Rabbit Anti-Human ET-1 (a.a. 131-180) Polyclonal antibody

Sarcoidosis is a chronic inflammatory disease, characterized by granulomatous inflammation, prominently involving the respiratory system. The etiology of this disease has not yet been elucidated and the contribution of genetic is not yet completely understood. We searched for novel candidate genes, utilizing a system biology approach, based on data from published transcriptional, proteomic and linkage studies of sarcoidosis. The search revealed several new potential candidate genes involved in the pathogenesis of inflammatory lung diseases: 25-(OH)-vitamin D-3-1 alpha-hydroxylase (CYP27B1), endothelin-1 (EDN1) and glutathione S-transferase Pi (GSTP1). Variants of selected polymorphisms: -1260/C>A in CYP27B1, Lys198Asn in EDN1, and Ile105Val in GSTP1, were examined to determine if they confer susceptibility to sarcoidosis, based on an analysis of 180 Slovenian patients in comparison with 283 healthy controls. Polymerase chain reactions using allele-specific oligonucleotides were performed. This disease was not significantly associated with genotypes CC at -1260/C>A polymorphism in CYP27B1 (P = 0.68, odds ratio (OR) = 1.10, 95% confidence interval (CI) = 0.75-1.61), GG genotype at Lys198Asn polymorphism in EDN1 (P = 1.00, OR = 0.97, 95% CI = 0.65-1.44) and AA genotypes at Ile105Val polymorphism in GSTP1 (P = 0.53, OR = 0.87, 95% CI = 0.60-1.27). There was no association of polymorphisms in any of the genes with sarcoidosis.

Endothelin 1 (Edn1), a secreted peptide expressed ventrally in the primordia of the zebrafish pharyngeal arches, is required for correct patterning of pharyngeal cartilage development. We have studied mutants and morpholino-injected larvae to examine the role of the Edn1 signal in patterning anterior pharyngeal arch bone development during the first week after fertilization. We observe a remarkable variety of phenotypic changes in dermal bones of the anterior arches after Edn1 reduction, including loss, size reduction and expansion, fusion and shape change. Notably, the changes that occur appear to relate to the level of residual Edn1. Mandibular arch dermal bone fusions occur with severe Edn1 loss. In the dorsal hyoid arch, the dermal opercle bone is usually absent when Edn1 is severely reduced and is usually enlarged when Edn1 is only mildly reduced, suggesting that the same signal can act both positively and negatively in controlling development of a single bone. Position also appears to influence the changes: a branchiostegal ray, a dermal hyoid bone normally ventral to the opercle, can be missing in the same arch where the opercle is enlarged. We propose that Edn1 acts as a morphogen; different levels pattern specific positions, shapes and sizes of bones along the dorso-ventral axis. Changes involving Edn1 may have occurred during actinopterygian evolution to produce the efficient gill-pumping opercular apparatus of teleosts.