PMID- 23271640
OWN - NLM
STAT- MEDLINE
DCOM- 20130904
LR  - 20220331
IS  - 1573-6830 (Electronic)
IS  - 0272-4340 (Linking)
VI  - 33
IP  - 3
DP  - 2013 Apr
TI  - Reduced levels of brain derived neurotrophic factor (BDNF) in the serum of 
      diabetic retinopathy patients and in the retina of diabetic rats.
PG  - 359-67
LID - 10.1007/s10571-012-9901-8 [doi]
AB  - Diabetic retinopathy (DR) is widely recognized as a neurovascular disease. 
      Retina, being a neuronal tissue of the eye, produces neurotrophic factors for its 
      maintenance. However, diabetes dysregulates their levels and thereby may damage 
      the retina. Among neurotrophins, brain derived neurotrophic factor (BDNF) is the 
      most abundant in the retina. In this study, we investigated the level of BDNF in 
      the serum of patients with DR and also in the serum and retina of 
      streptozotocin-induced diabetic rats. The level of BDNF was significantly 
      decreased in the serum of proliferative diabetic retinopathy patients as compared 
      to that of non-diabetic healthy controls (25.5 +/- 8.5-10.0 +/- 8.1 ng/ml, p < 0.001) 
      as well as compared to that of diabetic patients with no retinopathy (21.8 +/- 
      4.7-10.0 +/- 8.1 ng/ml, p < 0.001), as measured by ELISA techniques. The levels of 
      BDNF in the serum and retina of diabetic rats were also significantly reduced 
      compared to that of non-diabetic controls (p < 0.05). In addition, the expression 
      level of tropomyosin-related kinase B (TrkB) was significantly decreased in 
      diabetic rat retina compared to that of non-diabetic controls as determined by 
      Western blotting technique. Caspase-3 activity was increased in diabetic rat 
      retina after 3 weeks of diabetes and remained elevated until 10 weeks, which 
      negatively correlated with the level of BDNF (r = -0.544, p = 0.013). Our results 
      indicate that reduced levels of BDNF in diabetes may cause apoptosis and 
      neurodegeneration early in diabetic retina, which may lead to neuro-vascular 
      damage later in DR.
FAU - Ola, M Shamsul
AU  - Ola MS
AD  - Department of Biochemistry, College of Science, King Saud University, Riyadh, 
      11415, Saudi Arabia. mola@ksu.edu.sa
FAU - Nawaz, Mohd Imtiaz
AU  - Nawaz MI
FAU - El-Asrar, Ahmed Abu
AU  - El-Asrar AA
FAU - Abouammoh, Marwan
AU  - Abouammoh M
FAU - Alhomida, Abdullah S
AU  - Alhomida AS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121228
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/*blood
MH  - Case-Control Studies
MH  - Caspase 3/metabolism
MH  - Demography
MH  - Diabetes Mellitus, Experimental/blood/*metabolism
MH  - Diabetic Retinopathy/*blood/enzymology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Rats
MH  - Receptor, trkB/metabolism
MH  - Retina/enzymology/*metabolism/pathology
EDAT- 2012/12/29 06:00
MHDA- 2013/09/05 06:00
CRDT- 2012/12/29 06:00
PHST- 2012/10/18 00:00 [received]
PHST- 2012/12/13 00:00 [accepted]
PHST- 2012/12/29 06:00 [entrez]
PHST- 2012/12/29 06:00 [pubmed]
PHST- 2013/09/05 06:00 [medline]
AID - 10.1007/s10571-012-9901-8 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2013 Apr;33(3):359-67. doi: 10.1007/s10571-012-9901-8. Epub 
      2012 Dec 28.