Chromatin distribution pattern and cell functioning

Chromatin distribution patterns of the nuclei of the follicular epithelial cell of Dendroctonus pseudotsugae Hopk. (Scolytidae: Coleoptera) were analyzed after creating their digital images. The five cell populations examined consisted of follicular epithelial cells at three different stages of structural and functional differentiation and two populations in which this differentiation was blocked. The results show that chromatin distribution patterns differ when cells are structurally and functionally different but are not different in cells that are structurally, developmentally, and functionally similar. The procedures are capable of detecting minute differences and appear useful for early detection of developmental and functional changes in relation to normal and pathological conditions.

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Basal Autophagy Deficiency Causes Thyroid Follicular Epithelial Cell Death in Mice

Endocrinology ◽

10.1210/en.2019-00312 ◽

2019 ◽

Vol 160 (9) ◽

pp. 2085-2092 ◽

Cited By ~ 3

Author(s):

Tomomi Kurashige ◽

Yasuyo Nakajima ◽

Mika Shimamura ◽

Mutsumi Matsuyama ◽

Masanobu Yamada ◽

...

Keyword(s):

Cell Death ◽

Epithelial Cell ◽

Gene Knockout ◽

Tissue Degeneration ◽

Serum T4 ◽

Follicular Epithelial Cell ◽

Thyroid Morphology ◽

And Function ◽

Cellular Components ◽

Follicular Epithelial

Abstract Autophagy is a catabolic process that involves the degradation of cellular components through the lysosomal machinery, relocating nutrients from unnecessary processes to more pivotal processes required for survival. It has been reported that systemic disruption of the Atg5 or Atg7 gene, a component of autophagy, is lethal and that its tissue-specific disruption causes tissue degeneration in several organs. However, the functional significance of autophagy in the thyroid glands remains unknown. Our preliminary data imply the possible involvement of dysfunctional autophagy in radiation-induced thyroid carcinogenesis. Therefore, we evaluated the effect of Atg5 gene knockout (KO) on thyroid morphology and function. To this end, Atg5flox/flox mice were crossed with TPO-Cre mice, yielding the thyroid follicular epithelial cell (thyrocyte)‒specific ATG5-deficient mice (Atg5thyr-KO/KO). Atg5 gene KO was confirmed by a lack of ATG5 expression, and disruption of autophagy was demonstrated by a decrease in microtubule-associated protein 1 light chain 3–II puncta and an increase in p62. Atg5thyr-KO/KO mice were born normally, and thyroid morphology, thyroid weights, and serum T4 and TSH levels were almost normal at 4 months. However, at 8 and 12 months, a decrease in the number of thyrocytes and an increase in TUNEL+-thyrocytes were observed in Atg5thyr-KO/KO mice even though thyroid function was still normal. The number of irregularly shaped (gourd-shaped) follicles was also increased. Excess oxidative stress was indicated by increased 8-hydroxy-2′-deoxyguanosine and 53BP1 foci in Atg5thyr-KO/KO mice. These data demonstrate that thyrocytes gradually undergo degradation/cell death in the absence of basal levels of autophagy, indicating that autophagy is critical for the quality control of thyrocytes.

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