Association of Vascular Calcification with Serum lncRNA H19 and Runx2 mRNA Expression in Patients with Uremia.

Background: The objective of this study was to investigate the relationship between vascular calcification, serum lncRNA H19, and Runt-Related Transcription Factor 2 mRNA expression in patients with uremia.

Methods: This study is a retrospective study which recruited 146 patients with uremia on dialysis from December 2021 to November 2022. Participants were divided into the VC and non-VC groups based on their chest X-ray calcification ratings.

Hypomethylation of the LncRNA H19 promoter accelerates osteogenic differentiation of vascular smooth muscle cells by activating the Erk1/2 pathways.

Objective: Vascular calcification is a common chronic kidney disease complication. This study aimed to investigate the function of long non-coding RNA (LncRNA) H19 in vascular calcification to explore new therapeutic strategies.

Methods: We induced osteogenic differentiation and calcification of vascular smooth muscle cells (VSMCs) using β-glycerophosphate.

Interference of periostin attenuates pathological changes, proinflammatory markers and renal fibrosis in diabetic kidney injury.

Background: Diabetic nephropathy (DN) is a prevalent complication of diabetes, in which inflammation and fibrosis are the significant pathogenesis. Periostin is a matricellular protein that functions on stabilizing the extracellular matrix by binding to integrins during development. This study aimed to explored the role of periostin in DN.

LncTUG1 ameliorates renal tubular fibrosis in experimental diabetic nephropathy through the miR-145-5p/dual-specificity phosphatase 6 axis.

The renal interstitial fibrosis contributes to the progression and deterioration of diabetic nephropathy (DN). Long noncoding RNA taurine-up-regulated gene 1 (TUG1) in kidneys may be down-regulated by hyperglycemia. We aim to explore its role in tubular fibrosis caused by high glucose and the possible target genes of TUG1.

Zinc finger protein A20 regulates the development and progression of osteoarthritis by affecting the activity of NF-κB p65.

Objective: To investigate the role of Zinc finger protein A20 in osteoarthritis (OA) by regulating NF-κB p65.

Methods: and expressions in human OA cartilage samples were detected by qRT-PCR. IL-1β-induced chondrocyte was treated with A20 lentivirus activation particle, pyrrolidine dithiocarbamate (PDTC, a NF-κB inhibitor) with/without A20 siRNA.

Knockout of NGAL aggravates tubulointerstitial injury in a mouse model of diabetic nephropathy by enhancing oxidative stress and fibrosis.

Neutrophil gelatinase-associated lipocalin (NGAL), also called lipocalin 2, is considered a promising biomarker for acute and chronic kidney injuries. Several studies have demonstrated that its levels increase in plasma and urine in diabetic nephropathy (DN), and its urine concentration increases upon kidney function deterioration. However, its role in DN progression remains unclear.

Effects of hyperosmolality on expression of urea transporter A2 and aquaporin 2 in mouse medullary collecting duct cells.

In this study, the effects of hyperosmolality on the expression of urea transporter A2 (UTA2) and aquaporin 2 (AQP2) were investigated in transfected immortalized mouse medullary collecting duct (mIMCD3) cell line. AQP2-GFP-pCMV6 and UTA2-GFP-pCMV6 plasmids were stably transfected into mIMCD3 cells respectively. Transfected mIMCD3 and control cells were cultured in different hypertonic media, which were made by NaCl alone, urea alone, or an equiosmolar mixture of NaCl and urea.

PKCα regulates vasopressin-induced aquaporin-2 trafficking in mouse kidney collecting duct cells in vitro via altering microtubule assembly.

Aim: Aquaporin-2 (AQP2) is a vasopressin-regulated water channel located in the collecting tubule and collecting duct cells of mammalian kidney. The aim of this study is to investigate whether PKCα plays a role in vasopressin-induced AQP2 trafficking in mouse inner medullary collecting duct 3 (mIMCD3) cells.

Methods: AQP2-mIMCD3 stable cell line was constructed by transfection of mouse inner medullary collecting duct 3 (mIMCD3) cells with AQP2-GFP construct.