scholarly journals Dual Switch in Lipid Metabolism in Cervical Epithelial Cells during Dysplasia Development Observed Using Raman Microscopy and Molecular Methods

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1997
Author(s):  
Katarzyna Sitarz ◽  
Krzysztof Czamara ◽  
Joanna Bialecka ◽  
Malgorzata Klimek ◽  
Slawa Szostek ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Lipid Content ◽  
Raman Microscopy ◽  
Molecular Methods ◽  
Gene Methylation ◽  
Squamous Carcinoma Cells ◽  
Cervical Epithelial Cells ◽  
Srebf1 Gene

Cellular lipid metabolism is significantly transformed during oncogenesis. To assess how dysplasia development influences lipid cellular metabolisms and what is the molecular background behind it, cervical epithelial cells of 63 patients assigned to seven groups (based on the cytological examination and HPVhr test results) were studied using a multimethodological approach including Raman microscopy and molecular methods. The consistent picture obtained studying the lipid content, cell inflammation, SREBF1 gene methylation (hence SREBP1 inhibition) and level of mitochondrial DNA copies (indirectly the number of mitochondria) showed that changes in lipid metabolism were multidirectional. Cells from patients classified as mildly dysplastic (LSIL) exhibited a unique behavior (the highest level of inflammation and SREBF1 methylation, the lowest lipid content and mitochondrial DNA). On the contrary, cells from severe dysplastic (HSIL) and cancer (SCC) groups showed the opposite characteristics including the lowest SREBF1 gene methylation as well as the highest level of mitochondrial DNA and lipid cellular concentration (for HSIL/HPVhr+ and SCC groups). Following dysplastic progression, the lipid content decreases significantly (compared to the control) for mildly abnormal cells, but then increases for HSIL/HPVhr+ and SCC groups. This intriguing dual switch in lipid metabolism (reflected also in other studied parameters) on the way from normal to squamous carcinoma cells is of potential diagnostic interest.

scholarly journals miR-15b negatively correlates with lipid metabolism in mammary epithelial cells

2018 ◽  
Vol 314 (1) ◽  
pp. C43-C52 ◽  
Author(s):  
Meiqiang Chu ◽  
Yong Zhao ◽  
Shuai Yu ◽  
Yanan Hao ◽  
Pengfei Zhang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Steroid Hormones ◽  
Lipid Content ◽  
Mammary Epithelial Cells ◽  
Lipid Production ◽  
Fatty Acid Synthetase ◽  
Lipid Synthesis ◽  
Mammary Epithelial ◽  
Lipid Formation

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.

BIOASSAY OF PROLACTIN

1969 ◽  
Vol 60 (1) ◽  
pp. 91-100 ◽  
Author(s):  
Charles S. Nicoll
Keyword(s):  
Epithelial Cells ◽  
Lipid Content ◽  
Dry Weight ◽  
Fat Content ◽  
Assay Sensitivity ◽  
Mucosal Epithelium ◽  
Wet Weight ◽  
Total Dry Weight

ABSTRACT The response of the pigeon crop-sac to systemically acting prolactin (injected subcutaneously) was evaluated by measuring the wet weight of the responsive lateral lobes of the organ and by determining the dry weight of a 4 cm diameter disc of mucosal epithelium taken from one hemicrop. Of several different injection schedules tested, administration of prolactin in four daily injections was found to yield optimal responses. When compared with a graded series of prolactin doses, measurement of the mucosal dry weight proved to be a better method of response quantification than determination of the crop-sac wet weight with respect to both assay sensitivity and precision. The submucosal tissue of the crop-sac was estimated to constitute about 64 % of the total dry weight of the unstimulated organ and it was found to be relatively unresponsive to prolactin stimulation in comparison with the mucosa. The lipid content of the mucosal epithelium was determined using unstimulated crop-sacs or tissues which showed varying degrees of prolactin-induced proliferation. The fat content of the mucosal epithelial cells increased only slightly more rapidly than the dry weight or the defatted dry weight of the mucosa. Suggestions are made for the further improvement of the systemic crop-sac assay for prolactin.

