scholarly journals YAP and TAZ control peripheral myelination and the expression of laminin receptors in Schwann cells

2016 ◽  
Vol 19 (7) ◽  
pp. 879-887 ◽  
Author(s):  
Yannick Poitelon ◽  
Camila Lopez-Anido ◽  
Kathleen Catignas ◽  
Caterina Berti ◽  
Marilena Palmisano ◽  
...  
2002 ◽  
Vol 156 (1) ◽  
pp. 199-210 ◽  
Author(s):  
M. Laura Feltri ◽  
Diana Graus Porta ◽  
Stefano C. Previtali ◽  
Alessandro Nodari ◽  
Barbara Migliavacca ◽  
...  

In dystrophic mice, a model of merosin-deficient congenital muscular dystrophy, laminin-2 mutations produce peripheral nerve dysmyelination and render Schwann cells unable to sort bundles of axons. The laminin receptor and the mechanism through which dysmyelination and impaired sorting occur are unknown. We describe mice in which Schwann cell–specific disruption of β1 integrin, a component of laminin receptors, causes a severe neuropathy with impaired radial sorting of axons. β1-null Schwann cells populate nerves, proliferate, and survive normally, but do not extend or maintain normal processes around axons. Interestingly, some Schwann cells surpass this problem to form normal myelin, possibly due to the presence of other laminin receptors such as dystroglycan and α6β4 integrin. These data suggest that β1 integrin links laminin in the basal lamina to the cytoskeleton in order for Schwann cells to ensheath axons, and alteration of this linkage contributes to the peripheral neuropathy of congenital muscular dystrophy.


Author(s):  
Å. Thureson-Klein

Giant mitochondria of various shapes and with different internal structures and matrix density have been observed in a great number of tissues including nerves. In most instances, the presence of giant mitochondria has been associated with a known disease or with abnormal physiological conditions such as anoxia or exposure to cytotoxic compounds. In these cases degenerative changes occurred in other cell organelles and, therefore the giant mitochondria also were believed to be induced structural abnormalities.Schwann cells ensheating unmyelinated axons of bovine splenic nerve regularly contain giant mitochondria in addition to the conventional smaller type (Fig. 1). These nerves come from healthy inspected animals presumed not to have been exposed to noxious agents. As there are no drastic changes in the small mitochondria and because other cell components also appear reasonably well preserved, it is believed that the giant mitochondria are normally present jin vivo and have not formed as a post-mortem artifact.


Author(s):  
R.L. Martuza ◽  
T. Liszczak ◽  
A. Okun ◽  
T-Y Wang

Neurofibromatosis (NF) is an autosomal dominant genetic disorder with a prevalence of 1/3,000 births. The NF mutation causes multiple abnormalities of various cells of neural crest origin. Schwann cell tumors (neurofibromas, acoustic neuromas) are the most common feature of neurofibromatosis although meningiomas, gliomas, and other neoplasms may be seen. The schwann cell tumors commonly develop from the schwann cells associated with sensory or sympathetic nerves or their ganglia. Schwann cell tumors on ventral spinal roots or motor cranial nerves are much less common. Since the sensory neuron membrane is known to contain a mitogenic factor for schwann cells, we have postulated that neurofibromatosis may be due to an abnormal interaction between the nerve and the schwann cell and that this interaction may be hormonally modulated. To test this possibility a system has been developed in which an enriched schwannoma cell culture can be obtained and co-cultured with pure neurons.


2006 ◽  
Vol 22 (06) ◽  
Author(s):  
Deborah Yu ◽  
Sherri Wood ◽  
Keri Smith ◽  
Keith Bishop ◽  
Paul Cederna

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