School of Biomedical Engineering, Colorado State University, Fort Collins, Colorado.
Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois.
Toxicol Sci. 2020 Apr 1;174(2):266-277. doi: 10.1093/toxsci/kfaa003.
Primary human hepatocyte (PHH) cultures have become indispensable to mitigate the risk of adverse drug reactions in human patients. In contrast to dedifferentiating monocultures, coculture with nonparenchymal cells maintains PHH functions for 2-4 weeks. However, because the functional lifespan of PHHs in vivo is 200-400 days, it is desirable to further prolong PHH functions in vitro toward modeling chronic drug exposure and disease progression. Fasting has benefits on the longevity of organisms and the health of tissues such as the liver. We hypothesized that a culturing protocol that mimics dynamic fasting/starvation could activate starvation pathways and prolong PHH functional lifetime. To mimic starvation, serum and hormones were intermittently removed from the culture medium of micropatterned cocultures (MPCCs) containing PHHs organized onto collagen domains and surrounded by 3T3-J2 murine fibroblasts. A weekly 2-day starvation optimally prolonged PHH functional lifetime for 6+ weeks in MPCCs versus a decline after 3 weeks in nonstarved controls. The 2-day starvation also enhanced the functions of PHH monocultures for 2 weeks, suggesting direct effects on PHHs. In MPCCs, starvation activated 5' adenosine monophosphate-activated protein kinase (AMPK) and restricted fibroblast overgrowth onto PHH islands, thereby maintaining hepatic polarity. The effects of starvation on MPCCs were partially recapitulated by activating AMPK using metformin or growth arresting fibroblasts via mitomycin-C. Lastly, starved MPCCs demonstrated lower false positives for drug toxicity tests and higher drug-induced cytochrome-P450 activities versus nonstarved controls even after 5 weeks. In conclusion, intermittent serum/hormone starvation extends PHH functional lifetime toward enabling clinically relevant drug screening.
原代人肝细胞 (PHH) 培养已成为减轻人类患者药物不良反应风险的不可或缺手段。与去分化的单一培养物相比,与非实质细胞共培养可维持 PHH 功能 2-4 周。然而,由于 PHH 在体内的功能寿命为 200-400 天,因此理想情况下,需要在体外进一步延长 PHH 的功能,以模拟慢性药物暴露和疾病进展。禁食对生物体的寿命和肝脏等组织的健康都有益处。我们假设,一种模拟动态禁食/饥饿的培养方案可以激活饥饿途径并延长 PHH 的功能寿命。为了模拟饥饿,血清和激素被间歇性地从含有 PHH 的微图案共培养物 (MPCC) 的培养基中去除,这些 PHH 组织在胶原蛋白域上排列并被 3T3-J2 鼠成纤维细胞包围。每周 2 天的饥饿最优化地将 PHH 在 MPCC 中的功能寿命延长了 6 周以上,而在未饥饿对照中则在 3 周后下降。2 天的饥饿还增强了 PHH 单一培养物的功能 2 周,这表明对 PHH 有直接影响。在 MPCC 中,饥饿激活了 5' 腺苷一磷酸激活蛋白激酶 (AMPK),限制了成纤维细胞在 PHH 岛上的过度生长,从而维持了肝脏极性。使用二甲双胍或通过丝裂霉素 C 使成纤维细胞生长停滞来激活 AMPK,部分再现了饥饿对 MPCCs 的影响。最后,与未饥饿对照相比,饥饿的 MPCCs 在药物毒性试验中假阳性率较低,药物诱导的细胞色素 P450 活性较高,即使在 5 周后也是如此。总之,间歇性血清/激素饥饿可延长 PHH 的功能寿命,从而实现具有临床相关性的药物筛选。