scholarly journals PPARγ regulates meibocyte differentiation and lipid synthesis of cultured human meibomian gland epithelial cells (hMGEC)

2018 ◽  
Vol 16 (4) ◽  
pp. 463-469 ◽  
Author(s):  
Sun Woong Kim ◽  
Yilu Xie ◽  
Paul Q. Nguyen ◽  
Vickie T. Bui ◽  
Kelly Huynh ◽  
...  
Cornea ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Jillian F. Ziemanski ◽  
Landon Wilson ◽  
Stephen Barnes ◽  
Kelly K. Nichols

2014 ◽  
Vol 55 (6) ◽  
pp. 3866 ◽  
Author(s):  
David A. Sullivan ◽  
Yang Liu ◽  
Wendy R. Kam ◽  
Juan Ding ◽  
Karin M. Green ◽  
...  

2018 ◽  
Vol 314 (1) ◽  
pp. C43-C52 ◽  
Author(s):  
Meiqiang Chu ◽  
Yong Zhao ◽  
Shuai Yu ◽  
Yanan Hao ◽  
Pengfei Zhang ◽  
...  

Mammary epithelial cells are regulated by steroid hormones, growth factors, and even microRNAs. miR-15b has been found to regulate lipid metabolism in adipocytes; however, its effects on lipid metabolism in mammary epithelial cells, the cells of lipid synthesis and secretion, are as yet unknown. The main purpose of this investigation was to explore the effect of miR-15b on lipid metabolism in mammary epithelial cells, along with the underlying mechanisms. miR-15b was overexpressed or inhibited by miRNA mimics or inhibitors; subsequently, lipid formation in mammary epithelial cells, and proteins related to lipid metabolism, were investigated. Through overexpression or inhibition of miR-15b expression, the current investigation found that miR-15b downregulates lipid metabolism in mammary epithelial cells and is expressed differentially at various stages of mouse and goat mammary gland development. Inhibition of miR-15b expression increased lipid content in mammary epithelial cells through elevation of the lipid synthesis enzyme fatty acid synthetase (FASN), and overexpression of miR-15b reduced lipid content in mammary epithelial cells with decreasing levels of FASN. Moreover, the steroid hormones estradiol and progesterone decreased miR-15b expression with a subsequent increase in lipid formation in mammary epithelial cells. The expression of miR-15b was lower during lactation and negatively correlated with lipid synthesis proteins, which suggests that it may be involved in lipid synthesis and milk production. miR-15b might be a useful target for altering lipid production and milk yield.


Biology ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1226
Author(s):  
Yujia Jing ◽  
Yifei Chen ◽  
Shan Wang ◽  
Jialiang Ouyang ◽  
Liangyu Hu ◽  
...  

PER2, a circadian clock gene, is associated with mammary gland development and lipid synthesis in rodents, partly via regulating peroxisome proliferator-activated receptor gamma (PPARG). Whether such a type of molecular link existed in bovines was unclear. We hypothesized that PER2 was associated with lipid metabolism and regulated cell cycles and apoptosis in bovine mammary epithelial cells (BMECs). To test this hypothesis, BMECs isolated from three mid-lactation (average 110 d postpartum) cows were used. The transient transfection of small interfering RNA (siRNA) was used to inhibit PER2 transcription in primary BMECs. The silencing of PER2 led to lower concentrations of cellular lipid droplets and triacylglycerol along with the downregulation of lipogenic-related genes such as ACACA, FASN, LPIN1, and SCD, suggesting an overall inhibition of lipogenesis and desaturation. The downregulation of PPARG and SREBF1 in response to PER2 silencing underscored the importance of circadian clock signaling and the transcriptional regulation of lipogenesis. Although the proliferation of BMECs was not influenced by PER2 silencing, the number of cells in the G2/GM phase was upregulated. PER2 silencing did not affect cell apoptosis. Overall, the data provided evidence that PER2 participated in the coordination of mammary lipid metabolism and was potentially a component of the control of lipid droplets and TAG synthesis in ruminant mammary cells. The present data suggested that such an effect could occur through direct effects on transcriptional regulators.


Cornea ◽  
2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Di Chen ◽  
Jingyi Wang ◽  
David A. Sullivan ◽  
Wendy R. Kam ◽  
Yang Liu

2021 ◽  
pp. 108719
Author(s):  
Minh Anh Thu Phan ◽  
Michele C. Madigan ◽  
Mark Willcox ◽  
Fiona Stapleton ◽  
Blanka Golebiowski

1994 ◽  
Vol 42 (9) ◽  
pp. 1187-1199 ◽  
Author(s):  
A Khoor ◽  
M T Stahlman ◽  
M E Gray ◽  
J A Whitsett

We determined the temporal and spatial distribution of surfactant protein B (pro-SP-B) and C (pro-SP-C) mRNAs and proteins by immunohistochemistry and in situ hybridization in fetal, neonatal, and adult human lung. Pro-SP-B and SP-B mRNA were detected in bronchi and bronchioles by 15 weeks' gestation. After 25 weeks, pro-SP-B, active SP-B peptide, and SP-B mRNA were co-localized in bronchiolo-alveolar portal cells and in Type II epithelial cells. In adult lung, pro-SP-B and SP-B mRNA were detected primarily in non-ciliated bronchiolar epithelial cells and in Type II cells in the alveolus. Pro-SP-C and SP-C mRNA were detected in cells lining terminal airways from 15 weeks' gestation and thereafter. After 25 weeks, SP-C mRNA and precursor protein were detected in epithelial cells of the bronchiolo-alveolar portals and in Type II cells, where expression increased with advancing gestational age. Distinct cellular patterns of staining for pro-SP-B compared with SP-B active peptide support the concept that its proteolytic processing or cellular routing may be influenced by cell type and/or cell differentiation. SP-B and SP-C are expressed primarily in distal conducting and terminal airway epithelium of human fetal lung well in advance of surfactant lipid synthesis or physiologic requirements to produce pulmonary surfactant at the time of birth.


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