Passino Melissa A, Adams Ryan A, Sikorski Shoana L, Akassoglou Katerina
Department of Pharmacology, University of California, San Diego (UCSD), La Jolla, CA 92093-0636, USA.
Science. 2007 Mar 30;315(5820):1853-6. doi: 10.1126/science.1137603.
Differentiation of hepatic stellate cells (HSCs) to extracellular matrix- and growth factor-producing cells supports liver regeneration through promotion of hepatocyte proliferation. We show that the neurotrophin receptor p75NTR, a tumor necrosis factor receptor superfamily member expressed in HSCs after fibrotic and cirrhotic liver injury in humans, is a regulator of liver repair. In mice, depletion of p75NTR exacerbated liver pathology and inhibited hepatocyte proliferation in vivo. p75NTR-/- HSCs failed to differentiate to myofibroblasts and did not support hepatocyte proliferation. Moreover, inhibition of p75NTR signaling to the small guanosine triphosphatase Rho resulted in impaired HSC differentiation. Our results identify signaling from p75NTR to Rho as a mechanism for the regulation of HSC differentiation to regeneration-promoting cells that support hepatocyte proliferation in the diseased liver.
肝星状细胞(HSCs)向产生细胞外基质和生长因子的细胞分化,通过促进肝细胞增殖来支持肝脏再生。我们发现神经营养因子受体p75NTR,一种在人类肝纤维化和肝硬化损伤后的肝星状细胞中表达的肿瘤坏死因子受体超家族成员,是肝脏修复的调节因子。在小鼠中,p75NTR的缺失加剧了肝脏病理变化并在体内抑制了肝细胞增殖。p75NTR基因敲除的肝星状细胞无法分化为肌成纤维细胞,也不支持肝细胞增殖。此外,抑制p75NTR向小GTP酶Rho的信号传导会导致肝星状细胞分化受损。我们的研究结果确定了从p75NTR到Rho的信号传导是调节肝星状细胞分化为促进再生细胞的一种机制,这些细胞在患病肝脏中支持肝细胞增殖。