An article published this year in “Scielo” using our “Apoptosis Detection Kit FITC”, by our customers from several Centers, Hospitals and Universities of Portugal, in the analysis of how Intestinal inflammatory and redox responses to the perioperative administration of teduglutide in rats. Congrats and Thanks.

Summay:

Glucagon-like peptide 2 (GLP-2) is a gastrointestinal growth factor, synthetized in enteroendocrine L cells, that exerts a relevant role on the control of energy absorption and the preservation of intestinal mucosa morphology and function. Teduglutide is a long-acting dipeptidylpeptidase IV-resistant equivalent of GLP-2 currently accepted for pharmacological rehabilitation of patients with short-bowel syndrome associated intestinal failure and also considered a promising medication for moderate-to-severe Crohn’s disease. Several studies have demonstrated that, in patients with short-bowel syndrome, teduglutide treatment is safe, well tolerated and efficacious, with improvement of intestinal absorption and reduction of parenteral support requirements. Teduglutide was recently approved by the European Medicines Agency for treatment of patients with short-bowel syndrome related parenteral support dependence despite optimized medical and dietetic treatment, aged more than one year and who are stable following a period of postsurgical intestinal adaptation. Furthermore, in the recently published guidelines of the European Society for Clinical Nutrition and Metabolism, teduglutide was considered the first choice for carefully selected patients with chronic intestinal failure who are candidates for growth factor treatment.

Reference:

http://www.scielo.br/scielo.php?pid=S0102-86502017000800648&script=sci_arttext

Product link:

Apoptosis Detection Kit FITC

http://www.immunostep.com/apoptosis/3727-anxvkf-100t.html

An article published this year in “The International Journal of Biochemistry & Cell Biology” using our “ApoptosisDetection Kit FITC”, by our customers from Institute for Maternal and Child Health, Trieste, Italy, in the analysis of how 25-Hydroxycholesterol and inflammation in Lovastatin-deregulated mevalonate pathway. Congrats and Thanks.

Summay:

Mevalonate pathway deregulation has been observed in several diseases, including Mevalonate kinase deficiency (MKD). MKD is a hereditary auto-inflammatory disorder, due to mutations at mevalonate kinase gene (MVK), encoding mevalonate kinase (MK) enzyme. MVK mutations have been reported as associated with impairment of mevalonate pathway with consequent decrease of protein prenylation levels, defective autophagy and increase of IL-1β secretion, followed by cell death. Since 25-hydroxycholesterol (25-HC), a metabolite of cholesterol, can suppress IL-1β production, thus reducing inflammation, we evaluated the effect of 25-HC in an in vitro model of mevalonate pathway alteration, obtained using Lovastatin. Human glioblastoma cell line (U87-MG) was chosen to mimic, at least in part, the central nervous system impairment observed in MKD; 25-HC effects were evaluated aimed at disclosing if this compound could be considered as novel potential drug for MKD.

Our results showed that 25-HC is able to reduce inflammation but it is ineffective to restore autophagy flux and to decrease apoptosis levels, both caused by lower protein prenylation; so, in spite of its anti-inflammatory action it is not useful to rescue defective prenylation/autophagy impairment-driven apoptosis in Lovastatin impaired mevalonate pathway.

We hypothesize the presence in the mevalonate pathway of alternative mechanisms acting between inflammation and apoptotic autophagy impairment.

Reference:

http://www.sciencedirect.com/science/article/pii/S1357272517302339

Product link:

Apoptosis Detection Kit FITC

http://www.immunostep.com/apoptosis/3727-anxvkf-100t.html

ESCCA 2017 meeting will be held in Thessaloniki, from Sunday 24 September - Wednesday 27 September 2017.

As every year, IMMUNOSTEP will attend to this important meeting. We are proud to invite you to visit our booth S4 and give you further details about our new products.

See you in Thessaloniki!

IMMUNOSTEP S.L.

