Overexpression of HIF1α in Hunner Lesions of Interstitial Cystitis: Pathophysiological Implications
Yoshiyuki Akiyama, Jimpei Miyakawa, Michael A. O’Donnell, Karl J. Kreder, Yi Luo, Daichi Maeda, Tetsuo Ushiku, Haruki Kume, Yukio Homma
Abstract
PURPOSE: The aim of our study was to elucidate biological changes in Hunner lesions, which underlie the pathophysiology of Hunner-type interstitial cystitis, by characterizing their whole transcriptome and immunopathological profiles. MATERIALS AND METHODS: . The results were compared between the lesion and nonlesion areas. RESULTS: , and the HIF1α protein level were significantly higher in lesion areas. Otherwise, there were no significant differences between the lesion and nonlesion samples in terms of mRNA levels of inflammatory cytokines or histological features such as lymphoplasmacytic and mast cell infiltration, epithelial denudation and CD4/CD8 T-lymphocyte ratio. CONCLUSIONS: Our findings demonstrate significant overexpression of HIF1α and up-regulation of its related biological pathways in Hunner lesions. The results indicate that ischemia, in conjunction with inflammation, plays a pathophysiological role in this subtype of interstitial cystitis/bladder pain syndrome, particularly in Hunner lesions.