scholarly journals Identification of the molecular regulation of differences in lipid deposition in dedifferentiated preadipocytes from different chicken tissues

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Zheng Ma ◽  
Na Luo ◽  
Lu Liu ◽  
Huanxian Cui ◽  
Jing Li ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Lipid Content ◽  
Regulatory Network ◽  
Total Lipid Content ◽  
Fatty Acid Transport ◽  
Lipid Deposition ◽  
Ppar Signaling ◽  
The Difference

Abstract Background A body distribution with high intramuscular fat and low abdominal fat is the ideal goal for broiler breeding. Preadipocytes with different origins have differences in terms of metabolism and gene expression. The transcriptome analysis performed in this study of intramuscular preadipocytes (DIMFPs) and adipose tissue-derived preadipocytes (DAFPs) aimed to explore the characteristics of lipid deposition in different chicken preadipocytes by dedifferentiation in vitro. Results Compared with DAFPs, the total lipid content in DIMFPs was reduced (P < 0.05). Moreover, 72 DEGs related to lipid metabolism were screened, which were involved in adipocyte differentiation, fatty acid transport and fatty acid synthesis, lipid stabilization, and lipolysis. Among the 72 DEGs, 19 DEGs were enriched in the PPAR signaling pathway, indicating its main contribution to the regulation of the difference in lipid deposition between DAFPs and DIMFPs. Among these 19 genes, the representative APOA1, ADIPOQ, FABP3, FABP4, FABP7, HMGCS2, LPL and RXRG genes were downregulated, but the ACSL1, FABP5, PCK2, PDPK1, PPARG, SCD, SCD5, and SLC27A6 genes were upregulated (P < 0.05 or P < 0.01) in the DIMFPs. In addition, the well-known pathways affecting lipid metabolism (MAPK, TGF-beta and calcium) and the pathways related to cell communication were enriched, which may also contribute to the regulation of lipid deposition. Finally, the regulatory network for the difference in lipid deposition between chicken DAFPs and DIMFPs was proposed based on the above information. Conclusions Our data suggested a difference in lipid deposition between DIMFPs and DAFPs of chickens in vitro and proposed a molecular regulatory network for the difference in lipid deposition between chicken DAFPs and DIMFPs. The lipid content was significantly increased in DAFPs by the direct mediation of PPAR signaling pathways. These findings provide new insights into the regulation of tissue-specific fat deposition and the optimization of body fat distribution in broilers.

scholarly journals Thioredoxin Reductase Is Essential for Protection ofNeisseria gonorrhoeaeagainst Killing by Nitric Oxide and for Bacterial Growth during Interaction with Cervical Epithelial Cells

2009 ◽  
Vol 199 (2) ◽  
pp. 227-235 ◽  
Author(s):  
Adam J. Potter ◽  
Stephen P. Kidd ◽  
Jennifer L. Edwards ◽  
Megan L. Falsetta ◽  
Michael A. Apicella ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Bacterial Growth ◽  
Thioredoxin Reductase ◽  
Cervical Epithelial Cells

scholarly journals Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism

2016 ◽  
Vol 230 (1) ◽  
pp. 67-79 ◽  
Author(s):  
Giselle Adriana Abruzzese ◽  
Maria Florencia Heber ◽  
Silvana Rocio Ferreira ◽  
Leandro Martin Velez ◽  
Roxana Reynoso ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Glucose Tolerance ◽  
Fatty Liver ◽  
Lipid Content ◽  
Liver Lipid ◽  
Acid Oxidation ◽  
Liver Lipid Content ◽  
Increased Risk ◽  
Liver Lipid Metabolism

