000 | 03377 am a22004933u 4500 | ||
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042 | _adc | ||
100 | 1 | 0 |
_aMelica, Maria Elena _eauthor _92055 |
700 | 1 | 0 |
_aAntonelli, Giulia _eauthor _92056 |
700 | 1 | 0 |
_aSemeraro, Roberto _eauthor _92057 |
700 | 1 | 0 |
_aAngelotti, Maria Lucia _eauthor _92058 |
700 | 1 | 0 |
_aLugli, Gianmarco _eauthor _92059 |
700 | 1 | 0 |
_aLandini, Samuela _eauthor _92060 |
700 | 1 | 0 |
_aRavaglia, Fiammetta _eauthor _92061 |
700 | 1 | 0 |
_aLa Regina, Gilda _eauthor _92062 |
700 | 1 | 0 |
_aConte, Carolina _eauthor _92063 |
700 | 1 | 0 |
_aDe Chiara, Letizia _eauthor _92064 |
700 | 1 | 0 |
_aPeired, Anna Julie _eauthor _92065 |
700 | 1 | 0 |
_aMazzinghi, Benedetta _eauthor _92066 |
700 | 1 | 0 |
_aDonati, Marta _eauthor _92067 |
700 | 1 | 0 |
_aMolli, Alice _eauthor _92068 |
700 | 1 | 0 |
_aSteiger, Stefanie _eauthor _92069 |
700 | 1 | 0 |
_aMagi, Alberto _eauthor _92070 |
700 | 1 | 0 |
_aBartalucci, Niccolò _eauthor _92071 |
700 | 1 | 0 |
_aRaglianti, Valentina _eauthor _92072 |
700 | 1 | 0 |
_aGuzzi, Francesco _eauthor _92073 |
700 | 1 | 0 |
_aMaggi, Laura _eauthor _92074 |
700 | 1 | 0 |
_aAnnunziato, Francesco _eauthor _92075 |
700 | 1 | 0 |
_aBurger, Alexa _eauthor _92076 |
700 | 1 | 0 |
_aLazzeri, Elena _eauthor _92077 |
700 | 1 | 0 |
_aAnders, Hans-Joachim _eauthor _92078 |
700 | 1 | 0 |
_aLasagni, Laura _eauthor _92079 |
700 | 1 | 0 |
_aRomagnani, Paola _eauthor _92080 |
245 | 0 | 0 | _aCrescents derive from single podocyte progenitors and a drug enhancing their differentiation attenuates crescentic glomerulonephritis* |
260 | _c2022-08-10. | ||
500 | _a/pmc/articles/PMC7614034/ | ||
500 | _a/pubmed/35947676 | ||
520 | _aCrescentic glomerulonephritis is characterized by vascular necrosis and the formation of parietal epithelial cell (PEC) hyperplasia, but little is known about the molecular mechanisms driving this process. Inducing crescentic glomerulonephritis in several Pax2Cre reporter mouse lines revealed that crescents derive from clonal expansion of single immature PECs. Preemptive and delayed histone deacetylase inhibition with panobinostat, a drug used for the treatment of hematopoietic stem cell disorders, attenuated crescentic glomerulonephritis, and recovered kidney function. 3D confocal microscopy and STED super-resolution imaging of glomeruli showed that, in addition to exerting an anti-inflammatory and immunosuppressive effect, panobinostat turned the uncontrolled hyperplasia of a specific immature PEC subset into a controlled differentiation into podocytes thereby restoring the injured glomerular filtration barrier. Single cell RNA sequencing of human renal progenitor cultures identified an immature stratifin+ subset and expansion of a stratifin-expressing progenitor in human crescentic glomerulonephritis was associated with a poor outcome. Treatment of human PECs with panobinostat attenuated stratifin expression in podocyte progenitors, reduced their proliferation but promoted their differentiation into podocytes. These results offer mechanistic insights into the formation of glomerular crescents and demonstrate that selective targeting of progenitors can attenuate crescent formation and the deterioration of kidney function in crescentic glomerulonephritis. | ||
540 | _a | ||
546 | _aen | ||
690 | _aArticle | ||
655 | 7 |
_aText _2local |
|
786 | 0 | _nSci Transl Med | |
856 | 4 | 1 |
_uhttp://dx.doi.org/10.1126/scitranslmed.abg3277 _zConnect to this object online. |
999 |
_c870 _d870 |