Glomerular expression pattern of long non-coding RNAs in the type 2 diabetes mellitus BTBR mouse model

Reichelt-Wurm, Simone; Wirtz, Tobias; Chittka, Dominik; Lindenmeyer, Maja T.; Reichelt, Robert; Beck, Sebastian; Politis, Panagiotis K.; Charonis, Aristidis S.; Kretz, Markus; Huber, Tobias B.; Liu, Shuya; Banas, Bernhard; Banas, Miriam C.

doi:10.1038/s41598-019-46180-1

Cited by 7 publications

(7 citation statements)

References 51 publications

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“…Diabetic nephropathy (DN) is the leading cause of CKD and ESRD in the world [44,45]. A growing number of published studies suggest that lncRNAs play key roles in the development and progression of DN [46][47][48][49]. Interestingly, many lncRNAs were linked to mitochondrial function, highlighting the importance of mitochondrial dysfunction in progression of DN [46,49,50].…”

Section: Lncrna In Diabetic Nephropathymentioning

confidence: 99%

Long Noncoding RNAs and Their Therapeutic Promise in Diabetic Nephropathy

Coellar

Jiang

Danesh

2021

Nephron

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Recent advances in large-scale RNA sequencing and genome-wide profiling projects have unraveled a heterogeneous group of RNAs, collectively known as long noncoding RNAs (lncRNAs), which play central roles in many diverse biological processes. Importantly, an association between aberrant expression of lncRNAs and diverse human pathologies has been reported, including in a variety of kidney diseases. These observations have raised the possibility that lncRNAs may represent unexploited potential therapeutic targets for kidney diseases. Several important questions regarding the functionality of lncRNAs and their impact in kidney diseases, however, remain to be carefully addressed. Here, we provide an overview of the main functions and mechanisms of actions of lncRNAs, and their promise as therapeutic targets in kidney diseases, emphasizing on the role of some of the best-characterized lncRNAs implicated in the pathogenesis and progression of diabetic nephropathy.

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Section: Lncrna In Diabetic Nephropathymentioning

confidence: 99%

Long Noncoding RNAs and Their Therapeutic Promise in Diabetic Nephropathy

Coellar

Jiang

Danesh

2021

Nephron

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“…We obtained kidneys from different transgenic mouse models of DM: mice expressing a dominant-negative GIP receptor (GIPR dn ) which served as insulin-deficient DM type 1 model and black and tan brachyuric (BTBR) ob/ob mice, which represent a mouse model for DM type 2. The time points of kidney tissue harvesting were chosen to correspond to the early stages of DKD [ 22 , 23 , 24 , 25 , 26 ]. A distinct PLVAP signal was detectable in the glomeruli of GIPR dn transgenic mice ( Figure 1 ).…”

Section: Resultsmentioning

confidence: 99%

PLVAP as an Early Marker of Glomerular Endothelial Damage in Mice with Diabetic Kidney Disease

Wolf

Steglich

Kessel

et al. 2023

IJMS

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Plasmalemma vesicle-associated protein (PLVAP) is the main component of endothelial diaphragms in fenestrae, caveolae, and transendothelial channels. PLVAP is expressed in the adult kidney glomerulus upon injury. Glomerular endothelial injury is associated with progressive loss of kidney function in diabetic kidney disease (DKD). This study aimed to investigate whether PLVAP could serve as a marker for glomerular endothelial damage in DKD. Glomerular PLVAP expression was analyzed in different mouse models of DKD and their respective healthy control animals using automatic digital quantification of histological whole kidney sections. Transgenic mice expressing a dominant-negative GIP receptor (GIPRdn) in pancreatic beta-cells as a model for diabetes mellitus (DM) type 1 and black and tan brachyuric (BTBR) ob/ob mice, as a model for DM type 2, were used. Distinct PLVAP induction was observed in all diabetic models studied. Traces of glomerular PLVAP expression could be identified in the healthy control kidneys using automated quantification. Stainings for other endothelial injury markers such as CD31 or the erythroblast transformation-specific related gene (ERG) displayed no differences between diabetic and healthy groups at the time points when PLVAP was induced. The same was also true for the mesangial cells marker α8Integrin, while the podocyte marker nephrin appeared to be diminished only in BTBR ob/ob mice. Glomerular hypertrophy, which is one of the initial morphological signs of diabetic kidney damage, was observed in both diabetic models. These findings suggest that PLVAP is an early marker of glomerular endothelial injury in diabetes-induced kidney damage in mice.

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“…They can affect virtually every step of gene expression including pre- and post-transcriptional and -translational control, splicing, and genomic imprinting [ 20 , 21 ]. Research has revealed their relevance in development, cancer, and various diseases, like DKD [ 22 , 23 ] and renal fibrosis [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

The Interplay of NEAT1 and miR-339-5p Influences on Mesangial Gene Expression and Function in Various Diabetic-Associated Injury Models

Reichelt-Wurm

Pregler

Wirtz

et al. 2022

ncRNA

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Mesangial cells (MCs), substantial cells for architecture and function of the glomerular tuft, take a key role in progression of diabetic kidney disease (DKD). Despite long standing researches and the need for novel therapies, the underlying regulatory mechanisms in MCs are elusive. This applies in particular to long non-coding RNAs (lncRNA) but also microRNAs (miRNAs). In this study, we investigated the expression of nuclear paraspeckle assembly transcript 1 (NEAT1), a highly conserved lncRNA, in several diabetes in-vitro models using human MCs. These cells were treated with high glucose, TGFβ, TNAα, thapsigargin, or tunicamycin. We analyzed the implication of NEAT1 silencing on mesangial cell migration, proliferation, and cell size as well as on mRNA and miRNA expression. Here, the miRNA hsa-miR-339-5p was not only identified as a potential interaction partner for NEAT1 but also for several coding genes. Furthermore, overexpression of hsa-miR-339-5p leads to a MC phenotype comparable to a NEAT1 knockdown. In-silico analyses also underline a relevant role of NEAT1 and hsa-miR-339-5p in mesangial physiology, especially in the context of DKD.

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Glomerular expression pattern of long non-coding RNAs in the type 2 diabetes mellitus BTBR mouse model

Cited by 7 publications

References 51 publications

Long Noncoding RNAs and Their Therapeutic Promise in Diabetic Nephropathy

Long Noncoding RNAs and Their Therapeutic Promise in Diabetic Nephropathy

PLVAP as an Early Marker of Glomerular Endothelial Damage in Mice with Diabetic Kidney Disease

The Interplay of NEAT1 and miR-339-5p Influences on Mesangial Gene Expression and Function in Various Diabetic-Associated Injury Models

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