Published ahead of print on December 12, 2003, doi:10.1165/rcmb.2003-0145OC Am. J. Respir. Cell Mol. Biol., Volume 30, Number 6, June 2004, 784-792 A more recent version of this article appeared on June 1, 2004
Submitted on April 24, 2003 Epithelial-mesenchymal interactions are linked to neovascularizationMargaret A Schwarz1*,1 Surgery, UMDNJ RWJMS, New Brunswick, NJ, USA; Pediatrics, Cardiothoracic Surgery, and Cranio-Facial Center for Molecular Biology, University of Southern California Keck School of Medicine, Los Angeles, CA, USA, 2 Pediatrics, Cardiothoracic Surgery, and Cranio-Facial Center for Molecular Biology, University of Southern California Keck School of Medicine, Los Angeles, CA, USA, 3 Surgery, UMDNJ RWJMS, New Brunswick, NJ, USA * To whom correspondence should be addressed. E-mail: m.schwarz{at}umdnj.edu.
Lung morphogenesis is dependent on interactions between mesenchymal and epithelial cells. We have previously demonstrated that inhibition of neovascularization by EMAP II also attenuates fetal lung morphogenesis in vivo, and hypothesized that epithelial-mesenchymal interactions are regulated by vascular signals. To address this postulate, we evaluated the formation of epithelial cysts in vitro and assessed this complex interaction through: 1) identification of vascular formation in vitro, 2) assessment of the effect of selective vascular inhibition on cell viability, proliferation, and cellular interactions as measured by epithelial cyst formation, and 3) examination of whether there is an interdependent relationship between epithelial and mesenchymal cells and a vascular mediator's protein expression. Vascular networks in vitro formed in direct relationship to the presence of epithelial cysts. Disruption of the vasculature by delivery of a selective anti-angiogenic protein EMAP II was associated with disruption of epithelial cyst formation. Lastly, control of the vascular formation regulatory protein EMAP II, is a direct result of epithelial - mesenchymal cell interactions. These findings suggest that vascular formation modulate and is modulated by the normal cellular communication and interactions that direct lung morphology.
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