Khalaf Fatimah K, Mohammed Chrysan J, Dube Prabhatchandra, Connolly Jacob A, Lad Apurva, Ashraf Usman M, Breidenbach Joshua D, Su Robin C, Kleinhenz Andrew L, Malhotra Deepak, Gohara Amira F, Haller Steven T, Kennedy David J
Department of Medicine, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43606, USA.
Department of Clinical Pharmacy, University of Alkafeel, Najaf 54001, Iraq.
Antioxidants (Basel). 2022 Apr 30;11(5):900. doi: 10.3390/antiox11050900.
Papraoxonase-1 (PON1) is a hydrolytic lactonase enzyme that is synthesized in the liver and circulates attached to high-density lipoproteins (HDL). Clinical studies have demonstrated an association between diminished PON-1 and the progression of chronic kidney disease (CKD). However, whether decreased PON-1 is mechanistically linked to renal injury is unknown. We tested the hypothesis that the absence of PON-1 is mechanistically linked to the progression of renal inflammation and injury in CKD. Experiments were performed on control Dahl salt-sensitive rats (SSMcwi, hereafter designated SS rats) and Pon1 knock-out rats (designated SS-Pon1em1Mcwi, hereafter designated SS-PON-1 KO rats) generated by injecting a CRISPR targeting the sequence into SSMcwi rat embryos. The resulting mutation is a 7 bp frameshift insertion in exon 4 of the PON-1 gene. First, to examine the renal protective role of PON-1 in settings of CKD, ten-week-old, age-matched male rats were maintained on a high-salt diet (8% NaCl) for up to 5 weeks to initiate the salt-sensitive hypertensive renal disease characteristic of this model. We found that SS-PON-1 KO rats demonstrated several hallmarks of increased renal injury vs. SS rats including increased renal fibrosis, sclerosis, and tubular injury. SS-PON-1 KO also demonstrated increased recruitment of immune cells in the renal interstitium, as well as increased expression of inflammatory genes compared to SS rats (all p < 0.05). SS-PON-1 KO rats also showed a significant (p < 0.05) decline in renal function and increased renal oxidative stress compared to SS rats, despite no differences in blood pressure between the two groups. These findings suggest a new role for PON-1 in regulating renal inflammation and fibrosis in the setting of chronic renal disease independent of blood pressure.
对氧磷酶-1(PON1)是一种水解性内酯酶,在肝脏中合成,并与高密度脂蛋白(HDL)结合在血液循环中。临床研究表明,PON-1水平降低与慢性肾脏病(CKD)的进展之间存在关联。然而,PON-1降低是否在机制上与肾损伤相关尚不清楚。我们检验了以下假设:PON-1缺失在机制上与CKD中肾炎症和损伤的进展相关。实验在对照Dahl盐敏感大鼠(SSMcwi,以下简称SS大鼠)和通过将靶向该序列的CRISPR注射到SSMcwi大鼠胚胎中产生的Pon1基因敲除大鼠(命名为SS-Pon1em1Mcwi,以下简称SS-PON-1 KO大鼠)上进行。产生的突变是PON-1基因外显子4中的7个碱基对移码插入。首先,为了研究PON-1在CKD情况下的肾保护作用,将10周龄、年龄匹配的雄性大鼠维持在高盐饮食(8%氯化钠)中长达5周,以引发该模型特有的盐敏感性高血压肾病。我们发现,与SS大鼠相比,SS-PON-1 KO大鼠表现出肾损伤增加的几个特征,包括肾纤维化、硬化和肾小管损伤增加。与SS大鼠相比,SS-PON-1 KO还表现出肾间质中免疫细胞募集增加,以及炎症基因表达增加(所有p<0.05)。尽管两组之间血压没有差异,但与SS大鼠相比,SS-PON-1 KO大鼠的肾功能也显著下降(p<0.05),肾氧化应激增加。这些发现表明,PON-1在慢性肾病情况下调节肾炎症和纤维化方面具有独立于血压的新作用。