Abstract
PurposeThe purpose of our study was to investigate alterations in the meibomian gland (MG) in Cu, Zn-Superoxide Dismutase-1 knockout (Sod1 −/−) mouse.MethodsTear function tests [Break up time (BUT) and cotton thread] and ocular vital staining test were performed on Sod1 −/− male mice (n = 24) aged 10 and 50 weeks, and age and sex matched wild–type (+/+) mice (n = 25). Tear and serum samples were collected at sacrifice for inflammatory cytokine assays. MG specimens underwent Hematoxylin and Eosin staining, Mallory staining for fibrosis, Oil Red O lipid staining, TUNEL staining, immunohistochemistry stainings for 4HNE, 8-OHdG and CD45. Transmission electron microscopic examination (TEM) was also performed.ResultsCorneal vital staining scores in the Sod1 −/− mice were significantly higher compared with the wild type mice throughout the follow-up. Tear and serum IL-6 and TNF-α levels also showed significant elevations in the 10 to 50 week Sod1 −/− mice. Oil Red O staining showed an accumulation of large lipid droplets in the Sod1 −/− mice at 50 weeks. Immunohistochemistry revealed both increased TUNEL and oxidative stress marker stainings of the MG acinar epithelium in the Sod1 −/− mice compared to the wild type mice. Immunohistochemistry staining for CD45 showed increasing inflammatory cell infiltrates from 10 to 50 weeks in the Sod1 −/− mice compared to the wild type mice. TEM revealed prominent mitochondrial changes in 50 week Sod1 −/− mice.ConclusionsOur results suggest that reactive oxygen species might play a vital role in the pathogensis of meibomian gland dysfunction. The Sod1 −/− mouse appears to be a promising model for the study of reactive oxygen species associated MG alterations.
Highlights
Meibomian glands (MG) are large sebaceous glands located in the tarsal plates of the eyelid that secrete a mixture of lipids and proteins called meibum onto the ocular surface, forming a superficial lipid layer that prevents the evaporation of tears [1].Abnormalities in the MGs cause instability of the tear film, resulting in either chronic irritation of, or damage to, the ocular surface epithelium
The mean weight adjusted aqueous tear production was significantly lower in the Sod12/2 mice compared to the WT mice at 10 and 50 weeks (p = 0.0079, p,0.0001, respectively) (Figure 1A)
The mean corneal vital staining score was significantly worse in the Sod12/2 mice at 10 (p = 0.0005) and 50 (p = 0.0006) weeks compared to the age matched WT mice (Figure 1C)
Summary
Meibomian glands (MG) are large sebaceous glands located in the tarsal plates of the eyelid that secrete a mixture of lipids and proteins called meibum onto the ocular surface, forming a superficial lipid layer that prevents the evaporation of tears [1].Abnormalities in the MGs cause instability of the tear film, resulting in either chronic irritation of, or damage to, the ocular surface epithelium. Hyposecretion of meibomian lipids (meibum) caused by obstruction of the gland orifices is the most common abnormality and is usually referred to as obstructive meibomian gland dysfunction (MGD). MGD is an age related disease that leads to decreased expression of glandular lipids and an increase in tear instability, leading to dry eye disease and ocular surface abnormalities [1,2,3,4,5,6]. It has been reported that the incidence of dry eye is extensive in the Japanese population aged over 60, with MGD being the predominant associated disease process, as evidenced by transillumination of the eyelids [7]. The overall prevalence of MGD is 38.9% in the US, but it increases markedly with age, from 0% for subjects under the age of 10 to 67.2% for those over the age of 60 [8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
