Early detection and initiation of treatment is important to prevent the loss of visual function due to glaucoma, which is one of the leading causes of blindness worldwide. Moreover, it may be important to establish strategies for controlling intraocular pressure (IOP) in glaucoma patients via clarification of morphological abnormalities in aqueous outflow routes. It has been reported that in healthy eyes, 49% to 75% of the total aqueous outflow resistance is located between the anterior chamber and Schlemm's canal (SC).
1,2 Previous research related to aqueous outflow has focused on juxtacanalicular tissue (JCT), as it is considered to be the primary site of outflow resistance, which causes an increase in IOP. In particular, JCT is reportedly considered to be the site of highest aqueous humor outflow resistance.
3 Moreover, it has been reported that the occurrence of juvenile glaucoma is related to abnormality of the JCT.
4 On the other hand, although it has been reported that minimum outflow resistance of aqueous humor exists at the SC inner wall,
3 SC endothelial cells (ECs) do play some roles in the outflow of aqueous humor. Pathological changes of SC (e.g., closure of SC due to uveitis and primary angle-closure glaucoma [PACG]), may cause severe obstruction of the outflow pathways.
5–7 Aging is known to be one of the leading risk factors for primary open-angle glaucoma (POAG),
8–15 and the results of most epidemiological studies have shown that age is an important risk factor for glaucoma. Several studies have shown a relationship between IOP elevation in POAG patients and the age-related morphological changes (i.e., thickening of the trabecular meshwork [TM]),
16 progressive decrease in trabecular cellularity,
17 and accumulation of extracellular matrix in JCT.
18 Although the findings of previous reports have shown a relationship between aging and the function of SC in healthy eyes,
19,20 there has yet to be a study regarding age-related SC abnormalities in the eyes of POAG patients. Gramer et al.
21 reported that patients with a family history of glaucoma, including POAG, were significantly younger at diagnosis than patients without a family history of glaucoma. Therefore, we theorized that it would be interesting to investigate morphological abnormalities of SC in POAG from the aspect of aging by comparing the patients with a family history and without a family history of POAG. Blood vessel endothelium expresses anticoagulant thrombomodulin and procoagulant von Willebrand factor; however, expression of these opposing substances is different according to the function of the organs where those blood vessels exist. Thrombomodulin-dominant endothelial cells have been reported in alveolar capillaries
22 and SC endothelial cells (SC-ECs).
23 Immunohistochemical staining of thrombomodulin and/or CD34 is an excellent marker for identification of SC-ECs.
23 Thrombomodulin immunostaining is especially useful for identification of SC-ECs in PACG eyes with partial EC loss.
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