Prenatal hyperandrogenism is hypothesized as one of the main factors contributing to the development of polycystic ovary syndrome (PCOS). PCOS patients have high risk of developing fatty liver and steatosis. This study aimed to evaluate the role of prenatal hyperandrogenism in liver lipid metabolism and fatty liver development. Pregnant rats were hyperandrogenized with testosterone. At pubertal age, the prenatally hyperandrogenized (PH) female offspring displayed both ovulatory (PHov) and anovulatory (PHanov) phenotypes that mimic human PCOS features. We evaluated hepatic transferases, liver lipid content, the balance between lipogenesis and fatty acid oxidation pathway, oxidant/antioxidant balance and proinflammatory status. We also evaluated the general metabolic status through growth rate curve, basal glucose and insulin levels, glucose tolerance test, HOMA-IR index and serum lipid profile. Although neither PH group showed signs of liver lipid content, the lipogenesis and fatty oxidation pathways were altered. The PH groups also showed impaired oxidant/antioxidant balance, a decrease in the proinflammatory pathway (measured by prostaglandin E2 and cyclooxygenase-2 levels), decreased glucose tolerance, imbalance of circulating lipids and increased risk of metabolic syndrome. We conclude that prenatal hyperandrogenism generates both PHov and PHanov phenotypes with signs of liver alterations, imbalance in lipid metabolism and increased risk of developing metabolic syndrome. The anovulatory phenotype showed more alterations in liver lipogenesis and a more impaired balance of insulin and glucose metabolism, being more susceptible to the development of steatosis.

Polymorphism of TP53 gene and the risk of high human papillomavirus load in cervical epithelial cells

Gene Reports ◽  
2022 ◽  
Vol 26 ◽  
pp. 101456
Author(s):  
Abbas Hadi Albosale ◽  
Olga Andreevna Garbuzova ◽  
Konstantin Alekseevich Kovalenko ◽  
Elena Vladimirovna Mashkina
Keyword(s):  
Human Papillomavirus ◽  
Epithelial Cells ◽  
Tp53 Gene ◽  
Cervical Epithelial Cells

scholarly journals Pycnogenol protects against diet-induced hepatic steatosis in apolipoprotein-E-deficient mice

2018 ◽  
Vol 315 (2) ◽  
pp. E218-E228 ◽  
Author(s):  
Difei Wang ◽  
Huiying Cong ◽  
Xiaoli Wang ◽  
Yanli Cao ◽  
Shoichiro Ikuyama ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Apolipoprotein E ◽  
Hepatic Steatosis ◽  
Inflammatory Cytokines ◽  
Lipid Content ◽  
Acid Uptake ◽  
Short Term Treatment ◽  
Hepatic Lipid ◽  
Deficient Mice ◽  
Hepatic Lipid Content

PycnogenolR (PYC), a combination of active flavonoids derived from French maritime pine bark, is a natural antioxidant that has various pharmacological activities. Here, we investigated the beneficial effect of PYC on diet-induced hepatic steatosis. Apolipoprotein E (ApoE)-deficient male mice were administered PYC at oral doses of 30 or 100 mg·kg−1·day−1 for 2 wk in advance and were then fed a high-cholesterol and -fat diet (HCD) for 8 wk. Biochemical, immunohistochemical, and gene expression analyses were conducted to explore the effect of PYC on lipid metabolism in ApoE-deficient mice on a HCD. Short-term treatment with HCD in ApoE-deficient mice induced hepatic injuries, such as lipid metabolism disorder and hepatic histopathological changes. We found that PYC reduced body weight and the increase of serum lipids that had been caused by HCD. Supplementation of PYC significantly reduced lipid deposition in the liver, as shown by the lowered hepatic lipid content and histopathological lesions. We subsequently detected genes related to lipid metabolism and inflammatory cytokines. The study showed that PYC markedly suppressed the expression of genes related to hepatic lipogenesis, fatty acid uptake, and lipid storage while increasing the lipolytic gene, which thus reduced hepatic lipid content. Furthermore, PYC mainly reduced the expression of inflammatory cytokines and the infiltration of inflammatory cells, which were resistant to the development of hepatic steatosis. These results demonstrate that PYC protects against the occurrence and development of hepatic steatosis and may provide a new prophylactic approach for nonalcoholic fatty liver disease (NAFLD).

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