[Diabetes & Lipid Metabolism] [Cardiovascular Diseases] [Gene Functions] [Hypertension & Respiratory Function] [Neurology] [Behavioral Analysis] [Genetics & Breeding 1] [Genetics & Breeding 2] [Pathophysiology] [Animal Care & Husbandry] [Anesthesia] [Reproduction & Fertilization] [Developmental Engineering & Cryopreservation 1] [Developmental Engineering & Cryopreservation 2] [Microbiology] [ES Cells & Regenerative Medicine] [Immunity & Cancer 1] [Pharmacology & Toxicology] [Immunity & Cancer 2] [Diagnostic Technology]

Metabolic disorders (dyslipidemias) are currently crucial since they develop cardiovascular diseases. The work was aimed at studying age dynamics and its correlation with severity of dyslipidemia in basic lipid metabolism variables (in different age groups). Materials and methods: Examinees were Caucasians born and permanently residing in Magadan region: 55 mature men and 147 young men (mean ages were 36.8±0.8 and 18.7±0.8 yr, respectively). Blood serum lipid metabolism was examined by colorimetric and photometric method using AU 680 (Beckman Coulter, USA). Results: The data of obtained lipidogram showed dependence of rise in all indicators on subjective older age with higher percentage of dyslipidemia and increase in calculated indices reflecting degree of the lipid profile atherogenicity. Conclusion: Overall, the North study revealed a safer lipid profile in group of younger men, while biochemical picture of older residents demonstrated increased values. Lipid atherogenicity is a very alarming factor in developing cardiovascular diseases, and a predictor of risks for metabolic syndrome.

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Abstract 5276: Sumoylation Of Klf5 Is A Molecular Switch Regulating Ppar-δ-containing Transcriptional Programs Of Lipid Metabolism

Circulation ◽

10.1161/circ.118.suppl_18.s_518-a ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Yumiko Oishi ◽

Ichiro Manabe ◽

Kazuyuki Tobe ◽

Takashi Kadowaki ◽

Ryozo Nagai

Keyword(s):

Cardiovascular Disease ◽

Metabolic Syndrome ◽

Lipid Metabolism ◽

Cardiovascular Diseases ◽

Transcriptional Control ◽

Uncoupling Protein ◽

Molecular Switch ◽

Atherosclerotic Cardiovascular Disease ◽

Transcriptional Regulatory ◽

Reporter Assays

Metabolic syndrome is increasingly recognized as a major risk factor for cardiovascular disease. We have previously shown that a zinc finger transcription factor, Krüppel-like factor 5 (KLF5), plays an important role in cardiovascular diseases, such as atherosclerosis and cardiac hypertrophy. Interestingly, KLF5 is also expressed in metabolic tissues, such as adipose tissue, skeletal muscle and pancreatic β-cells. Moreover, we found that KLF5 is crucial for adipocyte differentiation. Therefore, it is very likely that KLF5 plays multiple roles in development and progression of metabolic syndrome and its cardiovascular and metabolic consequences including atherosclerotic cardiovascular disease. Indeed, KLF5 heterozygous knockout ( KLF5 +/− ) mice were resistant to high-fat-induced obesity and metabolic syndrome, despite consuming more food than wild-type mice. This appears to in part reflect their enhanced energy expenditure. Expression of the genes involved in lipid oxidation and energy uncoupling, including uncoupling protein (UCP) and carnitine-palmitoyl transferase 1b (CPT1b) was upregulated in the soleus muscles of KLF5 +/− mice. KLF5 could be reversibly modified by small ubiquitin-like modifier 1 (SUMO1), after which SUMOylated KLF5 strongly inhibited CPT1b , UCP3 and UCP2 promoter activity. Results of chromatin immunoprecipitation, two-hybrid, and reporter assays showed that under basal conditions SUMOylated KLF5 associated with transcriptionally repressive regulatory complexes containing unliganded PPARδ and corepressors. However, upon agonist stimulation of PPARδ, the deSUMOylating enzyme was recruited and KLF5 was deSUMOylated. The unSUMOylated KLF5 now formed transactivating complexes with liganded PPARδ and CBP. Thus, SUMOylation appears to be a molecular switch affecting function of KLF5 and the transcriptional regulatory programs governing lipid metabolism. Moreover, KLF5 is essential for the PPARδ agonist-dependent transcriptional control. Results of the present study have established KLF5 as a novel key molecule in lipid metabolism and suggest that the posttranscriptional modification of KLF5 is an attractive novel therapeutic target for both metabolic and cardiovascular diseases.

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Isolation, Characterization and Differentiation Potential of Chicken Spermatogonial Stem Cell Derived Embryoid Bodies

Annals of Animal Science ◽

10.1515/aoas-2015-0063 ◽

2016 ◽

Vol 16 (1) ◽

pp. 115-128 ◽

Cited By ~ 2

Author(s):

Thanh Luan Nguyen ◽

Jae Gyu Yoo ◽

Neelesh Sharma ◽

Sung Woo Kim ◽

Yong Jun Kang ◽

...

