CSF-1-activated macrophages are target-directed and essential mediators of schwann cell dedifferentiation and dysfunction in Cx32-deficient mice

Glia ◽  
2015 ◽  
Vol 63 (6) ◽  
pp. 977-986 ◽  
Author(s):  
Janos Groh ◽  
Ines Klein ◽  
Claudia Hollmann ◽  
Jennifer Wettmarshausen ◽  
Dennis Klein ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Activated Macrophages ◽  
Cell Dedifferentiation ◽  
Deficient Mice

scholarly journals Proteasome inhibition suppresses injury‐induced myelin ovoid formation and Schwann cell dedifferentiation in the peripheral nerves

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Hwan Tae Park ◽  
Hyun Kyoung Lee ◽  
Yoon Kyung Shin ◽  
Junyang Jung ◽  
Duk Joon Suh ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerves ◽  
Proteasome Inhibition ◽  
Cell Dedifferentiation

scholarly journals Cardiac Apoptosis in Severe Relapsing Fever Borreliosis

2005 ◽  
Vol 73 (11) ◽  
pp. 7669-7676 ◽  
Author(s):  
Diana Londoño ◽  
Yunhong Bai ◽  
Wolfram R. Zückert ◽  
Harald Gelderblom ◽  
Diego Cadavid
Keyword(s):  
Persistent Infection ◽  
Rnase Protection Assay ◽  
Cardiac Injury ◽  
Significant Loss ◽  
Activated Macrophages ◽  
Relapsing Fever ◽  
Rnase Protection ◽  
Caspase 1 ◽  
Reverse Transcription Pcr ◽  
Deficient Mice

ABSTRACT Previous studies revealed that the heart suffers significant injury during experimental Lyme and relapsing fever borreliosis when the immune response is impaired (D. Cadavid, Y. Bai, E. Hodzic, K. Narayan, S. W. Barthold, and A. R. Pachner, Lab. Investig. 84:1439-1450, 2004; D. Cadavid, T. O'Neill, H. Schaefer, and A. R. Pachner, Lab. Investig. 80:1043-1054, 2000; and D. Cadavid, D. D. Thomas, R. Crawley, and A. G. Barbour, J. Exp. Med. 179:631-642, 1994). To investigate cardiac injury in borrelia carditis, we used antibody-deficient mice persistently infected with isogenic serotypes of the relapsing fever agent Borrelia turicatae. We studied infection in hearts 1 to 2 months after inoculation by TaqMan reverse transcription-PCR and immunohistochemistry (IHC) and inflammation by hematoxylin and eosin and trichrome staining, IHC, and in situ hybridization (ISH). We studied apoptosis by terminal transferase-mediated DNA nick end labeling assay and measured expression of apoptotic molecules by RNase protection assay, immunofluorescence, and immunoblot. All antibody-deficient mice, but none of the immunocompetent controls, developed persistent infection of the heart. Antibody-deficient mice infected with serotype 2 had more severe cardiac infection and injury than serotype 1-infected mice. The injury was more severe around the base of the heart and pericardium, corresponding to sites of marked infiltration by activated macrophages and upregulation of interleukin-6 (IL-6). Infected hearts showed evidence of apoptosis of macrophages and cardiomyocytes as well as significant upregulation of caspases, most notably caspase-1. We conclude that persistent infection with relapsing fever borrelias causes significant loss of cardiomyocytes associated with prominent infiltration by activated macrophages, upregulation of IL-6, induction of caspase-1, and apoptosis.

scholarly journals Axon contact-driven Schwann cell dedifferentiation

Glia ◽  
2017 ◽  
Vol 65 (6) ◽  
pp. 864-882 ◽  
Author(s):  
Jennifer Soto ◽  
Paula V. Monje
Keyword(s):  
Schwann Cell ◽  
Cell Dedifferentiation

scholarly journals Heterophilic Binding of L1 on Unmyelinated Sensory Axons Mediates Schwann Cell Adhesion and Is Required for Axonal Survival

1999 ◽  
Vol 146 (5) ◽  
pp. 1173-1184 ◽  
Author(s):  
C.A. Haney ◽  
Z. Sahenk ◽  
C. Li ◽  
V.P. Lemmon ◽  
J. Roder ◽  
...  
Keyword(s):  
Nervous System ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Sensory Nerves ◽  
Sensory Function ◽  
Trophic Effect ◽  
Unmyelinated Fibers ◽  
Sensory Axons ◽  
Unmyelinated Axons ◽  
Deficient Mice

This study investigated the function of the adhesion molecule L1 in unmyelinated fibers of the peripheral nervous system (PNS) by analysis of L1- deficient mice. We demonstrate that L1 is present on axons and Schwann cells of sensory unmyelinated fibers, but only on Schwann cells of sympathetic unmyelinated fibers. In L1-deficient sensory nerves, Schwann cells formed but failed to retain normal axonal ensheathment. L1-deficient mice had reduced sensory function and loss of unmyelinated axons, while sympathetic unmyelinated axons appeared normal. In nerve transplant studies, loss of axonal-L1, but not Schwann cell-L1, reproduced the L1-deficient phenotype. These data establish that heterophilic axonal-L1 interactions mediate adhesion between unmyelinated sensory axons and Schwann cells, stabilize the polarization of Schwann cell surface membranes, and mediate a trophic effect that assures axonal survival.

scholarly journals A spontaneously immortalized Schwann cell line from aldose reductase-deficient mice as a useful tool for studying polyol pathway and aldehyde metabolism

2018 ◽  
Vol 144 (6) ◽  
pp. 710-722 ◽  
Author(s):  
Naoko Niimi ◽  
Hideji Yako ◽  
Shizuka Takaku ◽  
Hiroshi Kato ◽  
Takafumi Matsumoto ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Cell Line ◽  
Aldose Reductase ◽  
Polyol Pathway ◽  
Deficient Mice

Lysophosphatidic acid propagates post-injury Schwann cell dedifferentiation through LPA1 signaling

2018 ◽  
Vol 662 ◽  
pp. 136-141 ◽  
Author(s):  
Fabian Szepanowski ◽  
Leon-Phillip Szepanowski ◽  
Anne K. Mausberg ◽  
Christoph Kleinschnitz ◽  
Bernd C. Kieseier ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Lysophosphatidic Acid ◽  
Post Injury ◽  
Cell Dedifferentiation
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