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Yukitaka Danjo, Linda D. Hazlett, Ilene K. Gipson; C57BL/6 Mice Lacking Muc1 Show No Ocular Surface Phenotype. Invest. Ophthalmol. Vis. Sci. 2000;41(13):4080-4084.
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© ARVO (1962-2015); The Authors (2016-present)
purpose. To test the hypothesis that a membrane-spanning mucin, Muc1,
facilitates the spread of tear film and protects against bacterial
methods. Age-matched, Muc1 null mice and wild-type mice of
C57BL/6 genetic background were used for comparison. Eyes were examined
by slit lamp biomicroscopy with fluorescein solution to assess
epithelial damage and tear film stability. Structure of the ocular
surface epithelia was examined by light microscopy, scanning and
transmission electron microscopy, and wholemount confocal microscopy.
Bacterial adherence assay was performed on in vivo corneas with Pseudomonas aeruginosa containing a plasmid encoding
green fluorescent protein, followed by wholemount confocal microscopy.
Real-time reverse transcription–polymerase chain reaction was
performed using Muc4-specific primers to quantitate Muc4
mRNA expression in ocular surface tissues.
results. No differences were found between Muc1 null and control
mice in any parameter tested. Ocular surface epithelia of Muc1 null mice of the C57BL/6 strain had a normal
appearance of surface microplicae, a well-developed glycocalyx on the
apical cell membrane, and a normal appearance of goblet cell mucin
packets. There was no convincing evidence that bacterial adherence on
the cornea was increased in Muc1 null mice. Muc4 mRNA
expression was not upregulated in Muc1 null mice
compared with control. No ocular surface infections were observed in Muc1 null mice of the C57BL/6 strain (n = 204), which were housed in the animal facility over a period of 26
conclusions. Muc1 null mice of C57BL/6 background appeared normal in
all respects tested. These data differ from the reported phenotype in
the mice of the C57BL/6 x SVJ129 background, which show development of
blepharitis and conjunctivitis.
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