ArticleThe American journal of pathology2016
Inactivation of Tsc2 in Mesoderm-Derived Cells Causes Polycystic Kidney Lesions and Impairs Lung Alveolarization.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
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- mTOR/miR-142-3p/PRAS40 signaling cascade is critical for tuberous sclerosis complex-associated renal cystogenesis.Cellular & molecular biology letters · 2024Article
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- Defective mesenchymal Bmpr1a-mediated BMP signaling causes congenital pulmonary cysts.bioRxiv : the preprint server for biology · 2024Article
- Activation of mTOR signaling in adult lung microvascular progenitor cells accelerates lung aging.The Journal of clinical investigation · 2023Article
- Arginine depletion attenuates renal cystogenesis in tuberous sclerosis complex model.Cell reports. Medicine · 2023Article
- A Review of Signaling Transduction Mechanisms in Osteoclastogenesis Regulation by Autophagy, Inflammation, and Immunity.International journal of molecular sciences · 2022Review
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- Rheb1 protects against cisplatin-induced tubular cell death and acute kidney injury via maintaining mitochondrial homeostasis.Cell death & disease · 2020Article
- Inactivation ofAmerican journal of physiology. Renal physiology · 2019Article
- Alteration of cystic airway mesenchyme in congenital pulmonary airway malformation.Scientific reports · 2019Article
- Tsc1 ablation in Prx1 and Osterix lineages causes renal cystogenesis in mouse.Scientific reports · 2019Article
- Building and Regenerating the Lung Cell by Cell.Physiological reviews · 2019Review
- Renal disease in tuberous sclerosis complex: pathogenesis and therapy.Nature reviews. Nephrology · 2018Review
- Spatial and temporal changes in extracellular elastin and laminin distribution during lung alveolar development.Scientific reports · 2018Article
- A novel mouse model of anterior segment dysgenesis (ASD): conditional deletion ofDisease models & mechanisms · 2017Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The tuberous sclerosis complex (TSC) proteins are critical negative regulators of the mammalian/mechanistic target of rapamycin complex 1 pathway. Germline mutations of TSC1 or TSC2 cause TSC, affecting multiple organs, including the kidney and lung, and causing substantial morbidity and mortality. The mechanisms of organ-specific disease in TSC remain incompletely understood, and the impact of TSC inactivation on mesenchymal lineage cells has not been specifically studied. We deleted Tsc2 specifically in mesoderm-derived mesenchymal cells of multiple organs in mice using the Dermo1-Cre driver. The Dermo1-Cre-driven Tsc2 conditional knockout mice had body growth retardation and died approximately 3 weeks after birth. Significant phenotypes were observed in the postnatal kidney and lung. Inactivation of Tsc2 in kidney mesenchyme caused polycystic lesions starting from the second week of age, with increased cell proliferation, tubular epithelial hyperplasia, and epithelial-mesenchymal transition. In contrast, Tsc2 deletion in lung mesenchyme led to decreased cell proliferation, reduced postnatal alveolarization, and decreased differentiation with reduced numbers of alveolar myofibroblast and type II alveolar epithelial cells. Two major findings thus result from this model: inactivation of Tsc2 in mesoderm-derived cells causes increased cell proliferation in the kidneys but reduced proliferation in the lungs, and inactivation of Tsc2 in mesoderm-derived cells causes epithelial-lined renal cysts. Therefore, Tsc2-mTOR signaling in mesenchyme is essential for the maintenance of renal structure and for lung alveolarization.
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