Rabbit Anti-Human Smad3 Polyclonal Antibody Knockout Validated

Previous studies show that Long non-coding RNAs (LncRNAs) are involved in the regulation of various human diseases. This study aimed to reveal how LncRNA CRNDE regulated vascular smooth muscle cells (VSMCs) proliferation and apoptosis in abdominal aortic aneurysms (AAA). Here, we found CRNDE was down-regulated in AAA tissues and AngII-stimulated VSMCs. The overexpression of CRNDE promoted VSMCs proliferation and inhibited cell apoptosis. The interaction between CRNDE and Bcl-3 or Bcl-3 and Smad3 was verified. The interference with Bcl-3 or CRNDE reduced Smad3 stability or promoted Smad3 ubiquitination. After pcDNA-CRNDE or pcDNA-CRNDE+si-Bcl-3 was transfected into VSMCs and stimulated with AngII, CRNDE affected VSMCs proliferation and apoptosis via regulating Smad3 via Bcl-3. Vivo experiments showed the overexpression of CRNDE repressed AAA growth. Therefore, we concluded that CRNDE was down-regulated in AAA tissues and AngII-stimulated VSMCs. Furthermore, the overexpression of CRNDE promoted VSMCs proliferation and repressed cell apoptosis in AAA by up-regulating Smad3 via Bcl-3.

Keratoconus is a common ocular disorder that causes progressive corneal thinning and is the leading indication for corneal transplantation. Central corneal thickness (CCT) is a highly heritable characteristic that is associated with keratoconus. In this two-stage genome-wide association study (GWAS) of CCT, we identified a locus for CCT, namely STON2 rs2371597 (P=2.32 x 10(-13)), and confirmed a significant association between STON2 rs2371597 and keratoconus development (P=0.041). Additionally, strong STON2 expression was observed in mouse corneal epithelial basal cells. We also identified SMAD3 rs12913547 as a susceptibility locus for keratoconus development using predictive analysis with IBM's Watson question answering computer system (P=0.001). Further GWAS analyses combined with Watson could effectively reveal detailed pathways underlying keratoconus development. Yoshikatsu Hosoda et al. study the genetic basis for central corneal thickness (CCT) that is associated with keratoconus. They identify two susceptibility loci, STON2 rs2371597 and SMAD3 rs12913547, using two-step genome-wide association study (GWAS) and predictive analysis with IBM's Watson question answering computer system, respectively.