During endotoxemia, liver microcirculation disruption is characterized by a hypersensitivity to the constrictor effects of endothelin 1 (ET-1). The shift of ET-1-mediated effects toward vasoconstriction may result from depressed ET-1-mediated vasodilation through decreased ET-1-induced nitric oxide
Caveolin-1 secreting LNCaP cells induce tumor growth of caveolin-1 negative LNCaP cells in vivo
✍ Scribed by René Bartz; Jian Zhou; Jer-Tsong Hsieh; Yunshu Ying; Weiping Li; Pingsheng Liu
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- French
- Weight
- 542 KB
- Volume
- 122
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Abstract
Caveolin‐1 (Cav‐1) was originally identified as a structural protein of caveolae, which is a plasma membrane domain that regulates a variety of signaling pathways involved in cell growth and migration. Here, we show that expression of Cav‐1 in the Cav‐1‐deficient human prostate cancer cell line LNCaP both stimulates cell proliferation and promotes tumor growth in nude mice. Unexpectedly, Cav‐1 expressing LNCaP (LNCaP^Cav‐1^) cells injected into one side of a nude mouse promoted tumor growth of Cav‐1 negative LNCaP cells injected on the contralateral side of the same animal. The LNCaP tumors were positive for Cav‐1, however, this signal was not caused by migrated LNCaP^Cav‐1^ cells, but we show that this Cav‐1 was secreted by the LNCaP^Cav‐1^ tumors. We demonstrate that conditioned media from LNCaP^Cav‐1^ cells contained Cav‐1 that was associated with a lipoprotein particle ranging in size from 15 to 30 nm and a density similar to high density lipoprotein particle. These results suggest that LNCaP^Cav‐1^ cells secreting Cav‐1 particle produce an endocrine factor that stimulates tumor growth. © 2007 Wiley‐Liss, Inc.
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