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Volume 4, Issue 2, pp. 27 - 47, February 2020

Issue cover
Cover: This month in Cell Stress: Cellular tunneling nanotubes (TnTs) in development. Stylized image depicts a TnT structure in adherent mesothelioma cells stained with DAPI (red) and anti-fascin antibodies (yellow). Image modified by Cell Stress. Image Source: Lou E, Fujisawa S, Morozov A, Barlas A, Romin Y, et al. (2012) Tunneling Nanotubes Provide a Unique Conduit for Intercellular Transfer of Cellular Contents in Human Malignant Pleural Mesothelioma. PLOS ONE 7(3): e33093. Original image licensed under the CC BY 4.0 license. The cover is published under the CC BY 4.0 license. Enlarge issue cover

News and Thoughts

ACBP is an appetite stimulator across phylogenetic barriers

Frank Madeo, Nektarios Tavernarakis, José M. Bravo-San Pedro and Guido Kroemer

page 27-29 | 10.15698/cst2020.02.211 | Full text | PDF |


Fine intercellular connections in development: TNTs, cytonemes, or intercellular bridges?

Olga Korenkova, Anna Pepe and Chiara Zurzolo

page 30-43 | 10.15698/cst2020.02.212 | Full text | PDF | Abstract

Intercellular communication is a fundamental property of multicellular organisms, necessary for their adequate responses to changing environment. Tunneling nanotubes (TNTs) represent a novel means of intercellular communication being a long cell-to-cell conduit. TNTs are actively formed under a broad range of stresses and are also proposed to exist under physiological conditions. Development is a physiological condition of particular interest, as it requires fine coordination. Here we discuss whether protrusions shown to exist during embryonic development of different species could be TNTs or if they represent other types of cell structure, like cytonemes or intercellular bridges, that are suggested to play an important role in development.


Biomechanical stress provides a second hit in the establishment of BMP/TGFβ-related vascular disorders

Christian Hiepen, Jerome Jatzlau and Petra Knaus

page 44-47 | 10.15698/cst2020.02.213 | Full text | PDF | Abstract

Cardiovascular disorders are still the leading cause for mortality in the western world and challenge economies with steadily increasing healthcare costs. Understanding the precise molecular pathomechanisms behind and identifying players involved in the early onset of cardiovascular diseases remains crucial for the development of new therapeutic strategies. Taking advantage of CRISPR/Cas9 gene editing in human endothelial cells (ECs), we re-investigated the early molecular steps in a genetic vascular disorder termed pulmonary arterial hypertension (PAH) in our recent study (Hiepen C., Jatzlau J. et al.; PLOS Biol, 2019). Here, mutations in the Bone Morphogenetic Protein type II receptor (BMPR2) prime for the hereditary form (HPAH) with downregulated BMPR2 followed by a characteristic change in SMAD signaling, i.e. gain in both SMAD1/5 and SMAD2/3 responses. Remarkably these cells show increased susceptibility to signaling by TGFβ due to remodeling of the extracellular matrix (ECM) and increased biomechanics acting as a secondary stressor for ECs pathobiology. This clearly places BMPR2 not only as a BMP-signaling receptor, but also as a gatekeeper to protect ECs from excess TGFβ signaling.

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