Gingival Medicinal Signaling Cells Conditioned Medium effect on the Osteoclast and Osteoblast number in Lipopolysaccharide-induced Calvaria Bone Resorption in Wistar Rats’ (Rattus novergicus)

The gingival medicinal signaling cells conditioned medium (GMSCs-CM) is a biocompatible material which possessed beneficial cytokine, anti-microbial peptide, growth factor that can be collected after culture. GMSCs- CM may inhibit bone resorption in order to improve the patient’s quality of life. In this study, the potential effect of GMSCs-CM on the number of osteoclasts and osteoblasts in Lipopolysaccharide (LPS)-induced calvaria bone resorption in wistar rats (Rattus novergicus) has been analyzed. Twenty-eight male and healthy wistar rats (R. novergicus) at the age of 1-2 months old with 250-300 grams body weight were divided into 4 groups, namely PBS group: 100μg PBS day 1-7; LPS group: 100μg LPS day 1-7; LPS and GMSCs group: 100μg LPS + 100μg GMSCS-CM day 1 1-7, GMSCs group: 100μg M-GMSCs day 1-7. Escherichia Coli LPS was used to induce the bone resorption on the calvaria with subcutaneous injection. GMSCs-CM was collected after passage 4-5 then injected subcutaneously on the calvaria. All samples were examined on the. 8th day through cervical dislocation. The number of osteoblasts and osteoclasts in calvaria was then observed under 400x magnification. One Way ANOVA and Tukey HSD were conducted to analyze differences between groups (p<0.01). The number of osteoclasts in calvaria decreased significantly in the LPS + GMSCs-CM group compared to LPS group (p<0.01). The number of osteoblasts in calvaria increased significantly in the LPS + GMSCs-CM group compared to LPS group (p<0.01). GMSCs-CM can reduce the amount of osteoclast significantly and increases the production of osteoblast in LPS-induced calvaria bone resorption in wistar rats (R. novergicus).

Association of IGF-1 CA(n) and IGFBP3 rs2854746 Polymorphisms with Endometrial Polyp Risk

Introduction. Insulin-like growth factor 1 (IGF-1) is a peptide growth factor that promotes cell proliferation and inhibits apoptosis. The bioavailability of IGF-1 is regulated by the insulin-like growth factor binding protein 3 (IGFBP3). Genetic variations influence the levels of IGF-1 and IGFBP3. The purpose of this study was to examine the association of polymorphisms IGF-1 CA(n) and IGFBP3 rs2854746 with risk of endometrial polyps. Materials and Methods. Case control observational study, composed of 104 women with antecedent of endometrial polyp (case group) and 81 postmenopausal women without antecedent of endometrial diseases (control group). Genotyping of IGF-1 CA(n) was performed by PCR and fragment analysis by capillary electrophoresis, and genotyping of IGFBP3 rs2854746 was performed by PCR-HRM. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression. Results. The genotype IGF-1 CA(19)/CA(19) was associated with an increased endometrial polyp risk (OR=2,57; IC 95%= 1,09 - 6,01); this was also found when combining it with CA(>19)/CA(n) genotypes (OR=2,18; IC 95%= 1,06-4,47). The IGFBP3 rs2854746 analyses showed the CG genotype having a protective effect for endometrial polyp (OR=0,37; IC 95%= 0,19-0,73), fact also observed when grouping CG and GG carriers (OR=0,51; IC 95%= 0,28-0,93). Conclusion. The genotypes CA(19)/CA(19) and CA(19)/CA(19) + CA(>19)/CA(n) of the IGF-1 CA(n) may be considered a risk for endometrial polyp, whereas the genotypes CG and CG + GG of IGFBP3 rs2854746 polymorphism have an inverse effect of endometrial polyp risk.

