TY  - JOUR
A1  - Bachmann, Julia
A1  - Ehlert, Elias
A1  - Becker, Matthias
A1  - Otto, Christoph
A1  - Radeloff, Katrin
A1  - Blunk, Torsten
A1  - Bauer-Kreisel, Petra
T1  - Ischemia-like stress conditions stimulate trophic activities of adipose-derived stromal/stem cells
JF  - Cells
N2  - Adipose-derived stromal/stem cells (ASCs) have been shown to exert regenerative functions, which are mainly attributed to the secretion of trophic factors. Upon transplantation, ASCs are facing an ischemic environment characterized by oxygen and nutrient deprivation. However, current knowledge on the secretion capacity of ASCs under such conditions is limited. Thus, the present study focused on the secretory function of ASCs under glucose and oxygen deprivation as major components of ischemia. After exposure to glucose/oxygen deprivation, ASCs maintained distinct viability, but the metabolic activity was greatly reduced by glucose limitation. ASCs were able to secrete a broad panel of factors under glucose/oxygen deprivation as revealed by a cytokine antibody array. Quantification of selected factors by ELISA demonstrated that glucose deprivation in combination with hypoxia led to markedly higher secretion levels of the angiogenic and anti-apoptotic factors IL-6, VEGF, and stanniocalcin-1 as compared to the hypoxic condition alone. A conditioned medium of glucose/oxygen-deprived ASCs promoted the viability and tube formation of endothelial cells, and the proliferation and migration of fibroblasts. These findings indicate that ASCs are stimulated by ischemia-like stress conditions to secrete trophic factors and would be able to exert their beneficial function in an ischemic environment.
KW  - adipose-derived stromal/stem cells (ASCs)
KW  - regenerative medicine
KW  - secretion
KW  - trophic factors
KW  - ischemia
KW  - glucose starvation
KW  - hypoxia
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-211233
SN  - 2073-4409
VL  - 9
IS  - 9
ER  - 
TY  - JOUR
A1  - Ceteci, Fatih
A1  - Ceteci, Semra
A1  - Zanucco, Emanuele
A1  - Thakur, Chitra
A1  - Becker, Matthias
A1  - El-Nikhely, Nefertiti
A1  - Fink, Ludger
A1  - Seeger, Werner
A1  - Savai, Rajkumar
A1  - Rapp, Ulf R.
T1  - E-Cadherin Controls Bronchiolar Progenitor Cells and Onset of Preneoplastic Lesions in Mice
JF  - Neoplasia
N2  - Although progenitor cells of the conducting airway have been spatially localized and some insights have been gained regarding their molecular phenotype, relatively little is known about the mechanisms regulating their maintenance, activation, and differentiation. This study investigates the potential roles of E-cadherin in mouse Clara cells, as these cells were shown to represent the progenitor/stem cells of the conducting airways and have been implicated as the cell of origin of human non-small cell lung cancer. Postnatal inactivation of E-cadherin affected Clara cell differentiation and compromised airway regeneration under injury conditions. In steady-state adult lung, overexpression of the dominant negative E-cadherin led to an expansion of the bronchiolar stem cells and decreased differentiation concomitant with canonical Wnt signaling activation. Expansion of the bronchiolar stem cell pool was associated with an incessant proliferation of neuroepithelial body-associated Clara cells that ultimately gave rise to bronchiolar hyperplasia. Despite progressive hyperplasia, only a minority of the mice developed pulmonary solid tumors, suggesting that the loss of E-cadherin function leads to tumor formation when additional mutations are sustained. The present study reveals that E-cadherin plays a critical role in the regulation of proliferation and homeostasis of the epithelial cells lining the conducting airways.
KW  - injury
KW  - lung cancer
KW  - stem cells
KW  - clara cell
KW  - gene expression
KW  - basal cell
KW  - in vivo
KW  - epithelium
KW  - airway
KW  - renewal
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-135407
VL  - 14
IS  - 12
ER  -