alexa LAM/TSC Cell Migration to Uterus in an Experimental Model of Lymphangioleiomyomatosis. Regulation by Anti-Epidermal Growth Factor Receptor Antibody and Rapamycin
ISSN: 2157-7099

Journal of Cytology & Histology
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Research Article

LAM/TSC Cell Migration to Uterus in an Experimental Model of Lymphangioleiomyomatosis. Regulation by Anti-Epidermal Growth Factor Receptor Antibody and Rapamycin

Elena Lesma*, Eloisa Chiaramonte, Silvia Ancona, Anna Maria Di Giulio and Alfredo Gorio

Laboratory of Pharmacology, Department of Health Sciences, University of Milan, Italy

*Corresponding Author:
Elena Lesma
Laboratory of Pharmacology
Department of Health Sciences
University of Milan, via di Rudinì
8 20142 Milan, Italy
Tel: +39.02.503.23038
E-mail: [email protected]

Received Date: February 28, 2014; Accepted Date: March 26, 2014; Published Date: March 28, 2014

Citation: Lesma E, Chiaramonte E, Ancona S, DiGiulio AM, Gorio A (2014) LAM/TSC Cell Migration to Uterus in an Experimental Model of Lymphangioleiomyomatosis. Regulation by Anti-Epidermal Growth Factor Receptor Antibody and Rapamycin. JCytol Histol S4:007 doi:10.4172/2157-7099.S4-007

Copyright: © 2014 Lesma E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Lymphangioleiomyomatosis (LAM) is a rare lung disease affecting almost exclusively women, characterized by the invasion and abnormal proliferation of smooth muscle-like cells in pulmonary parenchyma and axial lymphatics. LAM cells bear mutations in Tuberous Sclerosis Complex (TSC) genes. It has been hypothesized that uterus might be the primary site of origin and one of the most frequent metastatic or disseminated site of LAM cells. We developed a mouse model to study the migratory and invasive properties of human LAM/TSC cells to the uterus. We also examined the action of rapamycin and anti-Epidermal Growth Factor Receptor (EGFR) antibody.
LAM/TSC cells were endonasally administered to 3 week old immunodeficient female nude mice. 5 months later mice were divided in 4 groups: control, LAM/TSC cell-administered mice, LAM/TSC cell-administered mice treated with rapamycin, and LAM/TSC cell-administered mice treated with anti-EGFR antibody. Drugs were administered for one months. Uteri were analysed for the presence of human LAM/TSC cells by COX IV antibody, lymphangiogenesis by LYVE 1 expression and angiogenesis by counting blood vessels.
LAM/TSC cells migrated to the uterus without causing any morphological lesion. Interestingly, LAM/TSC cells increased the number of blood vessels while did not cause any alteration in lymphatics vessels. Anti-EGFR antibody and rapamycin reduced the number of human LAM/TSC and counteracted the proliferation of blood vessels in uteri. Although both drugs did not change the expression of LYVE 1, localization of lymphatics was mainly in the perimetrium after drug treatment.
Our data describe the strong invasive capability of human LAM/TSC cells which migrated to the uterus. LAM/ TSC cells presence is accompanied by increased angiogenesis. Anti-EGFR antibody and rapamycin were effective in reducing the LAM/TSC cell number and blood vessel proliferation.

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