Early studies on the effect of peptide growth factor phytosulfokine-α on Brassica oleracea var. capitata L. protoplasts

<span>Phytosulfokines (PSK) are peptidyl growth factors with the potential of inducing cell proliferation. We examined the effect of supplementation of liquid culture medium with 0.1 µM phytosulfokine-α (PSK-α) on protoplast viability and division frequencies in seven accessions of <em>Brassica oleracea</em> var. <em>capitata</em> L., including cultivars and breeding lines. Protoplasts were isolated from leaves and hypocotyls of in vitro grown plants and immobilized in calcium-alginate layers. Cabbage protoplast-derived cells cultured in medium supplemented with 0.1 µM of PSK-α had higher viability and division frequencies compared to cells cultured in PSK-α-free control medium. The effect of PSK-α was more pronounced in low-responding accessions (‘Sława z Gołębiewa’, ‘Ramkila F1’, LM, and LM98); however, in two cultivars with very low response (‘Badger Shipper’ and ‘Oregon 123’), although the division frequencies in the media supplemented with PSK-α were increased over the control, the differences were not significant. Obtained callus colonies were subjected to regeneration. PSK-α supplemented into the liquid culture medium had an indirect effect on shoot regeneration by inducing sustained cell divisions leading to an increase in shoot regeneration in Sława z Gołębiewa and both breeding lines.</span>

TGFα expression in myeloid malignancies

BackgroundTransforming growth factor α (TGFα) is a peptide growth factor known to be expressed in normal haemopoiesis. It is also expressed in a range of epithelial neoplasms but has not been assessed in haemopoietic malignancies. We have performed an immunohistochemical evaluation of TGFα in acute and chronic myeloid malignancies.MethodsTGFα expression was semiquantitatively assessed in 69 normal bone marrow trephines and 157 cases of myeloid malignancy using an immunohistochemical approach.ResultsBlast cells of myeloid origin in acute myeloid leukaemia (AML), myelodysplasia and accelerated and blast phases of chronic myeloid leukaemia (CML) were TGFα positive. In acute promyelocytic leukaemia the neoplastic cells had significantly weaker TGFα expression than seen in other forms of AML. The blast cells in CML-accelerated and blast phases were positive with similar expression to AML.ConclusionsTGFα is expressed in neoplastic myeloblasts and could, therefore, be used as blast cell biomarker in diagnostic haematopathology. In addition, TGFα immunohistochemistry may be of use in identifying a therapeutic target.

Nestin upregulation characterizes vascular remodeling secondary to hypertension in the rat

Proliferation and hypertrophy of vascular smooth muscle cells represent hallmark features of vessel remodeling secondary to hypertension. The intermediate filament protein nestin was recently identified in vascular smooth muscle cells and in other cell types directly participated in proliferation. The present study tested the hypothesis that vessel remodeling secondary to hypertension was characterized by nestin upregulation in vascular smooth muscle cells. Two weeks after suprarenal abdominal aorta constriction of adult male Sprague-Dawley rats, elevated mean arterial pressure increased the media area and thickness of the carotid artery and aorta and concomitantly upregulated nestin protein levels. In the normal adult rat carotid artery, nestin immunoreactivity was observed in a subpopulation of vascular smooth muscle cells, and the density significantly increased following suprarenal abdominal aorta constriction. Filamentous nestin was detected in cultured rat carotid artery- and aorta-derived vascular smooth muscle cells and an analogous paradigm observed in human aorta-derived vascular smooth muscle cells. ANG II and EGF treatment of vascular smooth muscle cells stimulated DNA and protein synthesis and increased nestin protein levels. Lentiviral short-hairpin RNA-mediated nestin depletion of carotid artery-derived vascular smooth muscle cells inhibited peptide growth factor-stimulated DNA synthesis, whereas protein synthesis remained intact. These data have demonstrated that vessel remodeling secondary to hypertension was characterized in part by nestin upregulation in vascular smooth muscle cells. The selective role of nestin in peptide growth factor-stimulated DNA synthesis has revealed that the proliferative and hypertrophic responses of vascular smooth muscle cells were mediated by divergent signaling events.

A novel single nucleotide polymorphism (SNP) of the <i>IGF1R</i> gene and the association with growth traits in yak (Brief Report)

The insulin-like growth factor-I (IGF1) is a peptide growth factor that exerts mitogenic and metabolic activities, which are regulators of growth, survival and cell differentiation in a number of cell and tissue types. To elicit its effects, IGF1 must bind its receptors. The insulinlike growth factor 1 receptor (IGF1R) is similar to insulin receptor (INSR) and it mediates the growth-promoting effect of IGF1. The IGF1R gene, therefore, was selected as a biological candidate gene for growth, body composition, metabolic, and skeletal traits in animals (Rothschild et al. 1997). By now, no polymorphism of yak (Bos grunniensL) IGF1R gene is reported. In the present paper, the partial exon 1 region of IGF1R was screened to detect the SNPs in Chinese yak breeds. Associations of SNP of IGF1R with growth traits were analysed.