7 Taiwanesiska forskare som representerar 13 olika institut står bakom denna rapport benämnd :
Lipopolysaccharide promoted proliferation and adipogenesis of preadipocytes through JAK/STAT and AMPK-regulated cPLA2 expression
Received: 2017.11.28; Accepted: 2018.12.04 Published: 2019.01.01Studierna är publicerade i det vetenskapliga organet International Journal of Medical Sciences
Introduction
Obesity, defined as “abnormal or excessive fat accumulation, is a chronic disease and a worldwide epidemic problem. Obesity contributes to the development of a group of potentially life-threatening conditions including, insulin resistance, Type 2 Diabetes Mellitus, dyslipidemia, cardiovascular disease, metabolic syndrome, nonalcoholic fatty liver disease, osteoarthritis, stillbirth, and some cancer [1-3]. Adipose tissue consists of approximately one-third of mature adipocytes and two-thirds of stromal cells including macrophages, fibroblasts, endothelial cells and preadipocytes [4]. Preadipocytes originate from a multi-potent stem cell of mesodermal origin and function as source of new fat cells persists during the entire human life. The cellular changes of adipose tissue in obesity include fat depot hypertrophy (increase in adipocyte volumes) and hyperplasia (increase in adipocyte numbers) [5, 6]. Excess triglyceride accumulation in existing adipocytes due to a positive energy balance (energy intake in excess of energy expenditure) results in hypertrophy. On the other way, hyperplasia, regarded as 'adipogenesis', results from the recruitment of new adipocytes from precursor cells in adipose tissue and involves the proliferation and differentiation of preadipocytes [5]. Because increase in adipocyte number from preadipocyte proliferation and differentiation may result in more units to storage lipid. Hyperplastic fat expansion with poorest prognosis for treatment is addressed as more important than hypertrophic expansion [5].
Ur den klipper jag PHI-relevant.
Materials and methods
Cell viability assay and cell number counts
The working solution of XTT assay kit was prepared as manufacturer's direction.The Cultured cells (5000 cells/well) were treated with or without various inhibitors and then incubated with LPS for 48 h.
At the end of incubation, 50 μL of XTT kit reaction solution was added into each well and incubated in an incubator for 2 h. The absorbance of each well was detected at OD450 and OD630 (reference absorbance) by Epoch™ Multi-Volume Spectrophotometer System (BioTek, Vermont, USA).
Or cells were cultured in 6-cm dishes, and incubated with various treatments.
At the end of stimulation, cell numbers were counted by HoloMonitor M4 (Phase Holographic Imaging PHI AB, Lund, Sweden).
Figure 6
LPS enhanced proliferation of preadipocytes via JAK2 and AMPK-regulated cPLA2 protein.
Serum-starved 3T3-L1 cells were pretreated with AACOCF3 (1 μM), AG490 (100 nM) or BML-275 (0.1 μM) for 1 h. Or cells were transfected with siRNA against scramble, JAK2, AMPK or cPLA2 for 24 h. Then cells were incubated 20 μg/mL of LPS 48 h. Or, cells were incubated with 0.1 μM of arachidonic acid for 0, 24 or 48 h. At the end of incubation, (A) BrdU incorporation assay, (B, F, I) HoloM4 system detection, (C, G, J) cell number counts, and (D, H, K) XTT assay were performed. (E) Western blot was used to detect the expression of cPLA2. Data are expressed as means ± SEM of at least 3 independent experiments (n≥3). &P < 0.05, as compared with the control group or scramble siRNA transfected alone group. #P < 0.05, as compared with the LPS treated alone or the basal group.
Min kommentar
Med denna rapport kan vi addera ytterligare ett forskningsområde där PHI´s teknik är tillämpbar.
Obesity som man inledningsvis beskriver som ett världsomspännande problemområde med allvarliga följdsjukdomar som bland annat diabetes, hjärtproblematik och vissa typer av cancer.
HoloMonitor prickar av fler och fler användningsområden.
Mvh the99
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