Keyword(s):

Developmental Biology ◽

Regenerative Medicine ◽

Connexin 43 ◽

Es Cells ◽

Periodic Acid ◽

Embryonic Stem ◽

Embryoid Bodies ◽

Significant Finding ◽

Differentiation Potential

Abstract Human, murine and monkey spermatogonial stem cells (SSCs) have the capability to undergo self-renewal and differentiation into different body cell types in vitro, which are expected to serve as a powerful tool and resource for the developmental biology and regenerative medicine. We have successfully isolated and characterized the chicken SSCs from 3-day-old chicken testicular cells. The pluripotency was using Periodic Acid-Schiff (PAS ) staining or alkaline phosphatase staining, and antibodies to stage-specific embryonic antigens. In suspension culture conditions SSCs formed embryoid bodies (EBs) like embryonic stem (ES) cells. Subsequently EB differentiated into osteoblasts, adipocytes and most importantly into cardiomyocytes under induced differentiation conditions. The differentiation potential of EBs into cardiomyocyte-like cells was confirmed by using antibodies against sarcomeric α-actinin, cardiac troponin T and connexin 43. Cardiomyocytes-like cells were also confirmed by RT-PCR analysis for several cardiac cell genes like GATA-4, Nkx2-5, α-MHC, and ANF. We have successfully established an in vitro differentiation system for chicken SSCs into different body cells such as osteoblasts, adipocytes and cardiomyocytes. The most significant finding of this study is the differentiation potential of chicken SSCs into cardiomyocytes. Our findings may have implication in developmental biology and regenerative medicine by using chicken as the most potential animal model.

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Hepatic differentiation of pluripotent stem cells

Biological Chemistry ◽

10.1515/bc.2009.120 ◽

2009 ◽

Vol 390 (10) ◽

Cited By ~ 15

Author(s):

Komal Loya ◽

Reto Eggenschwiler ◽

Kinarm Ko ◽

Malte Sgodda ◽

Francoise André ◽

...

Keyword(s):

Stem Cells ◽

Regenerative Medicine ◽

Pluripotent Stem Cells ◽

Ethical Issues ◽

Es Cells ◽

Embryonic Stem ◽

Hepatic Differentiation ◽

Alternative Source ◽

Organ Specific

Abstract In regenerative medicine pluripotent stem cells are considered to be a valuable self-renewing source for therapeutic cell transplantations, given that a functional organ-specific phenotype can be acquired by in vitro differentiation protocols. Furthermore, derivatives of pluripotent stem cells that mimic fetal progenitor stages could serve as an important tool to analyze organ development with in vitro approaches. Because of ethical issues regarding the generation of human embryonic stem (ES) cells, other sources for pluripotent stem cells are intensively studied. Like in less developed vertebrates, pluripotent stem cells can be generated from the female germline even in mammals, via parthenogenetic activation of oocytes. Recently, testis-derived pluripotent stem cells were derived from the male germline. Therefore, we compared two different hepatic differentiation approaches and analyzed the generation of definitive endoderm progenitor cells and their further maturation into a hepatic phenotype using murine parthenogenetic ES cells, germline-derived pluripotent stem cells, and ES cells. Applying quantitative RT-PCR, both germline-derived pluripotent cell lines show similar differentiation capabilities as normal murine ES cells and can be considered an alternative source for pluripotent stem cells in regenerative medicine.

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Genetic defects in SAPK signalling, chromatin regulation, vesicle transport and CoA-related lipid metabolism are rescued by rapamycin in fission yeast

Open Biology ◽

10.1098/rsob.170261 ◽

2018 ◽

Vol 8 (3) ◽

pp. 170261 ◽

Cited By ~ 3

Author(s):

Kenichi Sajiki ◽

Yuria Tahara ◽

Alejandro Villar-Briones ◽

Tomáš Pluskal ◽

Takayuki Teruya ◽

...

Keyword(s):

Lipid Metabolism ◽

Fission Yeast ◽

Mechanisms Of Action ◽

Vesicle Transport ◽

Purine Biosynthesis ◽

Fibrodysplasia Ossificans Progressiva ◽

Genetic Defects ◽

Temperature Sensitive ◽

Chromatin Regulation ◽

Gene Functions

Rapamycin inhibits TOR (target of rapamycin) kinase, and is being used clinically to treat various diseases ranging from cancers to fibrodysplasia ossificans progressiva. To understand rapamycin mechanisms of action more comprehensively, 1014 temperature-sensitive (ts) fission yeast ( Schizosaccharomyces pombe ) mutants were screened in order to isolate strains in which the ts phenotype was rescued by rapamycin. Rapamycin-rescued 45 strains, among which 12 genes responsible for temperature sensitivity were identified. These genes are involved in stress-activated protein kinase (SAPK) signalling, chromatin regulation, vesicle transport, and CoA- and mevalonate-related lipid metabolism. Subsequent metabolome analyses revealed that rapamycin upregulated stress-responsive metabolites, while it downregulated purine biosynthesis intermediates and nucleotide derivatives. Rapamycin alleviated abnormalities in cell growth and cell division caused by sty1 mutants (Δ sty1 ) of SAPK. Notably, in Δ sty1 , rapamycin reduced greater than 75% of overproduced metabolites (greater than 2× WT), like purine biosynthesis intermediates and nucleotide derivatives, to WT levels. This suggests that these compounds may be the points at which the SAPK/TOR balance regulates continuous cell proliferation. Rapamycin might be therapeutically useful for specific defects of these gene functions.

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