Anti-FGF10 polyclonal antibody

Fibroblast growth factors (FGFs) are growth factors that regulate many important biological processes, including proliferation and differentiation of embryonic cells during organogenesis. In this review, we have summarized current information about the role of FGFs in pancreas organogenesis. The pancreas organogenesis is a complex process, which involves constant signaling from mesenchymal tissue and activation of various genes regulating particular stages thus determining specification of progenitor cells. Changes in the FGF/FGFR signaling pathway during this process result in incorrect activation of master genes, leading to different pathologies in pancreas development. Understanding the full picture about the role of FGFs in pancreas development will help better understanding of their role in other pathologies of the pancres, including carcinogenesis.

Cellular plasticity and de-differentiation are hallmarks of tissue/organ regenerative capacity in diverse species. Despite a more restricted capacity for regeneration, humans with age-related chronic diseases, such as cancer and fibrosis, show evidence of a recapitulation of developmental gene programs. We have previously identified a resident population of mesenchymal stromal cells (MSCs) in the terminal airways-alveoli by bronchoalveolar lavage (BAL) of human adult lungs. In this study, we characterized MSCs from BAL of patients with stable and progressive idiopathic pulmonary fibrosis (IPF), defined as <5% and >= 10% decline, respectively, in forced vital capacity over the preceding 6-month period. Gene expression profiles of MSCs from IPF subjects with progressive disease were enriched for genes regulating lung development. Most notably, genes regulating early tissue patterning and branching morphogenesis were differentially regulated. Network interactive modeling of a set of these genes indicated central roles for TGF-beta and SHH signaling. Importantly, fibroblast growth factor-10 (FGF-10) was markedly suppressed in IPF subjects with progressive disease, and both TGF-beta 1 and SHH signaling were identified as critical mediators of this effect in MSCs. These findings support the concept of developmental gene re-activation in IPF, and FGF-10 deficiency as a potentially critical factor in disease progression.