Nien Chyong Jy, Massei Salina, Lin Gloria, Nabavi Cameron, Tao Jeremiah, Brown Donald J, Paugh Jerry R, Jester James V
Gavin Herbert Eye Institute, Medical Center, University of California-Irvine, 101 The City Drive, Orange, CA 92868, USA.
Arch Ophthalmol. 2011 Apr;129(4):462-9. doi: 10.1001/archophthalmol.2011.69.
To identify age-related changes in human meibomian glands that may be associated with meibomian gland dysfunction (MGD).
Excess eyelid tissue from 36 patients (age range, 18-95 years, 19 female, 17 male) who underwent canthoplasty procedures were used. Dermatologic history, age, and presence of MGD were recorded. Samples were frozen, sectioned, and stained with specific antibodies against peroxisome proliferator-activated receptor γ (PPARγ) to identify meibocyte differentiation, Ki67 nuclear antigen to identify cycling cells, and CD45 to identify inflammatory cell infiltration.
Staining for PPARγ showed cytoplasmic and nuclear localization in the 2 youngest subjects (ages, 18 and 44 years). Older individuals (>60 years) showed predominantly nuclear staining, with cytoplasmic staining limited to the basal acinar cells in 17 of 31 subjects. The number of Ki67 positively stained basal cells were significantly elevated in the younger compared with older subjects based on linear regression analysis (r(2) = 0.35; P < .001). There was also a significant correlation between MG expression grade and CD45 cell infiltration (r = 0.414; P = .05).
These results indicate that aging human meibomian glands show decreased meibocyte differentiation and cell cycling that is associated with the development of MGD. Findings also suggest that altered PPARγ signaling may lead to acinar atrophy and development of an age-related hyposecretory MGD.
Meibomian gland dysfunction and evaporative dry eye are common age-related eyelid disorders. Understanding the underlying mechanism of MGD may lead to the development of novel therapeutic strategies to treat this disease.
确定人类睑板腺中可能与睑板腺功能障碍(MGD)相关的年龄相关变化。
使用36例接受眦成形术患者(年龄范围18 - 95岁,女性19例,男性17例)的多余眼睑组织。记录皮肤病史、年龄和MGD的存在情况。样本经冷冻、切片,并用抗过氧化物酶体增殖物激活受体γ(PPARγ)的特异性抗体染色以鉴定睑板腺细胞分化,用Ki67核抗原染色以鉴定增殖细胞,用CD45染色以鉴定炎性细胞浸润。
PPARγ染色显示,2名最年轻受试者(年龄分别为18岁和44岁)中PPARγ定位于细胞质和细胞核。年龄较大的个体(>60岁)主要表现为细胞核染色,31名受试者中有17名的细胞质染色仅限于基底腺泡细胞。基于线性回归分析,与老年受试者相比,年轻受试者中Ki67阳性染色的基底细胞数量显著升高(r² = 0.35;P < 0.001)。睑板腺表达分级与CD45细胞浸润之间也存在显著相关性(r = 0.414;P = 0.05)。
这些结果表明,衰老的人类睑板腺显示睑板腺细胞分化和细胞增殖减少,这与MGD的发生有关。研究结果还表明,PPARγ信号改变可能导致腺泡萎缩和与年龄相关的分泌减少型MGD的发生。
睑板腺功能障碍和蒸发过强型干眼是常见的与年龄相关的眼睑疾病。了解MGD的潜在机制可能会导致开发治疗该疾病的新治疗策略。