Lehman John G, Causey Robert D, LaGrasta Cristina V, Ruff Albert L
US Army Medical Research Institute of Chemical Defense.
US Army Medical Research Institute of Chemical Defense;
J Vis Exp. 2018 Jun 16(136):57372. doi: 10.3791/57372.
Toxicant-induced ocular injury is a true ocular emergency because chemicals have the potential to rapidly inflict significant tissue damage. Treatments for toxicant-induced corneal injury are generally supportive as no specific therapeutics exist to treat these injuries. In the efforts to develop treatments and therapeutics to care for exposure, it can be important to understand the molecular and cellular mechanisms of these injuries. We propose that utilization of high throughput small inhibitory RNA (siRNA) screening can be an important tool that could help to more rapidly elucidate the molecular mechanisms of chemical cornea epithelial injury. siRNA are double stranded RNA molecules that are 19-25 nucleotides long and utilize the post-transcriptional gene silencing pathway to degrade mRNA which have homology to the siRNA. The resulting reduction of expression of the specific gene can then be studied in toxicant exposed cells to ascertain the function of that gene in the cellular response to the toxicant. The development and validation of in vitro exposure models and methods for the high throughput screening (HTS) of hydrogen fluoride- (HF) and chloropicrin- (CP) induced ocular injury are presented in this article. Although we selected these two toxicants, our methods are applicable to the study of other toxicants with minor modifications to the toxicant exposure protocol. The SV40 large T antigen immortalized human corneal epithelial cell line SV40-HCEC was selected for study. Cell viability and IL-8 production were selected as endpoints in the screening protocol. Several challenges associated with the development of toxicant exposure and cell culture methods suitable for HTS studies are presented. The establishment of HTS models for these toxicants allows for further studies to better understand the mechanism of injury and to screen for potential therapeutics for chemical ocular injury.
毒物引起的眼损伤是真正的眼科急症,因为化学物质有可能迅速造成严重的组织损伤。由于不存在治疗这些损伤的特异性疗法,毒物引起的角膜损伤的治疗通常是支持性的。在努力开发治疗方法以应对暴露情况时,了解这些损伤的分子和细胞机制可能很重要。我们提出,利用高通量小干扰RNA(siRNA)筛选可能是一种重要工具,有助于更快速地阐明化学性角膜上皮损伤的分子机制。siRNA是长度为19 - 25个核苷酸的双链RNA分子,利用转录后基因沉默途径降解与siRNA具有同源性的mRNA。然后可以在暴露于毒物的细胞中研究特定基因表达的降低情况,以确定该基因在细胞对毒物反应中的功能。本文介绍了用于氟化氢(HF)和氯化苦(CP)诱导的眼损伤高通量筛选(HTS)的体外暴露模型和方法的开发与验证。尽管我们选择了这两种毒物,但我们的方法只需对毒物暴露方案进行微小修改,就适用于其他毒物的研究。选择SV40大T抗原永生化的人角膜上皮细胞系SV40 - HCEC进行研究。在筛选方案中选择细胞活力和白细胞介素 - 8产生作为终点指标。本文还介绍了与开发适用于HTS研究的毒物暴露和细胞培养方法相关的几个挑战。建立这些毒物的HTS模型有助于进一步研究,以更好地了解损伤机制并筛选化学性眼损伤的潜在治疗方法。