Bone marrow stromal cell conditioned media reduces endoplasmic reticulum stress in alveolar epithelial cells in vitro

Pneumologie ◽  
2013 ◽  
Vol 67 (05) ◽  
Author(s):  
I Nita ◽  
A Gazdhar ◽  
T Geiser
Keyword(s):  
Bone Marrow ◽  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Endoplasmic Reticulum Stress ◽  
Stromal Cell ◽  
Bone Marrow Stromal Cell ◽  
Alveolar Epithelial Cells ◽  
Marrow Stromal Cell ◽  
Alveolar Epithelial

A Mouse Bone Marrow Stromal Cell Line with Skeletal Stem Cell Characteristics to Study Osteogenesis In Vitro and In Vivo

2014 ◽  
Vol 23 (10) ◽  
pp. 1097-1108 ◽  
Author(s):  
Sebastian Raeth ◽  
Benedetto Sacchetti ◽  
Georg Siegel ◽  
Ulrike A. Mau-Holzmann ◽  
Jan Hansmann ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stromal Cell ◽  
Bone Marrow Stromal Cell ◽  
Mouse Bone Marrow ◽  
Marrow Stromal Cell ◽  
Stromal Cell Line ◽  
Skeletal Stem Cell ◽  
Osteogenesis In Vitro

scholarly journals The role of Endoplasmic Reticulum (ER) stress in pulmonary fibrosis

2016 ◽  
Vol 3 (1) ◽  
Author(s):  
Martina Korfei ◽  
Clemens Ruppert ◽  
Benjamin Loeh ◽  
Poornima Mahavadi ◽  
Andreas Guenther
Keyword(s):  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Er Stress ◽  
Replicative Senescence ◽  
Gene Mutations ◽  
Surfactant Protein ◽  
Alveolar Epithelial Cells ◽  
Gene Encoding ◽  
Alveolar Epithelial

AbstractThe activation of Endoplasmic Reticulum (ER) stress and Unfolded Protein Response (UPR) was first observed in patients with familial interstitial pneumonia (FIP) carrying mutations in the C-terminal BRICHOS domain of surfactant protein C (SFTPC). Here, aggresome formation and severe ER stress was demonstrated in type-II alveolar epithelial cells (AECII), which specifically express this very hydrophobic surfactant protein. In subsequent studies, FIP-patients with mutations in the gene encoding surfactant protein A2 (SFTPA2) were discovered, whose overexpression in epithelial cells in vitro also resulted in significant induction of ER stress. Moreover, prominent ER stress in AECII was also observed in FIP-patients not carrying the SFTPC/SFTPA2 mutations, as well as in patients with the more common sporadic forms of IP. Additionally, cases of adult-onset FIP with mutations in Telomerase genes and other telomereassociated components were reported. These mutations were associated with telomere shortening, which is a potential cause for triggering a persistent DNA damage response and replicative senescence in affected cells. Moreover, shortened telomeres were observed directly in the AECII of FIP-patients, and even sporadic IP cases, in the absence of any gene mutations. Here, we try to figure out the possible origins of ER stress in sporadic IP cases and non-SFTPC/SFTPA2-associated FIP.

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