Induction of meibocyte differentiation by three-dimensional, matrigel culture of immortalized human meibomian gland epithelial cells to form acinar organoids

Nuwormegbe, Selikem Abla; Park, Na-Young; Park, Hee Joo; Jin, Yeonwoo; Kim, Sun Woong; Jester, James V.

doi:10.1016/j.jtos.2022.10.004

Cited by 6 publications

(1 citation statement)

References 44 publications

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“… 27 We conducted immunofluorescence staining for Ki67 to assess the proliferative capacity of MG and found that the acini of UPM-treated mice had a lower number of Ki67-positive cells than those of control mice ( p < 0.001). P63 and Lrig1 were both important biomarkers for basal epithelial progenitor cells in human MG which represented the actively proliferating acinar basal cells and fed new differentiating meibocytes into the developing MG. 47 , 48 Immunofluorescence images demonstrated a marked reduction in the number of P63-labeled cells and the level of Lrig1 in the acini of UPM-treated mice ( p < 0.001) ( Figs. 2 C– 2 E).…”

Section: Resultsmentioning

confidence: 97%

Urban Particulate Matter Triggers Meibomian Gland Dysfunction

Tu,

Liu,

Xue

et al. 2024

Invest. Ophthalmol. Vis. Sci.

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Purpose The meibomian gland (MG), as the largest modified sebaceous gland, is potentially damaged by urban particulate matter (UPM) based on epidemiological evidence, but the specific experimental mechanisms remain unknown. This study investigated the effects of UPM on MG dysfunction (MGD) in rodent models. Methods Female C57BL/6J mice received eye drops containing UPM suspension or PBS for 14 days. The proliferative capacity and progenitor of MG were evaluated by immunofluorescence. Cell apoptosis was confirmed by TUNEL assay, along with the analysis of caspase family expression. Lipid accumulation was visualized by Oil Red O staining and LipidTox staining. Ductal hyperkeratinization, neutrophil infiltration, and pyroptosis activation were detected through immunostaining. The relative gene expression and signaling pathway activation were determined by Western blot analysis. Results Administration of UPM caused MGD-like clinical signs, manifested as distinct corneal epithelial erosion, increased MG orifice occlusion, and glandular dropout. UPM exposure significantly induced progenitor loss, cellular apoptosis, and lipogenic disorder in MG, by reducing P63/Lrig1 expression and increasing cleaved caspase-8, -9, and -3 and meibum lipogenic protein (HMGCR/SREBP-1) expression. UPM-treated mice exhibited ductal hyperkeratinization and neutrophil recruitment. Simultaneously, pyroptosis was motivated, as indicated by the heightened expression of NLRP3 and the cleavage of caspase-1 and -4 and gasdermin D, as well as the increase in IL-1β and IL-18 downstream. The underlying pathological mechanisms of UPM involve the phosphorylation of mitogen-activated protein kinase and nuclear factor-κB. Conclusions These results provided direct evidence for the toxicity of UPM in MG. UPM-induced activation of pyroptosis and mitogen-activated protein kinase/nuclear factor-κB signaling pathway might account for the inflammatory MGD.

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Section: Resultsmentioning

confidence: 97%

Urban Particulate Matter Triggers Meibomian Gland Dysfunction

Tu,

Liu,

Xue

et al. 2024

Invest. Ophthalmol. Vis. Sci.

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Global Literature Analysis of Organoid and Organ‐on‐Chip Research

Shoji

Davis

Mummery

et al. 2023

Adv Healthcare Materials

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Organoids and cells in organ‐on‐chip platforms replicate higher‐level anatomical, physiological, or pathological states of tissues and organs. These technologies are widely regarded by academia, the pharmacological industry and regulators as key biomedical developments. To map advances in this emerging field, a meta‐analysis based on a quality‐controlled text‐mining algorithm is performed. The analysis covers titles, keywords, and abstracts of categorized academic publications in the literature and preprint databases published after 2010. The algorithm identifies and tracks 149 and 107 organs or organ substructures modeled as organoids and organ‐on‐chip, respectively, stem cell sources, as well as 130 diseases, and 16 groups of organisms other than human and mouse in which organoid/organ‐on‐chip technology is applied. The meta‐analysis illustrates changing diversity and focus in organoid/organ‐on‐chip research and captures its geographical distribution. The downloadable dataset provided is a robust framework for researchers to interrogate with their own questions.

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