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Jul . 07, 2023 09:22 Back to list

Kisspeptin 10 (human) cas 374675-21-5



Kisspeptin 10 (human) cas 374675-21-5

Kisspeptin-10, human, is a potent vasoconstrictor and angiogenesis inhibitor. Kisspeptin-10, human, inhibits tumor metastasis through its receptor GPR54. The Kisspeptin-10-GPR54 system plays an important role in embryonic kidney development. Kisspeptin-10/GPR54 signaling induces osteoblast differentiation through NFATc4 mediated BMP2 expression

Kisspeptin-10 Property density 1.46±0.1g/cm3(Predicted) Storage conditions -20°C Solubility DMF:15mg/ml; DMSO:15mg/ml; DMSO:PBS(pH7.Chemicalbook2)(1:2):0.33mg/ml formacrystallinesolid Acidity coefficient (pKa)9.96±0.15(Predicted) Water Solubleinwaterat1mg/ml

in vitro study

Kisspeptin-10 (KP-10) significantly increased the adhesion of THP-1 cells to HUVEC 10-fold at 10μM. Pretreatment with GPR54 antagonist P234 (20μM) significantly inhibited Kisspeptin-10 (10μM) -induced THP-1 cell adhesion to HUVEC. These results suggest that Kisspeptin-10 increases the adhesion of THP-1 cells to HUVEC via GPR54. Kisspeptin-10 significantly enhanced mRNA expression of TNF-α, IL-6, MCP-1, ICAM-1, VCAM-1, and e-selective proteins in HUVEC. Kisspeptin-10 significantly increased protein expression of ICAM-1 and VCAM-1 in HUVECs, parallel to increased mRNA levels

in vivo study 

To evaluate the role of Kisspeptin-10 (KP-10) and the GPR54 antagonist P234 in the development of atherosclerotic lesions in two different ApoE - / - mice (C57 / B6 and BALB/c). In ApoE - / - mice (C57 / B6), the (entire) surface and cross-sectional area of the root (plaque size) of aortic atherosclerotic lesions with pentamer-3-positive areas, monocyte/macrophage infiltration and VSMC content were significantly increased at 17 weeks of age compared to 13 weeks of age. By 17 weeks of age, plasma Kisspeptin-10 concentrations were significantly higher in mice transfused with a high dose of Kisspeptin-10 (12.5μg/ kg/hour) compared to carrier controls. High doses of Kisspeptin-10 (12.5μg/ kg/hour) significantly enhanced atherosclerotic lesion areas of the aorta and atherosclerotic plaque size, significantly increased pentagramin-3 positive areas and monocyte/macrophage infiltration, and significantly decreased VSMC content. Among the 3 groups of ApoE - / - mice aged 17 weeks, there were no significant differences in body weight, food intake, systolic and diastolic blood pressure, and plasma concentrations of total cholesterol or glucose. Injections of Kisspeptin-10 slowed microvascular skin blood flow in mice. Changes in cardiac metabolites in rats treated with Kisspeptin-10 were investigated using GC/TOF-MS based metabolomics studies in rats. Identification of metabolic pathways and biomarkers may help to understand the mechanisms by which Kisspeptin-10 therapy alters cardiac function. The mitochondria undergoing energy metabolism are observed by transmission electron microscopy (TEM), and perturbations of energy metabolism can be inferred from changes in mitochondrial structure. There is a clear separation between the control (N) and Kisspeptin-10 (K) groups in the figure regarding serum samples.v

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