PMID- 9519752
OWN - NLM
STAT- MEDLINE
DCOM- 19980407
LR  - 20220409
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 47
IP  - 3
DP  - 1998 Mar
TI  - Muller cell changes in human diabetic retinopathy.
PG  - 445-9
AB  - Vascular cells may not be the only cells affected by diabetes in the retina. In 
      particular, abnormalities of the b-wave of the electroretinogram in diabetic 
      patients with absent or minimal microangiopathy have pointed to possible 
      dysfunction of Muller cells, the principal glia of the retina. In this study, we 
      sought evidence for diabetes-induced Muller cell abnormalities by testing the 
      expression of three proteins (Bcl-2, glutamine synthetase [GS], and glial 
      fibrillar acidic protein [GFAP]) that are solely or predominantly expressed in 
      Muller cells and show a reproducible pattern of changes in the context of retinal 
      injuries or degenerations. Retinas obtained postmortem from a total of 14 donors 
      aged 65 +/- 6 years with 10 +/- 4 years of diabetes and histological evidence of 
      microangiopathy and 18 age-matched nondiabetic donors were examined by 
      immunohistochemistry and immunoblotting. The typical Muller cell pattern of Bcl-2 
      and GS immunostaining was similar for both intensity and distribution in the 
      nondiabetic and diabetic retinas, as were the levels of the two proteins. In 
      contrast, GFAP staining, largely confined to the most proximal retina in the 
      nondiabetic donors, was in most diabetic retinas present along the entire length 
      of the Muller cell processes, throughout the outer retina. Accordingly, the level 
      of GFAP was increased in the diabetic retinas (161 +/- 106 densitometric 
      units/microg protein vs. 55 +/- 45 in the nondiabetic retinas, P = 0.03). These 
      data provide evidence for selective biosynthetic changes of Muller glial cells in 
      diabetes. Because Muller cells produce factors capable of modulating blood flow, 
      vascular permeability, and cell survival, and their processes surround all blood 
      vessels in the retina, a possible role of these cells in the pathogenesis of 
      retinal microangiopathy deserves to be investigated.
FAU - Mizutani, M
AU  - Mizutani M
AD  - Schepens Eye Research Institute and Department of Ophthalmology, Harvard Medical 
      School, Boston, Massachusetts 02114, USA.
FAU - Gerhardinger, C
AU  - Gerhardinger C
FAU - Lorenzi, M
AU  - Lorenzi M
LA  - eng
GR  - EY09122/EY/NEI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (BCL2L1 protein, human)
RN  - 0 (Bcl2l1 protein, mouse)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Immune Sera)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (bcl-X Protein)
RN  - EC 6.3.1.2 (Glutamate-Ammonia Ligase)
SB  - IM
MH  - Aged
MH  - Animals
MH  - Antibodies, Monoclonal/immunology
MH  - Cattle
MH  - Chickens
MH  - Cohort Studies
MH  - Diabetic Retinopathy/enzymology/*pathology
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Female
MH  - Glial Fibrillary Acidic Protein/*analysis
MH  - Glutamate-Ammonia Ligase/*analysis
MH  - Humans
MH  - Immune Sera/immunology
MH  - Immunoblotting
MH  - Immunohistochemistry
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - Proto-Oncogene Proteins c-bcl-2/*analysis
MH  - Rabbits
MH  - Retina/cytology/*pathology
MH  - Tissue Donors
MH  - bcl-X Protein
EDAT- 1998/03/31 00:00
MHDA- 1998/03/31 00:01
CRDT- 1998/03/31 00:00
PHST- 1998/03/31 00:00 [pubmed]
PHST- 1998/03/31 00:01 [medline]
PHST- 1998/03/31 00:00 [entrez]
AID - 10.2337/diabetes.47.3.445 [doi]
PST - ppublish
SO  - Diabetes. 1998 Mar;47(3):445-9. doi: 10.2337/diabetes.47.3.445.