PMID- 28002846
OWN - NLM
STAT- MEDLINE
DCOM- 20170615
LR  - 20171220
IS  - 1552-5783 (Electronic)
IS  - 0146-0404 (Linking)
VI  - 57
IP  - 15
DP  - 2016 Dec 1
TI  - Unchanged Neurotrophic Factors and Their Receptors Correlate With Sparing in 
      Extraocular Muscles in Amyotrophic Lateral Sclerosis.
PG  - 6831-6842
LID - 10.1167/iovs.16-20074 [doi]
AB  - PURPOSE: To investigate the impact of amyotrophic lateral sclerosis (ALS) on the 
      extraocular muscles (EOMs) by examining the distribution of neurotrophic factors 
      (NTFs) and their receptors in EOMs and limb muscles from ALS transgenic mice. 
      METHODS: Muscle samples collected from transgenic mice overexpressing human 
      superoxide dismutase type 1 mutations (SOD1G93A, the most widely used mouse model 
      of ALS) at 50 and 150 days as well as age-matched controls were analyzed with 
      immunohistochemistry using antibodies against brain-derived neurotrophic factor 
      (BDNF), neurotrophin-3 (NT-3), neurotrophin-4/5 (NT-4), glial cell line-derived 
      neurotrophic factor (GDNF), and the neurotrophin receptors p75NTR, tyrosine 
      kinase (Trk) receptor TrkB and TrkC, and GDNF family receptor alpha-1 (GFRalpha-1). 
      RESULTS: There was an intrinsic difference in NTF expression between EOMs and 
      limb muscles in control mice: EOMs presented significantly lower number of 
      neuromuscular junctions (NMJs) labeled for BDNF and NT-4 at 50 days, and for BDNF 
      and GDNF at 150 days, compared with the control limb muscles of corresponding 
      age. In ALS transgenic mice at 150 days, NTF expression in limb muscles was 
      significantly changed but not in EOMs: the limb muscles presented a significant 
      decline in the number of NMJs labeled for BDNF, NT-4, GDNF, p75NTR, TrkB, and 
      TrkC, which was not observed in EOMs. CONCLUSIONS: The significant differences in 
      expression of NTFs on NMJs between EOMs and limb muscles in both control and ALS 
      transgenic mice suggest that NTF may be involved in the pathogenesis of ALS and 
      the resistance of EOMs to the disease.
FAU - Harandi, Vahid M
AU  - Harandi VM
AD  - Department of Integrative Medical Biology, Section for Anatomy, Umea University, 
      Umea, Sweden 2Department of Clinical Sciences, Ophthalmology, Umea University, 
      Umea, Sweden.
FAU - Gaied, Aida R N
AU  - Gaied AR
AD  - Department of Clinical Sciences, Ophthalmology, Umea University, Umea, Sweden.
FAU - Brannstrom, Thomas
AU  - Brannstrom T
AD  - Department of Medical Biosciences, Pathology, Umea University, Umea, Sweden.
FAU - Pedrosa Domellof, Fatima
AU  - Pedrosa Domellof F
AD  - Department of Integrative Medical Biology, Section for Anatomy, Umea University, 
      Umea, Sweden 2Department of Clinical Sciences, Ophthalmology, Umea University, 
      Umea, Sweden.
FAU - Liu, Jing-Xia
AU  - Liu JX
AD  - Department of Integrative Medical Biology, Section for Anatomy, Umea University, 
      Umea, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Receptors, Nerve Growth Factor)
SB  - IM
MH  - Amyotrophic Lateral Sclerosis/*metabolism/pathology
MH  - Animals
MH  - Cell Line
MH  - Disease Models, Animal
MH  - Humans
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Motor Neurons/metabolism
MH  - Muscle, Skeletal/*metabolism/pathology
MH  - Nerve Growth Factors/*metabolism
MH  - Neuromuscular Junction/metabolism
MH  - Oculomotor Muscles/*metabolism/pathology
MH  - Receptors, Nerve Growth Factor/*metabolism
EDAT- 2016/12/22 06:00
MHDA- 2017/06/16 06:00
CRDT- 2016/12/22 06:00
PHST- 2016/12/22 06:00 [entrez]
PHST- 2016/12/22 06:00 [pubmed]
PHST- 2017/06/16 06:00 [medline]
AID - 2595000 [pii]
AID - 10.1167/iovs.16-20074 [doi]
PST - ppublish
SO  - Invest Ophthalmol Vis Sci. 2016 Dec 1;57(15):6831-6842. doi: 
      10.1167/iovs.16-20074.