Gorashi Rayyan M, Baddour Talia, Chittle Sarah J, Félix Vélez Nicole E, Wenning Michaela A, Anseth Kristi S, Mestroni Luisa, Peña Brisa, Guo Peng, Aguado Brian A
Shu Chien-Gene Lay Department of Bioengineering, University of California San Diego, La Jolla, CA 92093, USA.
Sanford Consortium for Regenerative Medicine, La Jolla, CA 92037, USA.
Sci Adv. 2025 Mar 14;11(11):eads5717. doi: 10.1126/sciadv.ads5717. Epub 2025 Mar 12.
Aortic valve stenosis (AVS) is a progressive disease, wherein males more often develop valve calcification relative to females that develop valve fibrosis. Valvular interstitial cells (VICs) aberrantly activate to myofibroblasts during AVS, driving the fibrotic valve phenotype in females. Myofibroblasts further differentiate into osteoblast-like cells and produce calcium nanoparticles, driving valve calcification in males. We hypothesized that the lysine demethylase UTY (ubiquitously transcribed tetratricopeptide repeat containing Y-linked) decreases methylation uniquely in male VICs responding to nanoscale extracellular matrix cues to promote an osteoblast-like cell phenotype. Here, we describe a hydrogel biomaterial cell culture platform to interrogate how nanoscale cues modulate sex-specific methylation states in VICs activating to myofibroblasts and osteoblast-like cells. We found that UTY modulates the osteoblast-like cell phenotype in response to nanoscale cues uniquely in male VICs. Overall, we reveal a previously unidentified role of UTY in the regulation of calcification processes in males during AVS progression.
主动脉瓣狭窄(AVS)是一种进行性疾病,相较于发生瓣膜纤维化的女性,男性更常出现瓣膜钙化。在AVS过程中,瓣膜间质细胞(VICs)异常激活为肌成纤维细胞,导致女性出现纤维化瓣膜表型。肌成纤维细胞进一步分化为成骨样细胞并产生钙纳米颗粒,导致男性瓣膜钙化。我们推测,赖氨酸去甲基化酶UTY(含Y连锁的泛转录四肽重复序列)在响应纳米级细胞外基质信号的雄性VICs中独特地降低甲基化,以促进成骨样细胞表型。在此,我们描述了一种水凝胶生物材料细胞培养平台,以探究纳米级信号如何调节激活为肌成纤维细胞和成骨样细胞的VICs中的性别特异性甲基化状态。我们发现,UTY仅在雄性VICs中响应纳米级信号调节成骨样细胞表型。总体而言,我们揭示了UTY在AVS进展过程中男性钙化过程调节中以前未被识别的作用。