derived pericytes (Hem-Pericytes) relaxed in response to epinephrine, but this was strongly inhibited if propranolol was added 5 minutes before epinephrine. These responses were blunted by silencing beta2-AR with siRNA. Propranolol had no effect on the contractility of placental or retinal pericytes in this assay. Propranolol also blocked proliferation of Hem-Pericytes and hemangioma-derived endothelial cells (HemECs), but not stem cells (HemSCs). In order to reproduce the clinical effect of propranolol on IH patients, a murine model of IH was utilized. HemECs and Hem-Pericytes suspended in Matrigel were implanted in mice and allowed to form blood vessels. At 7 days, vascular perfusion of the cell/Matrigel implants was verified; mice were divided into two groups and treated with vehicle or propranolol for 7 days. Contrast-enhanced micro-ultrasonography of the implants showed a significantly decreased vascular volume in propranolol-treated mice, but no reduction in those treated with vehicle. These experiments indicated that propranolol may affect contractility of Hem-Pericytes to reduce vascular volume of IH, to accomplish quick improvement seen in patients, and they identified HemECs, Hem-Pericytes and beta2-AR as likely targets of propranolol.

ISBN: 9781303724336Subjects--Topical Terms:

522710
Biology.

Cellular targets of propranolol in infantile hemangioma.
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502 $a Thesis (Ph.D.)--Harvard University, 2014.
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520 $a Infantile hemangioma (IH) is a vascular neoplasm that affects 4-10 percent of infants. Propranolol, a non-selective beta-adrenergic receptor (AR) antagonist, was serendipitously discovered to accelerate regression of IH in 2008; however, its mechanism in IH is unclear. A number of approaches were used to investigate the mechanism(s) by which propranolol accelerates the involution of IH. Two of the likely targets of propranolol, beta1- and beta2-ARs, were found expressed in IH tissues by quantitative real time polymerase chain reaction (qRT-PCR). In vitro contractility assays were developed to examine effects of propranolol on cellular activities, and they showed that wrinkles formed by hemangioma-derived pericytes (Hem-Pericytes) relaxed in response to epinephrine, but this was strongly inhibited if propranolol was added 5 minutes before epinephrine. These responses were blunted by silencing beta2-AR with siRNA. Propranolol had no effect on the contractility of placental or retinal pericytes in this assay. Propranolol also blocked proliferation of Hem-Pericytes and hemangioma-derived endothelial cells (HemECs), but not stem cells (HemSCs). In order to reproduce the clinical effect of propranolol on IH patients, a murine model of IH was utilized. HemECs and Hem-Pericytes suspended in Matrigel were implanted in mice and allowed to form blood vessels. At 7 days, vascular perfusion of the cell/Matrigel implants was verified; mice were divided into two groups and treated with vehicle or propranolol for 7 days. Contrast-enhanced micro-ultrasonography of the implants showed a significantly decreased vascular volume in propranolol-treated mice, but no reduction in those treated with vehicle. These experiments indicated that propranolol may affect contractility of Hem-Pericytes to reduce vascular volume of IH, to accomplish quick improvement seen in patients, and they identified HemECs, Hem-Pericytes and beta2-AR as likely targets of propranolol.
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