3D kidney organoids for bench-to-bedside translation

Gupta, Navin; Dilmen, Emre; Morizane, Ryuji

doi:10.1007/s00109-020-01983-y

Cited by 22 publications

(19 citation statements)

References 82 publications

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“…changes in DNA methylation and chromatin organization, in the developing kidney. Although we have gained many insights from mouse studies, additional studies are preferably conducted in human kidney models, given the recently described differences between human and mouse developmental programs during nephrogenesis [42,62].…”

Section: Directions For Future Researchmentioning

confidence: 99%

“…Since such a model may not recapitulate the crucial effects of TRIM28 loss during the earliest stages of nephrogenesis, TRIM28‐deficient human pluripotent stem cells (hPSCs) could be an interesting alternative. We speculate that differentiation of these hPSCs into kidney organoids will enable us to study the consequences of TRIM28 loss during the earliest stages of nephrogenesis, which is not possible in patient‐derived organoids [62]. By additionally knocking out REST and AMER1 , more insight into potential TRIM28–REST and TRIM28–AMER1 regulatory effects may also be provided.…”

Section: Directions For Future Researchmentioning

confidence: 99%

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TRIM28 variants and Wilms' tumour predisposition

Hol

Diets

Krijger

et al. 2021

The Journal of Pathology

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TRIM28 was recently identified as a Wilms' tumour (WT) predisposition gene, with germline pathogenic variants identified in around 1% of isolated and 8% of familial WT cases. TRIM28 variants are associated with epithelial WT, but the presence of other tumour components or anaplasia does not exclude the presence of a germline or somatic TRIM28 variant. In children with WT, TRIM28 acts as a classical tumour suppressor gene, with both alleles generally disrupted in the tumour. Therefore, loss of TRIM28 (KAP1/TIF1beta) protein expression in tumour tissue by immunohistochemistry is an effective strategy to identify patients carrying pathogenic TRIM28 variants. TRIM28 is a ubiquitously expressed corepressor that binds transcription factors in a context‐, species‐, and cell‐type‐specific manner to control the expression of genes and transposable elements during embryogenesis and cellular differentiation. In this review, we describe the inheritance patterns, histopathological and clinical features of TRIM28‐associated WT, as well as potential underlying mechanisms of tumourigenesis during embryonic kidney development. Recognizing germline TRIM28 variants in patients with WT can enable counselling, genetic testing, and potential early detection of WT in other children in the family. A further exploration of TRIM28‐associated WT will help to unravel the diverse and complex mechanisms underlying WT development. © 2021 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.

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Section: Directions For Future Researchmentioning

confidence: 99%

Section: Directions For Future Researchmentioning

confidence: 99%

TRIM28 variants and Wilms' tumour predisposition

Hol

Diets

Krijger

et al. 2021

The Journal of Pathology

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“…The kidney plays a major role in the filtration of various molecules and homeostasis regulation (Gupta et al, 2020). Nephrons, the functional units of the kidney, consist of Bowman's capsule glomerulus, and tubules, such as the proximal and distal convoluted tubules and loop of Henle.…”

Section: Convoluted Renal Proximal Tubule Models With Vascular Interfacesmentioning

confidence: 99%

3D Bioprinting-Based Vascularized Tissue Models Mimicking Tissue-Specific Architecture and Pathophysiology for in vitro Studies

Hwang

Choi

Jang

2021

Front. Bioeng. Biotechnol.

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A wide variety of experimental models including 2D cell cultures, model organisms, and 3D in vitro models have been developed to understand pathophysiological phenomena and assess the safety and efficacy of potential therapeutics. In this sense, 3D in vitro models are an intermediate between 2D cell cultures and animal models, as they adequately reproduce 3D microenvironments and human physiology while also being controllable and reproducible. Particularly, recent advances in 3D in vitro biomimicry models, which can produce complex cell structures, shapes, and arrangements, can more similarly reflect in vivo conditions than 2D cell culture. Based on this, 3D bioprinting technology, which enables to place the desired materials in the desired locations, has been introduced to fabricate tissue models with high structural similarity to the native tissues. Therefore, this review discusses the recent developments in this field and the key features of various types of 3D-bioprinted tissues, particularly those associated with blood vessels or highly vascularized organs, such as the heart, liver, and kidney. Moreover, this review also summarizes the current state of the three categories: (1) chemical substance treatment, (2) 3D bioprinting of lesions, and (3) recapitulation of tumor microenvironments (TME) of 3D bioprinting-based disease models according to their disease modeling approach. Finally, we propose the future directions of 3D bioprinting approaches for the creation of more advanced in vitro biomimetic 3D tissues, as well as the translation of 3D bioprinted tissue models to clinical applications.

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“…HC: They can make organoids from tissues that we cannot, central nervous system [11] in particular, also kidney [12,13].…”

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confidence: 99%