Ectopic expression of Thy-1 in the kidneys of transgenic mice induces functional and proliferative abnormalities

Kollias, George; Evans, David J.; Ritter, Mary A.; Beech, J. N.; Morris, Roger J.; Grosveld, Frank

doi:10.1016/0092-8674(87)90006-7

Cited by 64 publications

(34 citation statements)

References 28 publications

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“…6B) detected mRNA in normal spleen, thymus, and brain of (C57BL x CBA) mice. RNA of a similar size was detected in the brain and thymus of transgenic mice (35) and the transgenic kidney cell line GRK (34). Normalization of the values for the specific activities of probes Ia and Ib showed that exon lb is present in less than 5% of the total mRNA.…”

Section: Methodsmentioning

confidence: 76%

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Transcriptional unit of the murine Thy-1 gene: different distribution of transcription initiation sites in brain.

Spanopoulou¹,

Giguère²,

Grosveld³

1988

Mol. Cell. Biol.

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Structural analysis of the mouse Thy-1.2 gene has shown that the major promoter of the gene is characterized by a tissue-specific DNase I-hypersensitive site and is located within a methylation-free island. The gene is regulated at the transcriptional level, and steady-state mRNA analysis reveals that the previously reported exon Ib contributes at most 5% of the total mRNA. The major promoter uses several transcription initiation sites within a region of 100 base pairs. The frequency of usage of these sites in brain is markedly different from that in other tissues.

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Section: Methodsmentioning

confidence: 76%

“…Moreover, transgenic mice were shown to develop either a lymphoid hyperplasia or a proliferative kidney disorder as a result of an augmented ectopic expression of the Thy-1 gene in either progenitor B cells (15) or the kidney tubuli, respectively (34). The structure of the Thy-1 gene is as interesting as its expression pattern.…”

mentioning

confidence: 99%

Transcriptional unit of the murine Thy-1 gene: different distribution of transcription initiation sites in brain.

Spanopoulou¹,

Giguère²,

Grosveld³

1988

Mol. Cell. Biol.

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“…Kollias [42]. In 2002, Assman et al established an inducible model of FSGS in heterozygous animals by the injection of anti-Thy-1.1 monoclonal antibodies.…”

Section: Thy-11 Transgenic Mouse Modelmentioning

confidence: 99%

Recent advances of animal model of focal segmental glomerulosclerosis

Yang

Dettmar

Kronbichler³

et al. 2018

Clin Exp Nephrol

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In the last decade, great advances have been made in understanding the genetic basis for focal segmental glomerulosclerosis (FSGS). Animal models using specific gene disruption of the slit diaphragm and cytoskeleton of the foot process mirror the etiology of the human disease. Many animal models have been developed to understand the complex pathophysiology of FSGS. Therefore, we need to know the usefulness and exact methodology of creating animal models. Here, we review classic animal models and newly developed genetic animal models. Classic animal models of FSGS involve direct podocyte injury and indirect podocyte injury due to adaptive responses. However, the phenotype depends on the animal background. Renal ablation and direct podocyte toxin (PAN, adriamycin) models are leading animal models for FSGS, which have some limitations depending on mice background. A second group of animal models were developed using combinations of genetic mutation and toxin, such as NEP25, diphtheria toxin, and Thy1.1 models, which specifically injure podocytes. A third group of animal models involves genetic engineering techniques targeting podocyte expression molecules, such as podocin, CD2-associated protein, and TRPC6 channels. More detailed information about podocytopathy and FSGS can be expected in the coming decade. Different animal models should be used to study FSGS depending on the specific aim and sometimes should be used in combination.

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“…For studies in the CG model, the PEC-rtTA/ LC1/R26R mice were mated to the Thy-1.1 transgenic mouse line (T6 clone). 37 (B) Genetic labeling of PECs using doxycycline at the age of 4 wk in triple transgenic PEC-rtTA/LC1/R26R mice. After induction, Cre recombination occurred in more than 70% of all PECs (arrowheads, labeled PEC).…”

Section: De Novo Expression Of Cd44 In Activated Parietal Cellsmentioning

confidence: 99%

Tracing the Origin of Glomerular Extracapillary Lesions from Parietal Epithelial Cells

Smeets¹,

Uhlig²,

Fuss³

et al. 2009

Journal of the American Society of Nephrology

219

237

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Cellular lesions form in Bowman's space in both crescentic glomerulonephritis and collapsing glomerulopathy. The pathomechanism and origin of the proliferating cells in these lesions are unknown. In this study, we examined proliferating cells by lineage tracing of either podocytes or parietal epithelial cells (PECs) in the nephrotoxic nephritis model of inflammatory crescentic glomerulonephritis. In addition, we traced the fate of genetically labeled PECs in the Thy-1.1 transgenic mouse model of collapsing glomerulopathy. In both models, cellular bridges composed of PECs were observed between Bowman's capsule and the glomerular tuft. Genetically labeled PECs also populated larger, more advanced cellular lesions. In these lesions, we detected de novo expression of CD44 in activated PECs. In contrast, we rarely identified genetically labeled podocytes within the cellular lesions of crescentic glomerulonephritis. In conclusion, PECs constitute the majority of cells that compose early extracapillary proliferative lesions in both crescentic glomerulonephritis and collapsing glomerulopathy, suggesting similar pathomechanisms in both diseases.

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Ectopic expression of Thy-1 in the kidneys of transgenic mice induces functional and proliferative abnormalities

Cited by 64 publications

References 28 publications

Transcriptional unit of the murine Thy-1 gene: different distribution of transcription initiation sites in brain.

Transcriptional unit of the murine Thy-1 gene: different distribution of transcription initiation sites in brain.

Recent advances of animal model of focal segmental glomerulosclerosis

Tracing the Origin of Glomerular Extracapillary Lesions from Parietal Epithelial Cells

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