Niban protein regulates apoptosis in HK-2 cells via caspase-dependent pathway

Abstract

Purpose: To investigate whether Niban protein plays a role in renal interstitial fibrosis by regulating renal tubular epithelial cell apoptosis and explore the underlying mechanism. Methods: Unilateral ureteral obstruction (UUO) model was performed in C57B/6J mice, and divided into sham operation group and groups of days 3, days 7, and days 14. Niban expression was detected by immunohistochemistry and Western blot. TUNEL assays were used to detected apoptosis. Niban siRNA and overexpression Niban plasmid were transfected in HK-2 cells respectively to explore apoptosis related mechanisms of Niban during angiotensin II (AngII)and endoplasmic reticulum (ER) stress-induced injury. Results: With the development of obstruction, Niban's expression decreased gradually while apoptosis increased. Silencing of Niban not only increased the AngII-and ER stress-induced apoptosis, but also promoted the expression of caspase 8, caspase 9, Bip, and Chop. Overexpression of Niban reduced AngII-induced apoptosis and the expression of caspase 8 and caspase 9. Conclusions: Niban protein is involved in apoptosis regulation in HK-2 cells, and most likely via caspase-dependent pathway.

TUNEL Assay: A Powerful Tool for Kidney Injury Evaluation

“…Mixed acute-and-chronic injury, where toxic exposures, disease states, and/or assessments were both acute (i.e., hours, days) and chronic (i.e., weeks, months, years) in the same study, were observed in human transplant rejection (biopsy 1 week to 3 years post-transplant) [ 88 ], swine hepatitis E virus infection (7 and 14 days post-inoculation) [ 52 ], CO 2 pneumoperitoneum-induced stress in hydronephrotic kidneys (2 weeks hydronephrosis, 2 days post-pneumoperitoneum) [ 53 ], mesangial proliferative glomerulonephritis induced by snake venom (1 to 14 days post-injection) [ 99 ], unilateral ureteral obstruction (1 to 14 days of obstruction) [ 100 ], uranyl acetate exposure (1 to 28 days of exposure) [ 101 ], aristocholic acid nephropathy (5 and 30-day daily exposure) [ 102 ], and neonatal hyperoxia (tested 1 to 60 postnatal days, exposed to hyperoxia first 14 days) [ 103 ]. Fourteen days after impact is a very common assessment time point for these kinds of kidney injuries [ 52 , 53 , 99 , 101 , 103 ].…”

“…This is perhaps because cells are considered dead independent of the intensity of the TUNEL signal, as a cell cannot be “more dead” if the TUNEL staining is more intense. Although it is difficult to compare studies that use a wide variety of methods to quantify TUNEL results, the amount of TUNEL-positive cells in control animals is usually below 2% [ 75 , 99 , 100 , 116 , 126 ]. Acute injury is associated with a ~5–40× increase in TUNEL-positivity [ 79 , 126 , 127 ].…”

Differences in Cell-Intrinsic Inflammatory Programs of Yolk Sac and Bone Marrow Macrophages

“…Additionally, in BM Hoxb8 macrophages we identified an increased abundance of apoptosis-associated genes, such as Tgm2 , which promotes leukocyte apoptosis [ 19 ]. Fam129a encodes for the apoptosis-regulating protein Niban [ 20 , 21 ], which has recently been identified in human atherosclerotic plaques in a macrophage subpopulation and gives strong indications of being of BM origin [ 22 ].…”

Transcriptomic characterization of dying hair cells in the avian cochlea

“…Four of these genes were identified as significantly upregulated in D1T: TRIM35, BRCA2, IFIH1, and ATP4B (Figure 5). Additional genes in cluster 4 include FAM129A, a gene expressed in the early stage of apoptosis (Tang et al, 2019), and nebulin-like 1 (NEBL1) that regulates the stability and length of actin filaments (Moncman and Wang, 1995). CEMIP, a gene encoding a secreted hyaluronidase, was also transiently upregulated.…”