An article published this year in “EUROPEAN JOURNAL OF IMMUNOLOGY” using our “Custom Peptide Production Service” (MOG Peptide), by our customers from Facultad de Medicina (UCLM), Instituto de Investigación en Discapacidades Neurológicas (IDINE), Albacete, in the analysis of how Absence of Notch1 in murine myeloid cells attenuates the development of experimental autoimmune encephalomyelitis by affecting Th1 and Th17 priming. Congrats and Thanks.

Summary:

Inhibition of Notch signalling in T cells attenuates the development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Growing evidence indicates that myeloid cells are also key players in autoimmune processes. Thus, the present study evaluates the role of the Notch1 receptor in myeloid cells on the progression of myelin oligodendrocyte glycoprotein (MOG) _35-55-induced EAE, using mice with a myeloid-specific deletion of the Notch1 gene (MyeNotch1KO). We found that EAE progression was less severe in the absence of Notch1 in myeloid cells. Thus, histopathological analysis revealed reduced pathology in the spinal cord of MyeNotch1KO mice, with decreased microglia/astrocyte activation, demyelination and infiltration of CD4⁺ T cells. Moreover, these mice showed lower Th1 and Th17 cell infiltration and expression of IFN-γ and IL-17 mRNA in the spinal cord. Accordingly, splenocytes from MyeNotch1KO mice reactivated in vitro presented reduced Th1 and Th17 activation, and lower expression of IL-12, IL-23, TNF-α, IL-6, and CD86. Moreover, reactivated wild-type splenocytes showed increased Notch1 expression, arguing for a specific involvement of this receptor in autoimmune T cell activation in secondary lymphoid tissues. In summary, our results reveal a key role of the Notch1 receptor in myeloid cells for the initiation and progression of EAE.

Reference:

http://onlinelibrary.wiley.com/doi/10.1002/eji.201646901/full

Product link:

Peptide Custom Production Service

http://www.immunostep.com/content/25-peptide-production

An article published this year in “SCIENTIFIC REPORT” using our Polyclonal Antibody Development Service, by our customers from University of Extremadura, Spain, in the analysis of a Dioxin Receptor Adjusts Liver Regeneration after Acute Toxic Injury and Protects against Liver Carcinogenesis. Congrats and Thanks.

Summary:

The aryl hydrocarbon receptor (AhR) has roles in cell proliferation, differentiation and organ homeostasis, including the liver. AhR depletion induces undifferentiation and pluripotency in normal and transformed cells. Here, AhR-null mice (AhR−/−) were used to explore whether AhR controls liver regeneration and carcinogenesis by restricting the expansion of stem-like cells and the expression of pluripotency genes. Short-term CCl4 liver damage was earlier and more efficiently repaired in AhR−/− than in AhR+/+ mice. Stem-like CK14 + and TBX3 + and pluripotency-expressing OCT4 + and NANOG + cells expanded sooner in AhR−/− than in AhR+/+ regenerating livers. Stem-like side population cells (SP) isolated from AhR−/− livers had increased β-catenin (β-Cat) signaling with overexpression of Axin2, Dkk1 and Cyclin D1. Interestingly, β-Cat, Axin2 and Dkk1 also increased during regeneration but more notably in AhR-null livers. Liver carcinogenesis induced by diethylnitrosamine (DEN) produced large carcinomas in all AhR−/− mice but mostly premalignant adenomas in less than half of AhR+/+ mice. AhR-null tumoral tissue, but not their surrounding non-tumoral parenchyma, had nuclear β-Cat and Axin2 overexpression. OCT4 and NANOG were nevertheless similarly expressed in AhR+/+ and AhR−/− lesions. We suggest that AhR may serve to adjust liver repair and to block tumorigenesis by modulating stem-like cells and β-Cat signaling.

Reference:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5585208/

Product link:

Polyclonal Antibody Development Service:

http://www.immunostep.com/content/27-monoclonal-and-polyclonal-antibody-development-service