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Volume 6, Issue 4(Suppl) Transl Med 2016
ISSN: 2161-1025, an open access journal
Page 76
conferenceseries.com
Translation Medicine & World Oncologists 2016
November 28-30, 2016
Translational Medicine and Oncologists Meet
November 28-30, 2016 San Francisco, USA
14th Annual Conference on
Powerful preclinical mouse model to study live mucin and mucous cell differentiation
Jean-Luc Desseyn1, 2
1LIRIC UMR 995, France
2Universite Lille-II, France
Mucous cells are specialized cells that produce gelling mucins responsible for the mucus gel formation. Modification of mucous
cell density and gelling mucin production are established hallmarks of many mucosal diseases including solid tumors (breast
cancer, tumors from the digestive, respiratory and reproductive tract), otitis, rhinosinusitis, dry eye, cystic fibrosis, pulmonary fibrosis
and asthma. A genetically engineered Muc5b-GFP tagged reporter mouse line at the peptide level was obtained by homologous
recombination. Embryonic lung explants allowed to show that interleukine (IL) 13 stimulates Muc5b production. Live Muc5b was
easily monitored by probe-based confocal laser endomicroscopy (pCLE) in the nasal cavity, trachea, eye conjunctiva and vagina.
As proof of concept that the mouse strain was a valuable preclinical model, we first showed that Muc5b production greatly varied
during estrous cycle. We next demonstrated that the decrease in conjunctival goblet cell density monitored by pCLE in living mice
with chemically-induced dry eye was reversed by topical application of IL13. The transgenic mouse is unique and suitable for
preclinical drug development and suited for pharmacological studies to study the effect of compounds on mucosal homeostasis in
living animals.
Transl Med 2016, 6:4(Suppl)
Adipose-derived stem cells induce autophagic activation and inhibit catabolic response to pro-
inflammatory cytokines in rat chondrocytes
Li-Bo Jiang and Jian Zhang
Zhongshan Hospital- Fudan University, China
Aim: Adipose-derived stem cells (ADSCs) have been demonstrated to have an anti-apoptosis effect on chondrocytes. However, their
effect on autophagic activation remains unclear. We sought to explore whether ADSCs can activate autophagy and inhibit IL-1β- and
lipopolysacccharide (LPS)- induced catabolism in chondrocytes.
Methods: ADSCs and chondrocytes were collected from SD rats. The biologic characteristics of ADSCs were analyzed by flow
cytometric analysis, Oil red O and alizarin red staining. Autophagic level and autophagic flux were revealed by western blotting
for LC3-II and SQSTM1/P62, MDC (monodansylcadaverine) staining and mRFP-GFP-LC3 analysis. The mTOR pathway was
investigated by western blotting for p-mTOR. The mRNA level of matrix metalloproteinases (MMPs) and thrombospondin motifs
(ADAMTSs) was detected by real-time PCR.
Results: The typical surface markers and differentiation potentials of ADSCs were proved. ADSCs enhanced the expression of
LC3-II/LC3-I and reduced SQSTM1 levels in IL-1β-induced chondrocytes after 24 and 48 hours co-culturing and in LPS-induced
chondrocytes after 48 hours co-culturing respectively. mRFP-GFP-LC3 analysis suggested that autophagosomes and autolysosomes
were formed earlier in IL-1β-treated chondrocytes than in LPS-treated chondrocytes. Bafilomycin A1 treatment further increased the
LC3-II/LC3-I level in chondrocytes in co-culture with ADSCs. The mTOR pathway was inhibited in the chondrocytes in co-culture
with ADSCs. Finally, ADSCs inhibited the increase of MMPs and ADAMTSs in chondrocytes induced by IL-1β and LPS.