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Depletion of Flot1 attenuates macropinosome-dependent mTORC1 activation in podocytes
Yanan Li1, Yuxin He1, Longjiao Cheng1
1State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Frontiers Science Center for Cell Responses, Nankai University.
Abstract:
Podocytes are terminally differentiated renal epithelial cells that play a crucial role in kidney filtration. Given this essential function, podocyte dysfunction results in kidney diseases known as podocytopathies. Previous studies have demonstrated that maintaining the activation-deactivation balance of mechanistic target of rapamycin complex 1 (mTORC1) is vital for podocyte function. Podocyte-specific knockout (KO) mouse models revealed that abnormal mTORC1 activation leads to severe podocytopathy. Therefore, elucidating the mechanism underlying mTORC1 activation in podocytes may contribute to the development of treatments for certain podocytopathies. In our previous study, we showed that macropinocytosis-large-scale endocytosis-is involved in the molecular mechanism of mTORC1 activation in podocytes. Growth factor (GF) stimulation induces circular dorsal ruffles (CDRs), which are large membrane protrusions on the dorsal surface of podocytes. CDRs serve as precursors to macropinocytosis, generating vesicles called macropinosomes, which transport extracellular nutrients to lysosomes, thereby activating mTORC1. These findings suggest that CDRs-derived macropinosomes modulate the mTORC1 pathway. In the present study, we investigated the molecular mechanism underlying macropinosome formation in podocytes, focusing on flotillin-1 (Flot1), a protein enriched in lipid microdomains. Imaging analysis revealed the localization of Flot1 at CDRs, and Flot1 depletion reduced macropinosome formation. Biochemical analysis further demonstrated impaired GF-stimulated mTORC1 activation in Flot1-KO cells, which exhibited slower growth than control cells. Notably, immuno-staining analysis showed that Flot1 is expressed specifically in podocytes but not in other renal cells. These findings indicate that Flot1 participates in the formation of CDRs-derived macropinosomes and contributes to macropinosome-dependent mTORC1 activation in podocytes.Key words: Flot1, circular dorsal ruffles, macropinocytosis, mTORC1, podocytes.
Insights
Flotillin-1 (Flot1) is crucial for macropinosome formation and mechanistic target of rapamycin complex 1 (mTORC1) activation in kidney podocytes. This discovery offers new therapeutic targets for podocytopathies.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Biology
Background:
- Podocytes are vital for kidney filtration; their dysfunction causes podocytopathies.
- Maintaining mechanistic target of rapamycin complex 1 (mTORC1) activation balance is essential for podocyte function.
- Abnormal mTORC1 activation in podocytes leads to severe kidney disease.
Purpose of the Study:
- To investigate the molecular mechanism of macropinosome formation in podocytes.
- To elucidate the role of flotillin-1 (Flot1) in macropinosome formation and mTORC1 activation.
- To identify potential therapeutic targets for podocytopathies.
Main Methods:
- Imaging analysis to determine Flot1 localization at circular dorsal ruffles (CDRs).
- Macropinosome formation assays in Flot1-depleted podocytes.
- Biochemical analysis of mTORC1 activation in Flot1 knockout (KO) cells.
- Immunohistochemistry to assess Flot1 expression in renal cells.
Main Results:
- Flot1 localizes to CDRs, which are precursors to macropinocytosis.
- Flot1 depletion impairs macropinosome formation and growth factor-stimulated mTORC1 activation.
- Flot1 is specifically expressed in podocytes, not other kidney cells.
- Flot1-KO cells exhibit impaired growth compared to controls.
Conclusions:
- Flotillin-1 is a key mediator of CDR-derived macropinosome formation in podocytes.
- Flot1 contributes to macropinosome-dependent mTORC1 activation, crucial for podocyte function.
- Targeting Flot1 may offer a novel therapeutic strategy for podocytopathies.
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