The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease

Jianbing，Hao1; Xiaotian，Liu2; Jie，Tang3; Xueying，Chang3; Honge，Jin2; Bo，Zhu3; Lirong，Hao1; Lei，Zhang3

2022

10.1155/2022/1668000

Oxidative Medicine and Cellular Longevity   影响因子和分区

1942-0900

1942-0994

Increasing evidence suggests that disorders of inflammation, oxidative stress, and autophagy contribute to the pathogenesis of diabetic kidney disease (DKD). This study attempted to clarify the effect of allograft inflammatory factor-1 (AIF-1), miR-34a, and ATG4B on inflammation, oxidative stress, and autophagy in DKD both in vitro and in vivo experiments. In vivo, it was found that the levels of AIF-1, miR-34a, oxidative stress, and inflammatory factors were significantly increased in blood and urine samples of DKD patients and mouse models and correlated with the level of urinary protein. In vitro, it was also found that the expressions of AIF-1, miR-34a, ROS, and inflammatory factors were increased, while ATG4B and other autophagy related proteins were decreased in human renal glomerular endothelial cells (HRGECs) cultured with high concentration glucose medium (30 mmol/L). When AIF-1 gene was overexpressed, the levels of miR-34a, ROS, and inflammatory factors were significantly upregulated, and autophagy-related proteins such as ATG4B were downregulated, while downregulation of AIF-1 gene had the opposite effect. In addition, miR-34a inhibited the expression of ATG4B and autophagy-related proteins and increased the levels of ROS and inflammation. Furthermore, the result of luciferase reporter assay suggested that ATG4B was the target gene of miR-34a. When ATG4B gene was overexpressed, the level of autophagy was upregulated, and inflammatory factors were downregulated. Conversely, when ATG4B gene was inhibited, the level of autophagy was downregulated, and inflammatory factors were upregulated. Then, autophagy inducers inhibited the levels of inflammation and ROS, whereas autophagy inhibitors had the opposite function in HRGECs induced by glucose (30 mmol/L). In conclusion, the above data suggested that AIF-1 regulated the levels of inflammation, oxidative stress, and autophagy in HRGECs via miR-34a/ATG4B pathway to contribute to the pathogenesis of diabetic kidney disease.

SCI ; EI

英语

第一 ; 通讯

Heilongjiang Province Postdoctoral Science Foundation[LBH-Z18180] ; Scientific Research Project of Heilongjiang Provincial Health and Family Planning Commission[2017-019] ; Sanming project of medicine in Shenzhen Nanshan[SZSM202103002] ; foundation of Shenzhen science and innovation committee[202103243001365]

Cell Biology

Cell Biology

WOS:000880432200001

HINDAWI LTD

20224613113422

Cell death ; Genes ; Glucose ; Oxidative stress ; Pathology ; Proteins

Biological Materials and Tissue Engineering:461.2 ; Medicine and Pharmacology:461.6 ; Biology:461.9 ; Organic Compounds:804.1

2-s2.0-85141714807

Scopus

1.Department of Nephropathy and Hemodialysis,Southern University of Science and Technology Hospital,Shenzhen,518055,China
2.Department of Neurology,The Third Affiliated Hospital of Heilongjiang University of Chinese Medicine,Harbin,150040,China
3.Department of Blood Purification,The First Affiliated Hospital of Harbin Medical University,Harbin,150001,China

Jianbing，Hao,Xiaotian，Liu,Jie，Tang,et al. The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease[J]. Oxidative Medicine and Cellular Longevity,2022,2022.

Jianbing，Hao.,Xiaotian，Liu.,Jie，Tang.,Xueying，Chang.,Honge，Jin.,...&Lei，Zhang.(2022).The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease.Oxidative Medicine and Cellular Longevity,2022.

Jianbing，Hao,et al."The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease".Oxidative Medicine and Cellular Longevity 2022(2022).